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作者观察了大鼠原位灌注肺的缺氧性肺动脉 增压反应(HPPR)和D-2-脱氧葡萄糖(2DG)、异捕定和潘生丁对HPPR的影响。 呼吸性缺氧(3％-O_2,10分钟)使肺动脉压平均增高50％,2DG可抑制第一、二次、增强第七、八次的HPPR,异搏定和潘生丁均抑制NPPR。本实验结果提示:HPPR的机制主要在肺内,糖-能量代谢和HPPR的发生有关,Ca~#跨膜内流在HPPR的发生机制中可能起一定作用,腺苷可能参与HPPR的调节。
The authors observed the effects of hypoxic pulmonary hypertension (HPPR) and D-2-deoxyglucose (2DG), isocut and dipyridamole on HPPR in rats after orthotopic lung perfusion. Respiratory hypoxia (3% -O 2, 10 min) increased pulmonary arterial pressure by an average of 50%. 2DG inhibited the first and second, and enhanced the seventh and eighth HPPR. Verapamil and dipyridamole inhibited NPPR. Our results suggest that the mechanism of HPPR is mainly in the lung. The glucose-energy metabolism is related to the occurrence of HPPR. Ca ~ # transmembrane influx may play a role in the pathogenesis of HPPR, and adenosine may be involved in the regulation of HPPR.