Original Article
Cyclosporine-Induced Sympathetic Activation and Hypertension after Heart Transplantation
N Engl J Med 1990; 323:693-699September 13, 1990
- Abstract
- Abstract
Background.
Hypertension is a frequent complication of cyclosporine-induced immunosuppression, but the underlying mechanism is unknown. In anesthetized animals, the administration of cyclosporine increases sympathetic-nerve discharge, which may contribute to hypertension.
Methods.
To determine whether cyclosporine-induced hypertension is accompanied by sustained sympathetic neural activation in patients, we recorded sympathetic action potentials using intraneural microelectrodes (in the peroneal nerve) in heart-transplant recipients receiving azathioprine and prednisone alone (n = 5) or in combination with cyclosporine (n = 14). We performed the same studies in eight patients with myasthenia gravis who were receiving cyclosporine and eight who were not, in five patients with essential hypertension, and in nine normal controls.
Results.
Heart-transplant recipients receiving cyclo-sporine had higher mean arterial blood pressure (±SE) than those not receiving cyclosporine (112±3 vs. 96±4 mm Hg; P<0.05) and a 2.7-fold higher rate of sympathetic-nerve firing (80±3 vs. 30±4 bursts per minute; P<0.05). For patients with myasthenia gravis, similar doses of cyclosporine were associated with smaller elevations in mean arterial blood pressure (100±2 mm Hg, as compared with 91 ±4 mm Hg in those not receiving cyclosporine; P<0.05) and in the rate of sympathetic-nerve firing (46±3 bursts per minute, as compared with 25±4 bursts per minute; P<0.05). Sympathetic activity in patients with heart transplants or myasthenia gravis who were not being treated with cyclosporine was no different from that in patients with essential hypertension or in normal controls.
Conclusions.
Cyclosporine-induced hypertension is associated with sympathetic neural activation, which may be accentuated by the cardiac denervation that results from heart transplantation. (N Engl J Med 1990; 323: 693–9.)
Media in This Article
Figure 1
Recordings of Muscle Sympathetic-Nerve Activity in a Heart-Transplant Recipient Taking Cyclosporine, a Heart-Transplant Recipient Not Taking Cyclosporine, a Patient with Essential Hypertension, and a Normotensive Control Subject.Figure 2
Recordings of Muscle Sympathetic-Nerve Activity in One Patient with Myasthenia Gravis Obtained during Treatment with Cyclosporine and Three Months after Cyclosporine Had Been Replaced by Placebo.Article Activity
- Article
GYCLOSPORINE is a novel immunosuppressive agent that has greatly enhanced long-term survival after organ transplantation1 and has proved beneficial in the treatment of many autoimmune diseases.2 3 4 5 However, cyclosporine has also produced a new form of hypertension.1 , 6 , 7 The hypertensive effect of cyclosporine has been demonstrated most vividly in heart-transplant recipients, in whom the incidence of hypertension has increased from less than 20 percent in the precyclosporine era to more than 90 percent currently. 1 , 8 9 10 This hypertension typically is moderate to severe and often requires treatment with a number of antihypertensive agents. Thus, hypertension has become one of the most important problems in the medical care of heart-transplant recipients. Although this form of hypertension has been attributed directly to the administration of cyclosporine, the underlying mechanism is unknown.
In anesthetized animals, the short-term administration of cyclosporine stimulates sympathetic-nerve discharge.11 , 12 In heart-transplant recipients, this sympathoexcitatory effect of cyclosporine may be accentuated because cardiac transplantation interrupts the afferent (as well as efferent) neural connections from the transplanted ventricles to the central nervous system and thus removes ventricular-baroreceptor restraint on sympathetic outflow.13 , 14
Accordingly, the aims of this study were to determine whether the long-term administration of cyclosporine causes sustained sympathetic neural activation in humans and whether this effect is evident mainly in heart-transplant recipients, who have ventricular-baroreceptor denervation. To accomplish these aims, we performed microelectrode recordings of postganglionic sympathetic action potentials in heart-transplant recipients (denervated hearts) and in patients with myasthenia gravis (innervated hearts) undergoing immunosuppressive treatment with azathioprine and prednisone alone or in combination with cyclosporine.
Methods
Selection of Subjects
Four groups of subjects were studied: heart-transplant recipients, patients with myasthenia gravis, patients with essential hypertension, and control subjects. We studied 14 heart-transplant recipients who were being treated with azathioprine and prednisone plus cyclosporine (transplantations performed at either the University of Wisconsin at Madison or the University of Texas Southwestern Medical Center at Dallas) and 5 heart-transplant recipients who were being treated with azathioprine and prednisone alone and had never received cyclosporine (transplantations performed at either the Medical College of Virginia or the McGuire Veterans Affairs Medical Center in Richmond). We studied 14 patients with myasthenia gravis who were enrolled in a randomized, double-blind, crossover trial of cyclosporine and placebo. During the study period, one patient was switched from cyclosporine to placebo, and another patient from placebo to cyclosporine. We also studied five patients with uncomplicated essential hypertension and nine healthy, normotensive, middle-aged control subjects. The mean (±SE) ages of the four groups of subjects were similar: 47±4, 46±6, 49±2, and 45±3 years. The protocol was approved by the institutional review board on human investigation at all the facilities, and all subjects provided written informed consent before participation.
At the time of the study, none of the transplant recipients had any evidence of transplant rejection or congestive heart failure, as assessed by history and physical examination (all were in New York Heart Association class I), electrocardiography, multigated acquisition scanning at rest and during exercise, echocardiography, and cardiac catheterization with endomyocardial biopsy. None of the patients had orthostatic hypotension. All the patients had serum creatinine levels of less than 160 μmol per liter.
