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目的 :研究一种结构中含有半胱氨酸的新型一氧化氮供体 SP/ W- 5 186 ,在新西兰兔缺血 /再灌注心肌损伤中的作用和机制。方法 :兔缺血 45 min继之再灌注 180 min。再灌注前 5 min,通过静脉单剂量给予低剂量 (0 .3μmol/ kg)或高剂量 (1μm ol/ kg)的 SP/ W- 5 186。结果 :给予 0 .3μm ol/ kg SP/ W- 5 186对平均动脉压、心率等心功能指标没有影响 ,可显著地降低血小板聚集 ,减少白细胞聚集。类似物 SP/ W- 6 373则不产生任何保护作用。结论 :由 SP/ W- 5 186中释放的 NO可显著地保护心肌组织 ,减轻再灌注损伤。作用机制包括抑制血小板聚集 ,减少 PMN-内皮的相互作用和保护内皮功能
AIM: To investigate the role and mechanism of a new nitric oxide donor, SP / W-5 186, containing cysteine in ischemic / reperfusion-induced myocardial injury in New Zealand rabbits. Methods: Rabbits were subjected to ischemia for 45 min followed by 180 min of reperfusion. Five minutes prior to reperfusion, low dose (0.3 μmol / kg) or high dose (1 μm ol / kg) of SP / W-5 186 was given as a single intravenous dose. Results: The administration of 0.3 μmol / kg SP / W-5 186 had no effect on cardiac function indexes such as mean arterial pressure and heart rate, and significantly reduced platelet aggregation and leukocyte aggregation. The analog SP / W-6 373 does not produce any protective effect. CONCLUSIONS: NO released from SP / W-5 186 significantly protects cardiac tissue and reduces reperfusion injury. Mechanisms of action include inhibition of platelet aggregation, reduction of PMN-endothelium interactions and protection of endothelial function