Hiramatsu T, Imai Y, Takanashi Y, Hoshino S, Yashima M, Tanaka S A, Chang D, Nakazawa M
Department of Pediatric Cardiac Surgery, Tokyo Women's Medical College, Heart Institute of Japan, Japan.
Ann Thorac Surg. 1997 Mar;63(3):648-52. doi: 10.1016/s0003-4975(96)01055-7.
The endothelium-derived vasoconstrictor endothelin-1 (ET-1) may be involved in pulmonary hypertension (PH), but production of the endothelium-derived vasodilator nitric oxide (NO) after cardiopulmonary bypass (CPB) in congenital heart disease is unclear.
Twenty patients (age, 4 months to 12 years) were divided into three groups: severe PH (mean pulmonary-to-systemic arterial pressure ratio > 0.5) and high pulmonary flow (n = 8), mild PH (mean pulmonary-to-systemic arterial pressure ratio < 0.35) and high pulmonary flow (n = 6), and no PH and low pulmonary flow (n = 6). The mean pulmonary-to-systemic arterial pressure ratio was calculated and blood samples were taken, and NO3-, an NO metabolite, was measured.
Levels of ET-1 in the group with severe PH and high pulmonary flow were higher than in the other groups until 6 hours after CPB, and NO3- was not changed significantly in the group with severe PH and high pulmonary flow and or the group with mild PH and high pulmonary flow during CPB. Endothelin-1 in the group with no PH and low pulmonary flow was higher than in the group with mild PH and high pulmonary flow after CPB, and NO3- in the group with no PH and low pulmonary flow significantly decreased after CPB. A positive correlation was obtained between mean pulmonary-to-systemic arterial pressure ratio and ET-1 (r = 0.742 before CPB; r = 0.689 after CPB).
Imbalance between increased ET-1 and constant NO after CPB in the group with severe PH and high pulmonary flow could contribute to dominant effects of ET-1, which may injure the lung. The increased ET-1 and the decreased NO after CPB in the group with no PH and low pulmonary flow may induce a mechanism of protective vasoconstriction against an acute increase in pulmonary flow.
内皮源性血管收缩因子内皮素-1(ET-1)可能参与肺动脉高压(PH)的发生,但先天性心脏病患者体外循环(CPB)后内皮源性血管舒张因子一氧化氮(NO)的产生情况尚不清楚。
20例患者(年龄4个月至12岁)分为三组:重度PH(平均肺循环与体循环动脉压比值>0.5)且肺血流量高(n = 8),轻度PH(平均肺循环与体循环动脉压比值<0.35)且肺血流量高(n = 6),无PH且肺血流量低(n = 6)。计算平均肺循环与体循环动脉压比值并采集血样,检测NO代谢产物NO3-。
重度PH且肺血流量高的组中ET-1水平在CPB后6小时内高于其他组,重度PH且肺血流量高的组以及轻度PH且肺血流量高的组在CPB期间NO3-无明显变化。无PH且肺血流量低的组在CPB后ET-1高于轻度PH且肺血流量高的组,无PH且肺血流量低的组在CPB后NO3-显著降低。平均肺循环与体循环动脉压比值与ET-1之间呈正相关(CPB前r = 0.742;CPB后r = 0.689)。
重度PH且肺血流量高的组在CPB后ET-1升高与NO恒定之间的失衡可能导致ET-1起主导作用,这可能会损伤肺脏。无PH且肺血流量低的组在CPB后ET-1升高和NO降低可能诱导一种针对肺血流量急性增加的保护性血管收缩机制。