In all transplant recipients, both the recipient and donor hearts were in normal sinus rhythm. The cyclosporine-treated heart-transplant recipients and those not treated with cyclosporine were taking similar doses of azathioprine (mean ±SE, 110±15 vs. 130±10 mg per day; P>0.1) and prednisone (15±2 vs. 13±3 mg per day; P>0.1). One cyclosporine-treated patient with myasthenia gravis and two who had not received cyclosporine were taking azathioprine (100 mg per day). The average dose of prednisone tended to be higher in the patients with myasthenia gravis who had not received cyclosporine than in those who had (27.5±5.6vs. 12.5±10.3 mg per day; P>0.1). Transplant recipients and patients with myasthenia gravis were taking similar doses of cyclosporine (3.8±0.3 vs. 3.2±0.8 mg per kilogram of body weight per day; P>0.1).
Essential hypertension was present in two heart-transplant recipients before transplantation and in two patients with myasthenia gravis before the administration of cyclosporine. All antihypertensive medications were withheld for 72 to 96 hours before the study, except in the case of two heart-transplant recipients in whom it was deemed unsafe to do so.
General Procedures
All experiments were performed after a meal while the subjects were supine. Rates of both the donor heart and the recipient's atrial remnant (electrocardiography), respiratory excursions (pneumography), and efferent muscle sympathetic-nerve activity were recorded continuously on a TEAC R 71 tape recorder (Tokyo, Japan) and later transcribed to hard copy with a Gould ES1000 electrostatic recorder (Oxnard, Calif.). Respiratory excursions were monitored to detect inadvertent performance of a Valsalva maneuver or prolonged expiration, because these respiratory maneuvers markedly stimulate muscle sympathetic outflow.15 Blood pressure was measured in the right arm with an automated sphygmomanometer (Dinamap, Critikon, Tampa, Fla.).
Recording of Sympathetic-Nerve Discharge
Multiunit recordings of postganglionic sympathetic-nerve activity were obtained with unipolar tungsten microelectrodes inserted selectively into muscle nerve fascicles of the peroneal nerve posterior to the fibular head according to the technique of Vallbo et al.16 Briefly, the neural signals were amplified 20,000 to 50,000 times, filtered (bandwidth, 700 to 2000 Hz), rectified, and integrated (time constant, 0.1 second) to obtain a mean-voltage display of sympathetic activity. A recording of sympathetic activity was considered acceptable when the neurograms revealed spontaneous, pulse-synchronous bursts of neural activity, with the largest bursts showing a minimal signal-to-noise ratio of 3:1. In each experiment, we documented that we were recording sympathetic outflow to skeletal muscle by demonstrating that the neural activity had no response to arousal stimuli (loud noise or skin pinch) but had a characteristic biphasic response to the Valsalva maneuver.15 This response consists of sympathetic activation during Phases II and III (decrease in blood pressure) followed by sympathetic inhibition during Phase IV (increase in blood pressure on release), the latter being used to define the noise level.
Sympathetic bursts were detected by inspection of the filtered and mean-voltage neurograms. A deflection on the mean-voltage display was counted as a burst if it had a minimal signal-to-noise ratio of 2:1 and was pulse-synchronous (with an interburst interval equal to or a multiple of the RR interval). The interobserver and intraobserver variabilities in identifying bursts are less than 10 percent and less than 5 percent, respectively.17 Inadvertent contraction of the leg muscles adjacent to the recording electrode produces electromyographic artifacts that are easily distinguished from sympathetic bursts; neurograms that revealed such artifacts were excluded from analysis. Nerve traffic was expressed as the number of bursts of sympathetic activity per minute and as the number of sympathetic bursts per 100 heartbeats, the latter providing a measure of sympathetic activity that is controlled for heart rate. These indexes of sympathetic-burst frequency have been shown to be remarkably stable when a given subject is studied on repeated occasions; the intrasubject variability is less than 15 percent.16 No attempt was made to measure sympathetic-burst amplitude, which is dependent on the position of the recording electrode in the nerve fascicle.
In all experiments, nerve recordings were analyzed with the investigator blinded to the group assignment of the patients. In the studies performed in patients with myasthenia gravis, all data were collected and analyzed in a double-blind fashion.
Measurement of Calf Blood Flow
While recording sympathetic outflow to calf muscles in one leg, we simultaneously measured calf blood flow in the contralateral leg. Calf blood flow was measured by venous-occlusion plethysmography.18 The calf was elevated above the level of the right atrium to collapse the veins. The circulation to the foot was arrested during blood-flow determinations, which were performed at 15-second intervals. Calf vascular resistance was calculated as the mean arterial pressure (one third of the pulse pressure plus diastolic pressure) in millimeters of mercury divided by calf blood flow in milliliters per minute per 100 ml of tissue.
Determination of Plasma Norepinephrine Concentration
In 10 heart-transplant recipients taking cyclosporine, 5 transplant recipients not taking cyclosporine, and 9 normotensive control subjects, we obtained venous blood samples from an indwelling cannula in a forearm vein for the determination of norepinephrine levels; 10-ml aliquots were withdrawn after the subject had rested quietly for 30 minutes. The samples were collected in prechilled tubes treated with heparin and promptly centrifuged at 4°C. Norepinephrine levels were assayed by high-performance liquid chromatography with an electrochemical detector (Smith-Kline BioScience Laboratories, Van Nuys, Calif.). The assay was sensitive to 10 pgof norepinephrine per milliliter, with a coefficient of variation of 10 percent.
Experimental Protocol
To ensure a stable level of base-line values, all subjects rested quietly for 30 minutes, after which nerve activity and blood flow at rest were recorded for four 15-minute periods. The values for sympathetic activity and calf blood flow represent the mean of these four measurement periods. In 7 of the 14 heart-transplant recipients who received cyclosporine, neural recordings were performed on two consecutive days.
To document vagal denervation of the transplanted heart, we measured donor and recipient heart-rate responses to static handgrip. One minute of static handgrip at one third of the maximal voluntary contraction had no effect on the ventricular rate in any of the heart-transplant recipients, even though this maneuver increased the atrial remnant rate by 8± 1 beats per minute (P<0.05).
Statistical Analysis
The mean differences across groups were compared by analysis of variance with least-significant-difference post hoc tests. Student's two-tailed t-test was used for paired comparisons within groups. Correlation coefficients were calculated according to the method of least squares. A P value of less than 0.05 was considered to indicate significance. Results are expressed as means ±SE.
