NEW METHOD FOR MYOCARDIAL PROTECTION

本研究旨在从血管通透性和中性粒细胞活化的角度阐明一氧化氮（NO）在缺血再灌注诱导的内皮损伤中的作用。从成年大鼠心脏和血液中分离微血管内皮细胞和中性粒细胞。我们测量跨膜FITC-白蛋白渗漏作为渗透性、化学发光值和中性粒细胞粘附内皮细胞的指标（%）。在缺氧6小时后的复氧过程中，通过加入中性粒细胞增加渗透性。精氨酸和硝普钠通过抑制中性粒细胞活化和粘附内皮细胞，降低微血管通透性。结果提示，缺血后内皮细胞NO释放减少，可能导致中性粒细胞的通透性、粘附和活化增加，从而加重内皮损伤。

The present study was designed to elucidate the role of Nitric Oxide(NO) in ischemia-reperfusion induced endothelial injury in view of vascular permeability and neutrophil activation. Microvascular endothelial cells and neutrophils were isolated from adult rat heart and blood. We measured the transmembrane FITC-albumin leakage as indices of permeability, chemiluminescence value and neutrophil adherence to endothelial cell(%). Permeability was increased by addition of neutrophils during reoxygenation after 6 hours hypoxia. L-arginine and Nitroprusside decreased microvascular permeability by inhibiting neutrophil activation and adhesion to endothelial cell. These results indicate that decrease of constitutive NO release from endothelial cell after ischemia may cause the increase of permeability, adherence and activation of neutrophils resulting in enhancement of endothelial injury.