[Protective effect of endothelium-derived relaxing factor on ischemic (hypoxic) and reperfused (reoxygenated) myocardium].
The present study is undertaken to investigate the effects of NO, its inhibitor L-NNA and its procursor L-Arg on the status of myocardial tissue during ischemia (hypoxia) and reperfusion (reoxygenation) in two different models, i.e. Langendorff heart and cultured heart cells of rat. The results were as follows: (1) When heart perfusion was stopped for 30 min and reinstitued for 20 min with K-H buffer containing NO, the coronary flow rate (CFR), left ventricular pressure (LVP) and +/- dp/dtmax increased significantly. When NO was replaced by L-NNA opposite effects were observed. L-Arg alone was without effect on CFR, LVP and +/- dp/dtmax, but attenuated the decreasing effect of L-NNA on CFR. NO decreased MDA and NAGase content of myocardium while L-NNA increased them. (2) When cultured ventricular myocytes were subjected to hypoxia for 30 min and reoxygenated for 20 min, none of the substances under investigation showed any effects on Ca2+ content of heart cells, but all of them decreased MDA, NAGase content of the culture tissue after reoxygenation. The above findings show that NO plays an important role in protecting myocardium from ischemic and reperfused injury by improving blood supply of reperfused myocardium and attenuation of oxygen free radical injury.
Wan
M
M
Pathophysiology Laboratory, Hebei Academy of Medical Sciences, Shijiazhuang.
Yu
Z J
ZJ
D000818:Animals; D001783:Blood Flow Velocity / Q000187:drug effects; D003326:Coronary Circulation / Q000187:drug effects; D066298:In Vitro Techniques; D015428:Myocardial Reperfusion Injury / Q000378:metabolism / Q000517:prevention & control*; D009569:Nitric Oxide / Q000494:pharmacology* / Q000502:physiology; D051381:Rats
D009569:Nitric Oxide