Results
The characteristics of the heart-transplant recipients and the patients with myasthenia gravis, including individual values of sympathetic-nerve activity, are shown in Tables 1Table 1
Characteristics of the Heart-Transplant Recipients. and 2Table 2
Characteristics of the Patients with Myasthenia Gravis.. Values of mean arterial pressure, sympathetic activity, calf blood flow, and vascular resistance for all four groups of subjects are shown in Table 3Table 3
Characteristics ot the Four Study Groups..In heart-transplant recipients treated with cyclosporine, the rate of muscle sympathetic discharge was 2.9 times that in normal controls: 80±3 as compared with 28±4 sympathetic bursts per minute (P<0.05) (Table 3 and Fig. 1Figure 1
Recordings of Muscle Sympathetic-Nerve Activity in a Heart-Transplant Recipient Taking Cyclosporine, a Heart-Transplant Recipient Not Taking Cyclosporine, a Patient with Essential Hypertension, and a Normotensive Control Subject.). Similarly, the discharge rate in the cyclosporine-treated recipients was 2.7 times that in the recipients not treated with cyclosporine (P<0.05). In contrast, sympathetic activity was indistinguishable from normal both in heart-transplant recipients who were not treated with cyclosporine and in patients with essential hypertension (Table 3 and Fig. 1). Although ventricular rates were similar in both groups of heart-transplant recipients (91 ±4 vs. 90±4 beats per minute), sympathetic nerves fired during 88±2 percent of cardiac cycles in the group receiving cyclosporine but only during 34±6 percent of cardiac cycles in the group not treated with cyclosporine (P<0.05) (Table 3).In the transplant recipients treated with cyclosporine, sympathetic discharge was not significantly correlated with the time that had elapsed since transplantation (r = 0.34, P>0.1). In the three heart-transplant recipients receiving cyclosporine who had stopped taking clonidine before the study, the rate of sympathetic discharge (87±7 bursts per minute) was similar to that in the nine transplant recipients who had never received clonidine (76±4 bursts per minute) and in the two patients in whom clonidine therapy was continued (88 and 83 bursts per minute).
In the patients with myasthenia gravis, sympathetic discharge was 1.8 times higher in the cyclosporine group than in the placebo group: 46±3 as compared with 25±4 bursts per minute (P<0.05) (Table 3). Sympathetic activity increased from 32 to 47 bursts per minute in the one patient with myasthenia gravis who was switched from placebo to cyclosporine, and decreased from 49 to 26 bursts per minute in the patient who was switched from cyclosporine to placebo (Fig. 2Figure 2
Recordings of Muscle Sympathetic-Nerve Activity in One Patient with Myasthenia Gravis Obtained during Treatment with Cyclosporine and Three Months after Cyclosporine Had Been Replaced by Placebo.).Cyclosporine treatment was associated with higher blood pressure and calf vascular resistance in heart-transplant recipients and in patients with myasthenia gravis than in their respective non-cyclosporine-treated controls (Table 3). However, both mean arterial pressure (112±3 vs. 100±2 mm Hg) and sympathetic activity (80±3 vs. 46±3 bursts per minute) were significantly higher (P<0.05) in heart-transplant recipients than in patients with myasthenia gravis taking similar doses of cyclosporine.
Figure 3Figure 3
Relation between Muscle Sympathetic-Nerve Activity and Plasma Norepinephrine Levels in 10 Heart-Transplant Recipients Taking Cyclosporine (Solid Circles), 5 Heart-Transplant Recipients Not Taking Cyclosporine (Open Circles), and 9 Normal Control Subjects (Triangles). shows the relation between sympathetic-nerve activity and plasma norepinephrine levels in heart-transplant recipients and healthy control subjects. Although there was considerable overlap between groups, plasma norepinephrine levels were higher in the transplant recipients who received cyclosporine than in those who did not or in normal control subjects: 1.55±0.15, 1.03±2.7, and 0.90±0.11 nmol per liter (262±26, 174±45, and 152±18 pg per milliliter), respectively (P<0.05). Plasma norepinephrine concentrations showed a significant correlation with sympathetic activity in the heart-transplant recipients who received cyclosporine (r = 0.81, P<0.01); in contrast, no such relation was observed in the transplant recipients who did not receive cyclosporine or in the normal control subjects.Discussion
We used intraneural microelectrodes to measure sympathetic discharge in two groups of patients undergoing immunosuppressive treatment with or without cyclosporine. The principal conclusion of our study is that cyclosporine treatment is accompanied by sustained sympathetic activation both in heart-transplant recipients and in patients with myasthenia gravis. This sympathetic activation is directly related to the administration of cyclosporine and appears to be accentuated by the cardiac denervation that results from heart transplantation.
Previous studies in heart-transplant recipients suggested that cyclosporine did not cause sympathetic overactivity because plasma and urinary catecholamine concentrations were normal.8 , 19 In our heart-transplant recipients receiving cyclosporine, plasma norepinephrine levels also were within the normal range of the assay but nevertheless were 50 percent higher than in transplant recipients not receiving cyclosporine. This subtle elevation in plasma norepinephrine was accompanied by marked increases in sympathetic discharge and regional vascular resistance, indicating that sympathetic activation cannot be excluded on the basis of "normal" norepinephrine levels.
Increased sympathetic activity in patients receiving cyclosporine was not related to the withdrawal of clonidine or to preexisting essential hypertension. None of the patients with myasthenia gravis were taking clonidine before the study. In the three heart-transplant recipients in whom clonidine was withdrawn before the study, the level of sympathetic activation was similar to but not more than that seen in the nine transplant recipients who had never received clonidine. Sympathetic activity was normal in patients with uncomplicated essential hypertension, which confirms previous reports20 , 21 and indicates that sympathetic activation during cyclosporine treatment is not a nonspecific autonomic response to chronic hypertension.
