Cody R J, Haas G J, Binkley P F, Capers Q, Kelley R
Department of Medicine, Ohio State University Hospitals, College of Medicine, Columbus, Ohio 43210.
Circulation. 1992 Feb;85(2):504-9. doi: 10.1161/01.cir.85.2.504.
Endothelin is a family of potent vasoconstrictor peptides of vascular endothelial origin. Although it has been proposed that the vasoconstrictor effects of endothelin are produced at the local vascular level, increased plasma concentration of endothelin has been identified in cardiovascular disorders.
We tested whether immunoreactive endothelin-1 could be detected by radioimmunoassay in plasma of congestive heart failure patients and whether levels correlated with hemodynamic characteristics. Twenty congestive heart failure patients (New York Heart Association class II-IV) were sampled in the morning after an overnight fast, before medication. Cardiac index was decreased to 2.14 +/- 0.45 l/m/m2, and pulmonary wedge pressure was increased to 22 +/- 7 mm Hg. The ranges of pulmonary pressures were: systolic, 22-100 mm Hg, mean, 13-61 mm Hg, and diastolic, 8-42 mm Hg. The endothelin-1 level was 9.07 +/- 4.13 pg/ml (range, 4-19 pg/ml), which was increased compared with 12 normals (3.7 +/- 0.6 pg/ml; range, 2.8-4.7 pg/ml); the difference was statistically significant (p less than 0.0001). Endothelin-1 significantly correlated with pulmonary pressures (systolic, r = 0.78; mean, r = 0.80; diastolic, r = 0.77; all p less than 0.003) and pulmonary vascular resistance (r = 0.65, p less than 0.01). Endothelin-1 strongly correlated with the resistance ratio (pulmonary vascular resistance/systemic vascular resistance) (r = 0.88, p less than 0.0001). Stepwise multiple regression analysis confirmed the significance of these observations.
Elevated immunoreactive endothelin-1 specifically correlated with the extent of pulmonary hypertension in congestive heart failure patients. Whether endothelin-1 is a regional mediator of pulmonary hypertension or a marker for its occurrence requires additional evaluation.
内皮素是一族由血管内皮产生的强效血管收缩肽。尽管有人提出内皮素的血管收缩作用是在局部血管水平产生的,但在心血管疾病中已发现血浆内皮素浓度升高。
我们检测了放射免疫分析法能否检测充血性心力衰竭患者血浆中的免疫反应性内皮素-1,以及其水平是否与血流动力学特征相关。20例充血性心力衰竭患者(纽约心脏协会心功能II-IV级)在禁食过夜后、用药前的早晨进行采样。心脏指数降至2.14±0.45升/分钟/平方米,肺楔压升至22±7毫米汞柱。肺压范围为:收缩压22 - 100毫米汞柱,平均压13 - 61毫米汞柱,舒张压8 - 42毫米汞柱。内皮素-1水平为9.07±4.13皮克/毫升(范围4 - 19皮克/毫升),与12名正常人(3.7±0.6皮克/毫升;范围2.8 - 4.7皮克/毫升)相比有所升高;差异具有统计学意义(p < 0.0001)。内皮素-1与肺压(收缩压,r = 0.78;平均压,r = 0.80;舒张压,r = 0.77;所有p < 0.003)和肺血管阻力(r = 0.65,p < 0.01)显著相关。内皮素-1与阻力比(肺血管阻力/体循环血管阻力)密切相关(r = 0.88,p < 0.0001)。逐步多元回归分析证实了这些观察结果的重要性。
免疫反应性内皮素-1升高与充血性心力衰竭患者肺动脉高压的程度具体相关。内皮素-1是肺动脉高压的局部介质还是其发生的标志物,需要进一步评估。