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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。
To observe the role of calmodulin (CaM) in hemodynamic changes such as pulmonary hypertension induced by hypoxia, we used cyclic nucleotide phosphodiesterase assay to determine the effects of hypoxia on pulmonary arteries, lung and myocardium CaM levels, the effects of liposome-encapsulated CaM antagonist trifluoperazine (TFP) on the hemodynamics of hypoxic animals were observed. The results showed that: (1) There was no significant difference in the level of CaM activity in pulmonary artery, lung and myocardium between rabbits and hypoxia (simulated 4000m plateau 10 ~ 11 days), while CaM did not change significantly under the above experimental conditions; Pseudomonas aeruginosa hypoxia rabbits injected with liposome wrapped TFP, Ppa no significant change, PVR increased trend, and observed at 45 minutes end of the animal pulmonary artery CaM activity was significantly inhibited, indicating that hypoxic pulmonary hypertension is not necessarily increased Dependent on CaM; 3. Rabbit pulmonary circulation and systemic response to hypoxia are different in simulated 4000m plateau, liposome-wrapped TFP on the lungs, systemic hemodynamics of anoxic animals are also different, suggesting; pulmonary circulation and systemic circulation Vascular smooth muscle contraction regulation mechanism is not consistent.