Among the heart-transplant recipients who received cyclosporine, the degree of sympathetic overactivity was unrelated to the time that had elapsed since transplantation. This finding suggests that the lower levels of sympathetic activity in the heart-transplant recipients who had never received cyclosporine were not caused by either the gradual resolution of lingering sympathetic activation from preexisting heart failure22 23 24 or the gradual reinnervation of the transplanted heart. Reflex neurohumoral abnormalities accompanying heart failure resolve within the first few weeks or months after successful cardiac transplantation.19 , 25 Most human cardiac allografts do not undergo functional extrinsic reinnervation14 , 26 27 28 29 30 31 32; indeed, in our heart-transplant recipients, ventricular heart rates were dissociated from the rates of innervated atrial remnants at rest and failed to increase during static handgrip — a maneuver that consistently increased atrial-remnant rates by 8 to 10 beats per minute.
The finding that cyclosporine treatment was associated with increased sympathetic activity in patients with myasthenia gravis as well as in heart-transplant recipients indicates that this effect of cyclosporine does not depend on cardiac (ventricular-baroreceptor) denervation. Such denervation, however, may facilitate the sympathoexcitatory effect of cyclosporine. Similar doses of cyclosporine were associated with larger increases in sympathetic activity and blood pressure in heart-transplant recipients than in patients with myasthenia gravis. Although many mechanisms have been implicated in the pathogenesis of cyclosporine-induced hypertension,9 , 33 34 35 36 37 38 augmented sympathetic activation provides one possible explanation for the greater hypertensive effect of cyclosporine in heart-transplant recipients than in other groups of patients.1 , 39
Supported by grants from Sandoz Corporation, the Muscular Dystrophy Association, the Fondation Suisse de Bourses en Médecine et Biologie, the Policlinique Médicale Universitaire, Lausanne, Switzerland, the Danish Medical Research Council (12–6945 and 12–7663), the Danish Heart Foundation, the Ruby D. Hexter Estate, the National Heart, Blood, and Lung Institute (NHLBI) (HL44010, HL08085, and HL06296), the American Heart Association, Texas Affiliate (86G-098 and 87R-985), the Lawson and Rogers Lacy Research Fund in Cardiovascular Diseases, and the Department of Veterans Affairs; and by a NHLBI National Research Service Award (HL08085) to Dr. Morgan and a Clinical Investigator Award (HL01886) to Dr. Victor. Dr. Victor is an Established Investigator of the American Heart Association.
A preliminary report of this work was presented at the Annual Fall Conference of the Council for High Blood Pressure Research of the American Heart Association and at the 62nd Scientific Sessions of the American Heart Association.
We are indebted to Dr. Herbert A. Berkoff for allowing us to study patients under his care; to Dr. Jere H. Mitchell for his continued support and critical review of this work; to Drs. James T. Willerson and Norman M. Kaplan for their careful review of the manuscript; to Nancy Johnson, R.N., Carolyn McNamara, R.N., Catherine Murphy, R.N., and Helen Sheehan, R.N., for superb research assistance; to Ms. Patricia Powell and Mrs. Janet Batjer for assistance in the preparation of the manuscript; and to Sandoz Corporation for supplying cyclosporine to the patients with myasthenia gravis.
Source Information
From the Departments of Internal Medicine (Cardiology Division and the Harry S. Moss Heart Center) (U.S., S.V., B.J.M., R.G.V.), Neurology (J.A.R., R.S.A.T.), and Surgery (S.R.), University of Texas Southwestern Medical Center, Dallas; the Department of Medicine (Cardiology Section), University of Wisconsin, Madison (P.H.); and the Department of Internal Medicine (Cardiology Division), Medical College of Virginia, and the McGuire Veterans Affairs Medical Center, Richmond, Va. (P.K.M.). Address reprint requests to Dr. Victor at the Cardiology Division, U.T. Southwestern Medical Center, 5323 Harry Hines Blvd., Dallas, TX 75235–9034.
- References
References
1
Cohen
Web of Science | Medline2
Kahan BD, ed. Cyclosporine: applications in autoimmune diseases. Philadelphia: Grune & Stratton, 1988.
3
Tindall
Full Text | Web of Science | Medline4
Stiller
CrossRef | Web of Science | Medline5
Brynskov
Full Text | Web of Science | Medline6
Schachter
CrossRef | Web of Science | Medline7
Bennett
CrossRef | Web of Science | Medline8
Thompson
Web of Science9
Bellet
CrossRef | Web of Science | Medline10
Olivari
Medline11
Moss
CrossRef | Web of Science | Medline12
Morgan 13
Lower
Web of Science | Medline14
Mohanty
CrossRef | Web of Science | Medline15
Delius
CrossRef | Medline16
Vallbo
Web of Science | Medline17
Mark
Web of Science | Medline18
Greenfield
Web of Science | Medline19
Olivari
Web of Science20
Wallin
Web of Science | Medline21
Wallin
Web of Science | Medline22
Leimbach
CrossRef | Web of Science | Medline23
Davis 24
Hasking
CrossRef | Web of Science | Medline25
Ellenbogen
CrossRef | Web of Science | Medline26
Arrowood
CrossRef | Web of Science | Medline27
Stinson
Web of Science | Medline28
Yusuf
CrossRef | Web of Science | Medline29
Fallen
CrossRef | Medline30
Wharton
Web of Science | Medline31
Schwaiger
CrossRef32
Wilson
CrossRef33
Lamb
CrossRef | Web of Science | Medline34
Perico
Web of Science | Medline35
Myers
Full Text | Web of Science | Medline36
Thomson
CrossRef | Web of Science | Medline37
Curtis
CrossRef | Web of Science | Medline38
Meyer-Lehnert
Web of Science | Medline39
Weidle
Medline
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1
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CrossRef2
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CrossRef3
J A Lopes, S Jorge. (2011) Acute kidney injury following HCT: incidence, risk factors and outcome. Bone Marrow Transplantation 46:11, 1399-1408
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CrossRef5
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CrossRef6
Felix Seibert, Carolin Behrendt, Sven Schmidt, Markus van der Giet, Walter Zidek, Timm H. Westhoff. (2011) Differential effects of cyclosporine and tacrolimus on arterial function. Transplant International 24:7, 708-715
CrossRef7
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CrossRef8
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CrossRef9
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CrossRef10
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CrossRef11
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CrossRef12
Inge HHT Klein, Alferso C Abrahams, Thomas van Ede, P Liam Oey, Gerry Ligtenberg, Peter J Blankestijn. (2010) Differential effects of acute and sustained cyclosporine and tacrolimus on sympathetic nerve activity. Journal of Hypertension 28:9, 1928-1934
CrossRef13
Osman Najam, Nizar Yonan, Simon G. Williams, Steven M. Shaw. (2010) The Usefulness of Chronic Heart Failure Treatments in Chronic Cardiac Graft Failure. Cardiovascular Therapeutics 28:1, 48-58
CrossRef14
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CrossRef15
Mahmoud M. El-Mas, Amal G. Omar, Mai M. Helmy, Mahmoud M. Mohy El-Din. (2009) Interruption of central neuronal pathway of imidazoline I1 receptor mediates the hypertensive effect of cyclosporine in rats. Brain Research 1248, 96-106
CrossRef16
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CrossRef17
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CrossRef18
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CrossRef19
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CrossRef23
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CrossRef24
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CrossRef26
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CrossRef27
CLAUDIO PONTICELLI. (2005) Cyclosporine: From Renal Transplantation to Autoimmune Diseases. Annals of the New York Academy of Sciences 1051:1, 551-558
CrossRef28
Edmund Q. Sanchez, Goran B. Klintmalm. 2005. Postoperative Management Beyond the Intensive Care Unit: Adults. , 865-880.
