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Effects of successful cardiac transplantation on plasma endothelin
G J Haas1, M Wooding-Scott, P F Binkley
1Division of Cardiology, Ohio State University Hospitals, Columbus 43210.
Insights
Plasma endothelin-1 levels are significantly elevated in cardiac transplant patients, potentially contributing to post-transplant hypertension. Further research is needed to understand the mechanisms behind this increase.
Area of Science:
- Cardiovascular Medicine
- Nephrology
- Immunology
Background:
- Systemic hypertension is common after cardiac transplantation in patients treated with cyclosporine.
- The underlying mechanisms of post-transplant hypertension remain largely unknown.
- Endothelin, a potent vasoconstrictor, may play a role due to potential cyclosporine-induced endothelial injury.
Purpose of the Study:
- To investigate the presence and levels of immunoreactive endothelin-1 in the plasma of cardiac transplant recipients.
- To determine if endothelin-1 levels correlate with hemodynamic parameters, cyclosporine levels, or renal function (serum creatinine).
Main Methods:
- Plasma endothelin-1 was measured using radioimmunoassay in 22 stable cardiac transplant patients.
- Patients were assessed 9 days to 3 years post-transplantation.
- Measurements were compared to 12 healthy normal subjects.
Main Results:
- Plasma endothelin-1 levels were significantly higher in cardiac transplant recipients (5.2 +/- 1.8 pg/ml) compared to normal subjects (1.9 +/- 0.3 pg/ml).
- Elevated endothelin-1 levels were persistent in repeated measurements.
- No significant correlation was found between endothelin-1 levels and hemodynamic variables, serum creatinine, or cyclosporine levels.
Conclusions:
- Endothelin-1 is demonstrably increased in patients following successful cardiac transplantation.
- The specific characteristics and mechanisms driving elevated endothelin-1 in these patients require additional investigation.
- The role of endothelin-1 in post-transplant hypertension warrants further study.
Abstract:
After cardiac transplantation, cyclosporine-treated patients exhibit a high incidence of systemic hypertension, the mechanism of which is not known. Endothelin, a potent vasoconstrictor peptide of endothelial origin, may be activated by cyclosporine-induced endothelial injury and therefore may mediate post-transplant hypertension. In the present study, we tested whether immunoreactive endothelin-1 could be detected by radioimmunoassay in the plasma of cardiac transplant recipients and if levels correlated with hemodynamic characteristics, cyclosporine level, or renal function as assessed by serum creatinine. Plasma endothelin was measured in 22 stable cyclosporine-treated patients 9 days to 3 years after successful orthotopic cardiac transplantation before routine hemodynamic assessment and surveillance endomyocardial biopsy. Fifteen patients were receiving chronic therapy for hypertension. Plasma endothelin-1 was 5.2 +/- 1.8 pg/ml (range 3.1 to 10.5), which was increased compared with that in 12 normal subjects (1.9 +/- 0.3 pg/ml; range 1.4 to 2.4); the difference was statistically significant (p < 0.0001). Repeated sampling in 8 patients at weekly intervals identified a persistent increase in endothelin with only modest variability. Endothelin-1 did not correlate with any hemodynamic variable, serum creatinine or cyclosporine level. Thus, endothelin-1 is increased after successful orthotopic cardiac transplantation. In the absence of discrete correlations with hemodynamic variables, serum creatinine or cyclosporine levels, both the characteristics and mechanisms for increased endothelin in recipients of cardiac transplants require further evaluation.