缺氧家兔组织钙调蛋白水平及钙调蛋白拮抗剂对血流动力学的影响

为观察钙调蛋白(CaM)在缺氧所致的肺动脉高压等血流动力学改变中的作用,我们采用环核苷酸磷酸二脂酶的方法测定了缺氧家兔肺动脉、肺和心肌组织CaM水平,观察了脂质体包裹的CaM拮抗剂三氟啦嗪(TFP)对缺氧动物血流动力学的影响。结果表明:1.缺氧(模拟4000m高原10～11天)家兔肺动脉、肺和心肌组织CaM活性量水平与平原对照值无显著差异,CaM在上述实验条件下改变不甚显著;2.在模拟4000m高原为缺氧家兔注入脂质体包裹的TFP后,Ppa无显著改变,PVR有增高趋势,而观察45分钟末动物肺动脉的CaM活性受到显著抑制,说明缺氧性肺动脉压增高不一定依赖于CaM;3.家兔肺循环和体循环对缺氧反应不同,在模拟4000m高原,脂质体包裹的TFP对缺氧动物的肺、体循环的血流动力学影响也不同,提示;肺循环与体循环血管平滑肌收缩的调节机制不尽一致。

Calmodulin Levels and Effects of Calmodulin Antagonist on Hemodynamics in Hypoxic Rabbits

The calmodulin levels of the pulmonary arteries,lungs and myocardial tissues from hypoxic rabbits and their controls were determined by phosphodiesterase activation,and the effects of trifluperazine (TFP),a calmodulin antagonist,on the hemodynamics of hypoxic animals were also examined.The results were;(1) No significant changes of calmodulin levels of 3 kinds of tissue were observed in rabbits exposeded to 4000m simulated altitude for 10 days; (2) Even though the administration of TFP encapsulated by phosphatidylcholine liposomes inhibited markedly the calmodulin activity on pulmonary arteries,it failed to diminish the hypoxic pressor response in rabbits.The results suggest that the hypoxic pulmonary vasoconstriction is independent from calmodulin to certain degree; (3) The pulmonary arterial pressure and pulmonary vascular resistance exhibited no significant changes during TFP treatment while the femoral arterial pressure and systemic vascular resistance decresed markedly.It strongly suggests that the pulmonary and systemic circulation do not share a common molecular mechanism of vasoconstriction.