CrossRef29
Michael R. Charlton, K.V. Narayanan Menon. 2005. Late Complications of Liver Transplantation and Recurrence of Disease. , 995-1017.
CrossRef30
Amal G. Omar, Mahmoud M. El-Mas. (2004) Time-Domain Evaluation of Cyclosporine Interaction with Hemodynamic Variability in Rats. Cardiovascular Drugs and Therapy 18:6, 461-468
CrossRef31
Anne B. Taegtmeyer, Angela M. Crook, Paul J.R. Barton, Nicholas R. Banner. (2004) Reduced incidence of hypertension after heterotopic cardiac transplantation compared with orthotopic cardiac transplantation. Journal of the American College of Cardiology 44:6, 1254-1260
CrossRef32
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Matthew R Weir. (2004) Blood pressure management in the kidney transplant recipient. Advances in Chronic Kidney Disease 11:2, 172-183
CrossRef35
B. B. McCormick. (2004) Review of clinical outcomes in nocturnal haemodialysis patients after renal transplantation. Nephrology Dialysis Transplantation 19:3, 714-719
CrossRef36
Farzad Moien-Afshari, Bruce M. McManus, Ismail Laher. (2003) Immunosuppression and transplant vascular disease: benefits and adverse effects. Pharmacology & Therapeutics 100:2, 141-156
CrossRef37
Margarida Santiago, Flavio Reis, Luis Almeida, Teresa Alcobia, Joaquim Dionisio, Frederico Teixeira. (2003) Impairment of vascular and platelet levels of nitric oxide and cyclic guanosine-3',5'-monophosphate in cyclosporin A-induced hypertensive rats. Fundamental and Clinical Pharmacology 17:1, 43-50
CrossRef38
Randy W Braith, Roger M Mills, Christopher S Wilcox, Gary L Davis, James A Hill, Charles E Wood. (2003) High-dose angiotensin-converting enzyme inhibition restores body fluid homeostasis in heart-transplant recipients. Journal of the American College of Cardiology 41:3, 426-432
CrossRef39
Howard J Eisen. (2003) Hypertension in heart transplant recipients: more than just cyclosporine. Journal of the American College of Cardiology 41:3, 433-434
CrossRef40
Sakti Mookherjee. 2003. Heart, Autonomic Nervous System and. , 531-533.
CrossRef41
Stephane Cook, Urs Scherrer. (2002) Insulin resistance, a new target for nitric oxide-delivery drugs. Fundamental and Clinical Pharmacology 16:6, 441-453
CrossRef42
Maria Chiara Matteucci, Ugo Giordano, Armando Calzolari, Gianfranco Rizzoni. (2002) Total peripheral vascular resistance in pediatric renal transplant patients. Kidney International 62:5, 1870-1874
CrossRef43
John J. Curtis. (2002) Hypertensinogenic mechanism of the calcineurin inhibitors. Current Hypertension Reports 4:5, 377-380
CrossRef44
Mahmoud M El-Mas, Elham A Afify, Amal G Omar, Fouad M Sharabi. (2002) Cyclosporine attenuates the autonomic modulation of reflex chronotropic responses in conscious rats. Canadian Journal of Physiology and Pharmacology 80:8, 766-776
CrossRef45
Alice Schmidt, Johannes Pleiner, Michaela Bayerle-Eder, Gunther F Wiesinger, Suzanne Rodler, Michael Quittan, Gert Mayer, Michael Wolzt. (2002) Regular physical exercise improves endothelial function in heart transplant recipients. Clinical Transplantation 16:2, 137-143
CrossRef46
Michael Barenbrock, Markus Kosch, Elke Jöster, Klaus Kisters, Karl-Heinz Rahn, Martin Hausberg. (2002) Reduced arterial distensibility is a predictor of cardiovascular disease in patients after renal transplantation. Journal of Hypertension 20:1, 79-84
CrossRef47
E. Schwertfeger, J. Wehrens, V. Oberhauser, A. Katzenwadel, L. C. Rump. (2001) Contractile effects of tacrolimus in human and rat isolated renal arteries. Journal of Autonomic Pharmacology 21:4, 205-210
CrossRef48
Hiromi Shimizu, Toshio Kumai, Shinichi Kobayashi. (2001) Involvement of Tyrosine Hydroxylase Upregulation in Cyclosporine-Induced Hypertension.. The Japanese Journal of Pharmacology 85:3, 306-312
CrossRef49
Olivier Bongard, Daniel Weimer, Robert Lemoine, Jean-François Bolle, Michel Leski, Henri Bounameaux. (2000) Cyclosporine toxicity in renal transplant recipients detected by nailfold capillaroscopy with Na-fluorescein. Kidney International 58:6, 2559-2563
CrossRef50
Anders Åsberg, Knut Joachim Berg, Anders Hartmann. (2000) Each Administration of Cyclosporin A Enhances Skin Microvascular Reactivity in Renal Transplant Recipients. Microvascular Research 60:2, 81-90
CrossRef51
Wolf O. Bechstein. (2000) Neurotoxicity of calcineurin inhibitors: impact and clinical management. Transplant International 13:5, 313-326
CrossRef52
A. Elli, F. Quarto Palo, R. Rivolta, A. Tarantino, G. Montagnino, A. Aroldi, C. Ponticelli. (2000) Effect of increased arterial resistance index on long-term outcome of well-functioning kidney grafts. Transplant International 13:S1, S84-S89
