Yi G H, Zwas D, Wang J
Division of Circulatory Physiology, Department of Medicine, College of Physicians and Surgeons of Columbia University, New York, NY 10032, USA.
Prostaglandins Other Lipid Mediat. 2000 Mar;60(4-6):137-51. doi: 10.1016/s0090-6980(00)00057-5.
Although it has been shown that long-term exercise training preserves endothelium-mediated nitric oxide vasodilator function in chronic heart failure (CHF), whether exercise training exerts similar beneficial effects on endothelial/prostaglandin-mediated vasodilator capacity in coronary circulation during the development of CHF has not been determined. Fifteen mongrel dogs were surgically instrumented for measurement of left ventricular pressure, aortic pressure, coronary blood flow and left circumflex coronary artery diameter. Dogs (n = 5) who underwent 4 weeks of cardiac pacing (210 b/min for 3 weeks and 240 b/min for the 4th week) developed CHF as characterized by significant reduction in left ventricular systolic pressure, mean arterial pressure and left ventricular dP/dt, increases in left ventricular end-diastolic pressure and heart rate, as well as clinical signs of CHF. Endothelial prostaglandin-mediated vasodilation of the epicardial coronary artery was impaired, as manifested by an attenuated arachidonic acid (AA)-induced dilation of the artery (epicardial artery diameter increased by: 0.78 +/- 0. 84% in CHF versus 4.6 +/- 0.89% in normal, P < 0.05); however, prostacyclin (PGI(2))-induced and nitroglycerin-induced vasodilation of the coronary circulation were not altered. In contrast, dogs (n = 6) with cardiac pacing plus daily exercise training (4.4 +/- 0.3 km/h, 2 h/day) only developed mild cardiac dysfunction, and the response of the epicardial coronary artery diameter to AA was preserved (epicardial artery diameter increased by 4.2 +/- 0.98% from baseline, P 0.05 compared to its respective control). Thus, long-term exercise training preserves endothelial/prostaglandin-mediated dilation of epicardial coronary artery during development of CHF.
尽管已有研究表明，长期运动训练可保留慢性心力衰竭（CHF）患者内皮细胞介导的一氧化氮血管舒张功能，但在CHF发生发展过程中，运动训练对冠状动脉循环中内皮细胞/前列腺素介导的血管舒张能力是否具有类似的有益作用尚未确定。15只杂种犬接受手术植入仪器，用于测量左心室压力、主动脉压力、冠状动脉血流量和左旋冠状动脉直径。接受4周心脏起搏（第1至3周为210次/分钟，第4周为240次/分钟）的犬（n = 5）出现了CHF，其特征为左心室收缩压、平均动脉压和左心室dP/dt显著降低，左心室舒张末期压力和心率增加，以及CHF的临床症状。心外膜冠状动脉的内皮细胞前列腺素介导的血管舒张功能受损，表现为花生四烯酸（AA）诱导的动脉扩张减弱（CHF组心外膜动脉直径增加：0.78±0.84%，而正常组为4.6±0.89%，P < 0.05）；然而，前列环素（PGI2）诱导的和硝酸甘油诱导的冠状动脉循环血管舒张功能未改变。相比之下，接受心脏起搏加每日运动训练（4.4±0.3 km/h，每天2小时）的犬（n = 6）仅出现轻度心脏功能障碍，心外膜冠状动脉直径对AA的反应得以保留（心外膜动脉直径较基线增加4.2±0.98%，与各自对照组相比，P>0.05）。因此，长期运动训练可在CHF发生发展过程中保留心外膜冠状动脉内皮细胞/前列腺素介导的扩张功能。
