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Ann Thorac Surg 1993;55:450-458
© 1993 The Society of Thoracic Surgeons

Articles

Plasma endothelin levels and surgically correctable pulmonary hypertension

Hang Chang, MD*, Gong-Jhe Wu, MD, Shih-Ming Wang, MD, Chi-Ren Hung, MD

Departments of Emergency Medicine and Surgery, National Taiwan University Hospital, Taipei, Taiwan, Republic of China

Accepted for publication May 28, 1992.

* Address reprint requests to Dr Chang, National Taiwan University Hospital, No. 1, Chang-Te St, Taipei, Taiwan, ROC.

To know the changes in plasma endothelin of patients with pulmonary hypertension, we studied 32 patients with valvular heart disease. Among them, 22 patients had pulmonary hypertension (group I) and 10 had pulmonary arterial pressures in the normal range (group II). Plasma endothelin-1 concentrations of the patients in group I were significantly greater than those of the patients in group II (p < 0.05). No significant difference in plasma endothelin-3 concentrations existed between the two groups. Cardiac output and pulmonary capillary wedge pressure had a linear correlation with plasma endothelin-1 levels. There was also a significant correlation between plasma endothelin-1 levels and hemodynamic indicators of severity of pulmonary hypertension, such as mean pulmonary arterial pressure and pulmonary vascular resistance (p < 0.05). All patients in this study underwent surgical procedures for the correction of valvular lesions. All patients in group I showed a decrease in pulmonary arterial pressures, and their plasma endothelin-1 levels decreased from 3.84 ± 0.20 pg/mL to 1.66 ± 0.07 pg/mL (p < 0.05), whereas the plasma endothelin-3 levels had only slight variation from 0.64 ± 0.11 pg/mL to 0.75 ± 0.06 pg/mL (p > 0.05) between the preoperative and the postoperative stages. The results demonstrated that plasma endothelin-1 rather than endothelin-3 had a role in pulmonary hypertension. Several pieces of evidence pointed out that endothelin-1 functioned as a reactive mediator during vasoconstriction in the case of pulmonary hypertension rather than as a triggering factor of pulmonary hypertension.




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