CrossRef53
Scott T W Morris, John J V Mcmurray, R Stuart C Rodger, Rosemary Farmer, Alan G Jardine. (2000) Endothelial dysfunction in renal transplant recipients maintained on cyclosporine. Kidney International 57:3, 1100-1106
CrossRef54
Jeanne Salyer, Dianne V. Jewell, Rebecca J. Quigg. (1999) Predictors of Early Post-cardiac Transplant Exercise Capacity. Journal of Cardiopulmonary Rehabilitation 19:6, 381-388
CrossRef55
Juerg Schwitter, Teresa DeMarco, Sebastian Globits, Hajime Sakuma, Cindy Klinski, Kanu Chatterjee, William W Parmley, Charles B Higgins. (1999) Influence of felodipine on left ventricular hypertrophy and systolic function in orthotopic heart transplant recipients:. The Journal of Heart and Lung Transplantation 18:10, 1003-1013
CrossRef56
Donald R.J. Singer. (1999) Hypertension in heart transplantation. Current Opinion in Organ Transplantation 4:3, 234-240
CrossRef57
Nina Beyer, Mette Aadahl, Birgit Strange, Preben Kirkegaard, Bent Adel Hansen, Thomas Mohr, Michael Kjaer. (1999) Improved physical performance after orthotopic liver transplantation. Liver Transplantation and Surgery 5:4, 301-309
CrossRef58
Krzysztof Narkiewicz, Virend K. Somers. (1999) Obstructive sleep apnea as a cause of neurogenic hypertension. Current Hypertension Reports 1:3, 268-273
CrossRef59
Christiane Bracht, Xiao-Way Yan, Hans-Peter Brunner LaRocca, Gabor Sütsch, Wolfgang Kiowski. (1999) Cyclosporine A and control of vascular tone in the human forearm. Journal of Hypertension 17:3, 357-363
CrossRef60
U. Gerhardt, M. Riedasch, H. Hohage. (1999) Blood pressure control in kidney transplant recipients: influence of immunosuppression. Journal of Autonomic Pharmacology 19:1, 49-54
CrossRef61
Frans H. H. Leenen, Ross A. Davies, Anne Fourney. (1998) Catecholamines and heart function in heart transplant patients: Effects of β1- versus nonselective β-blockade*. Clinical Pharmacology & Therapeutics 64:5, 522-535
CrossRef62
Ruediger C. Braun-Dullaeus, Markus Feussner, Gerhard Walker, Harald Tillmanns, Werner Haberbosch. (1998) Comparison of In Vitro Cardiovascular Function with In Vivo Echocardiographic Assessment After Long-Term Administration of Cyclosporine to Rats. Journal of Cardiovascular Pharmacology 31:6, 828-832
CrossRef63
Marinus A. van den Dorpel, Anton H. van den Meiracker, Thomas W. Lameris, Willem Weimar, Arie J. Man inʼt Veld. (1998) Forearm vasorelaxation in hypertensive renal transplant patients. Journal of Hypertension 16:3, 331-337
CrossRef64
William M. Bennett. (1998) The nephrotoxicity of new and old immunosuppressive drugs. Renal Failure 20:5, 687-690
CrossRef65
Denis Bouchard, Marc-Antoine Despatis, Josie Buluran, Raymond Cartier. (1997) Vascular Effects of Cyclosporin A and Acute Rejection in Canine Heart Transplantation. The Annals of Thoracic Surgery 64:5, 1325-1330
CrossRef66
Hector O. Ventura, Mandeep R. Mehra, Dwight D. Stapleton, Frank W. Smart. (1997) CYCLOSPORINE-INDUCED HYPERTENSION IN CARDIAC TRANSPLANTATION. Medical Clinics of North America 81:6, 1347-1357
CrossRef67
WILLIAM G. COTTS, RON M. OREN. (1997) Function of the Transplanted Heart: Unique Physiology and Therapeutic Implications. The American Journal of the Medical Sciences 314:3, 164-172
CrossRef68
Janet R. Maurer, Sanjiv Tewari. (1997) NONPULMONARY MEDICAL COMPLICATIONS IN THE INTERMEDIATE AND LONG-TERM SURVIVOR. Clinics in Chest Medicine 18:2, 367-382
CrossRef69
Marianne Storogenko, Marie-Agnès Pech-amsellem, Saadia Kerdine, François Rousselet, Marc Pallardy. (1997) Cyclosporin-A inhibits human endothelial cells proliferation through interleukin-6-dependent mechanisms. Life Sciences 60:17, 1487-1496
CrossRef70
Bengt Rundqvist, Roberto Casale, Yrsa Bergmann-Sverrisdottir, Peter Friberg, Andrea Mortara, Mikael Elam. (1997) Rapid fall in sympathetic nerve hyperactivity in patients with heart failure after cardiac transplantation. Journal of Cardiac Failure 3:1, 21-26
CrossRef71
Jesper Melchior Hansen, Niels Fogh-Andersen, Niels Juel Christensen, Svend Strandgaard. (1997) Cyclosporine-induced hypertension and decline in renal function in healthy volunteers. Journal of Hypertension 15:3, 319-326
CrossRef72
Bernd Kutkuhn, Markus Hollenbeck, Peter Heering, Michael Koch, Adina Voiculescu, Thomas Reinhard, Bernd Grabensee. (1997) Development of Insulin Resistance and Elevated Blood Pressure during Therapy with Cyclosporine A. Blood Pressure 6:1, 13-17
CrossRef73
A. Lo Russo, A. C. Passaquin, C. Cox, U. T. Rüegg. (1997) Cyclosporin a Potentiates Receptor-Activated [Ca 2+ ] c Increase. Journal of Receptors and Signal Transduction 17:1-3, 149-161
CrossRef74
