聚集的血小板对血管张力的影响及内皮细胞舒血管因子的作用

EFFECT OF AGGREGATING PLATELET ON VASCULAR TENSION AND THE ROLE OF EDRF

缺氧─再给氧、机械方法分别作为大鼠胸主动脉环内皮损伤和去除的手段，观察聚集的血小板及血小板分泌产物二磷酸腺苷（ＡＤＰ）、５－羟色胺（５－ＨＴ）对血管张力的影响及内皮细胞舒血管因子（ＥＤＲＦ）的作用。发现聚集的血小板、ＡＤＰ和５－ＨＴ均引起内皮正常的血管环呈浓度依赖性舒张，且这种舒张作用可被ＥＤＲＦ特异抑制剂血红蛋白（Ｈｂ）逆转。缺氧─再给氧使血管环的此种舒张作用明显减弱，在去内皮的血管环几乎消失。提示正常血管内皮细胞通过释放ＥＤＲＦ，介导聚集血小板、ＡＤＰ和５－ＨＴ所致的血管舒张，缺氧一再给氧可致内皮分泌ＥＤＲＦ机制受损，去内皮则使该机制丧失。

The endothelium of rat isolated-thoracic aortic ring was either damaged by hypoxia-reoxygenation or removed by mechanical means. By bioassay the effects of aggregating platelets, adenosine diphosphate (ADP) and 5-hydroxytryptamine(5-HT) on vascular tension and the role of endothelium-derived relaxing factor (EDRF) were studied.Dose-dependent relaxation was elicited respectively by aggregating platelets (n=10),ADP (n=10) and 5-HT(n=11 in normal endothelial aortic rings. This vasodilation action was blocked by hemoglobin,a specific inhibitor of EDRF. The vasodilation was markedly reduced in hypoxic-reoxygenatied ring.(n=10), nearly lost in endothelial removed rings(n=10).It is suggested that normal vascular endothelium mediates the vasodilation of aggregating platelets, ADP and 5-HT by releasing EDRF. The mechanisms of endotbelium releasing EDRF are damaged by hypoxia-reoxygenation and lost by endothelium removal.