Arnon Blum, Dan Aravot. (1996) Heart transplantation-An update. Clinical Cardiology 19:12, 930-938
CrossRef75
William M Bennett, Angelo DeMattos, Mary M Meyer, Takeshi Andoh, John M Barry. (1996) Chronic cyclosporine nephropathy: The Achilles' heel of immunosuppressive therapy. Kidney International 50:4, 1089-1100
CrossRef76
Christiane Bracht, Klaus Hoerauf, Giuseppe Vassalli, Otto M. Hess, Peter Ueberfuhr, Berthold Hoefling. (1996) CIRCADIAN VARIATIONS OF BLOOD PRESSURE AND HEART RATE EARLY AND LATE AFTER HEART TRANSPLANTATION. Transplantation 62:8, 1187-1190
CrossRef77
J. F. Navarro, C. Mora, R. Marcén, J. L. Teruel, C. Gámez, J. J. Jiménez, L. Orofino, J. Ortuno. (1996) Acute cardiovascular effects of intravenous cyclosporine. International Urology and Nephrology 28:4, 575-581
CrossRef78
Susan C. Brozena, Maryl R. Johnson, Hector Ventura, Robert Hobbs, Leslie Miller, Maria Teresa Olivari, Barry Clemson, Robert Bourge, Rebecca Quigg, Roger M. Mills, David Naftel. (1996) Effectiveness and safety of diltiazem or lisinopril in treatment of hypertension after heart transplantation Results of a prospective, randomized multicenter trial. Journal of the American College of Cardiology 27:7, 1707-1712
CrossRef79
Urs Scherrer, Reza Owlya, Mattic Leport. (1996) Body fat and sympathetic nerve activity. Cardiovascular Drugs and Therapy 10:S1, 215-222
CrossRef80
Maria-Teresa Olivari. (1996) Cardiac transplantation: Current indications,short- and long-term results, economic implications, and future developments. Journal of Cardiac Failure 2:2, 141-152
CrossRef81
Hinchey, Judy, Chaves, Claudia, Appignani, Barbara, Breen, Joan, Pao, Linda, Wang, Annabel, Pessin, Michael S., Lamy, Catherine, Mas, Jean-Louis, Caplan, Louis R., . (1996) A Reversible Posterior Leukoencephalopathy Syndrome. New England Journal of Medicine 334:8, 494-500
Full Text82
Randy W. Braith, Roger M. Mills, Christopher S. Wilcox, Gary L. Davis, Charles E. Wood. (1996) Breakdown of blood pressure and body fluid homeostasis in heart transplant recipients. Journal of the American College of Cardiology 27:2, 375-383
CrossRef83
Peter A. Shapiro, Richard P. Sloan, Emilia Bagiella, J. Thomas Bigger, Jack M. Gorman. (1996) Heart rate reactivity and heart period variability throughout the first year after heart transplantation. Psychophysiology 33:1, 54-62
CrossRef84
Salvatore Badalamenti, Francesco Salerno, Elettra Lorenzano, Gianni Paone, Giovanna Como, Silvia Finazzi, Anna Cristina Sacchetta, Antoni Rimola, Giorgio Graziani, Dinangelo Galmarini, Claudio Ponticelli. (1995) Renal effects of dietary supplementation with fish oil in cyclosporine-treated liver transplant recipients. Hepatology 22:6, 1695-1701
CrossRef85
Randin, Denis, Vollenweider, Peter, Tappy, Luc, Jéquier, Eric, Nicod, Pascal, Scherrer, Urs, . (1995) Suppression of Alcohol-Induced Hypertension by Dexamethasone. New England Journal of Medicine 332:26, 1733-1738
Full Text86
J Defraigne. (1995) Successful abdominal aortic aneurysm resection in long-term survivors of cardiac transplantation. Cardiovascular Surgery 3:3, 321-324
CrossRef87
Allison MARTIN, Ming LI, Steven W. TURNER, Judith A. WHITWORTH. (1995) Effects of renal denervation on cyclosporin induced hypertension in the Wistar rat. Nephrology 1:3, 207-212
CrossRef88
Otto-Erich Brodde, Melanie Adamczyk, Frauke Busch, Claus Bossaller, Ellen Duske, Eckart Fleck, Stephan Götze, Wolfgang Auch-Schwelk. (1995) Selective downregulation of rat cardiac beta1-adrenoceptors by cyclosporine a: Prevention by diltiazem or angiotensin-converting enzyme inhibitors. Journal of the American College of Cardiology 25:3, 761-767
CrossRef89
James W Scholey, DE Mills. (1995) Dietary fatty acids and the glomerular hemodynamic response to cyclosporine in borderline hypertensive rats. Kidney International 47:2, 611-617
CrossRef90
DOMINIQUE BABUTY, MICHEL AUPART, PIERRE COSNAY, AGNES SIRINELLI, SERGE ROUCHET, MICHEL MARCHAND, JEAN PAUL FAUCHIER. (1994) Electrocardiographic and Electrophysiologic Properties of Cardiac Allografts. Journal of Cardiovascular Electrophysiology 5:12, 1053-1063
CrossRef91
Roy A. Patchell. (1994) Neurological complications of organ transplantation. Annals of Neurology 36:5, 688-703
CrossRef92
Raymond Cartier, François Dagenais, Charleen Hollmann, Helen Cambron, Josie Buluran. (1994) Chronic exposure to cyclosporine affects endothelial and smooth muscle reactivity in the rat aorta. The Annals of Thoracic Surgery 58:3, 789-794
CrossRef93
Luke, Robert G., . (1994) New Issues in Therapy after Renal Transplantation. New England Journal of Medicine 331:6, 393-394
Full Text94
William J. Sandborn, J. Eileen Hay, Michael K. Porayko, Gregory J. Gores, Jeffery L. Steers, Ruud A. F. Krom, Russell H. Wiesner. (1994) Cyclosporine withdrawal for nephrotoxicity in liver transplant recipients does not result in sustained improvement in kidney function and causes cellular and ductopenic rejection. Hepatology 19:4, 925-932
CrossRef95
Jun Amano, Akio Suzuki, Makoto Sunamori. (1994) Effects of cardiac denervation on coronary and systemic circulation. The Annals of Thoracic Surgery 57:4, 928-932
CrossRef96
R. L. MATHIEU, J. P. CASEZ, Ph. JAEGER, A. MONTANDON, E. PEHEIM, F. F. HORBER. (1994) Altered body composition and fuel metabolism in stable kidney transplant patients on immuno-suppressive monotherapy with cyclosporine A. European Journal of Clinical Investigation 24:3, 195-200
CrossRef97
David E. Mills, Roberto Antueno, James Scholey. (1994) Interaction of dietary fatty acids and cyclosporine a in the borderline hypertensive rat: Tissue fatty acids. Lipids 29:1, 27-32
CrossRef98
ROBERT F. REA, MARC D. THAMES. (1993) Neural Control Mechanisms and Vasovagal Syncope. Journal of Cardiovascular Electrophysiology 4:5, 587-595
CrossRef99
Leslie W. Miller, Robert C. Schlant, Jon Kobashigawa, Spencer Kubo, Dale G. Renlund. (1993) Task force 5: Complications. Journal of the American College of Cardiology 22:1, 41-54
CrossRef100
James B. Young, William L. Winters, Robert Bourge, Barry F. Uretsky. (1993) Task force 4: Function of the heart trnsplant recipient. Journal of the American College of Cardiology 22:1, 31-41
CrossRef101
W. H. REINHART. (1993) Binding of cyclosporine by erythrocytes: influence on cell shape and deformability. European Journal of Clinical Investigation 23:3, 177-181
CrossRef102
Miquel Navasa, Faust Feu, Joan Carles García-Pagan, Wladimiro Jiménez, Josep Llach, Antoni Rimola, Jaume Bosch, Joan Rodés. (1993) Hemodynamic and humoral changes after liver transplantation in patients with cirrhosis. Hepatology 17:3, 355-360
CrossRef103
Georges Mourad, Jean Ribstein, Albert Mimran. (1993) Converting-enzyme inhibitor versus calcium antagonist in cyclosporine-treated renal transplants. Kidney International 43:2, 419-425
CrossRef104
U. Christians, K.-F. Sewing. (1993) Cyclosporin metabolism in transplant patients. Pharmacology & Therapeutics 57:2-3, 291-345
CrossRef105
Converse, Richard L. Jr., Jacobsen, Tage N., Toto, Robert D., Jost, Charles M.T., Cosentino, Frank, Fouad-Tarazi, Fetnat, Victor, Ronald G., . (1992) Sympathetic Overactivity in Patients with Chronic Renal Failure. New England Journal of Medicine 327:27, 1912-1918
Full Text106
Jose López-Miranda, Francisco Pérez-Jiménez, Juan A. Gómez-Gerique, Antonio Espino-Montoro, Luis Hidalgo-Rojas, Javier Pedreño, Jose A. Jiménez-Perepérez. (1992) Effect of cyclosporin on plasma lipoprotein lipase activity in rats. Clinical Biochemistry 25:5, 387-394
CrossRef107
David A. Bull, Glenn C. Hunter, Jack G. Copeland, Victor M. Bernhard, Luis J. Rosado, Kenneth E. McIntyre, Gulshan K. Sethi, Charles W. Putnam. (1992) Peripheral vascular disease in heart transplant recipients. Journal of Vascular Surgery 16:4, 546-554
CrossRef108
Lynne Warner Stevenson, Gregg C. Fonarow. (1992) Endothelin and the vascular choir in heart failure. Journal of the American College of Cardiology 20:4, 854-857
CrossRef109
Karl L Skorecki, William P Rutledge, Robert W Schrier. (1992) Acute cyclosporine nephrotoxicity—Prototype for a renal membrane signalling disorder. Kidney International 42:1, 1-10
CrossRef110
Y. Takeda, I. Miyamori, T. Yoneda, R. Takeda. (1992) Endothelin-1 release from the mesenteric arteries of cyclosporine-treated rats. European Journal of Pharmacology 213:3, 445-447
CrossRef111
Heinrich R. Schelbert, Lynne Warner Stevenson. (1992) Toward an improved understanding and management of human heart transplant recipients. Journal of the American College of Cardiology 19:1, 107-109
CrossRef112
C. E. Angermann, C. H. Spes, P. Dominiak, J. Weil, R. Gerzer, H. -U. Stempfle, B. M. Kemkes, K. Theisen. (1992) Effects of graded exercise on blood pressure, heart rate, and plasma hormones in cardiac transplant recipients before and during antihypertensive therapy. The Clinical Investigator 70:1, 14-21
CrossRef113
Heinfried H Radeke, Uwe Christians, Jörg S Bleck, Karl-F Sewing, Klaus Resch. (1991) Additive and synergistic effects of cyclosporine metabolites on glomerular mesangial cells. Kidney International 39:6, 1255-1266
CrossRef114
Mark, Allyn L., . (1990) Cyclosporine, Sympathetic Activity, and Hypertension. New England Journal of Medicine 323:11, 748-750
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