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将大鼠置于不同模拟海拔高度低压舱内4d,观察其左、右心室功能代偿与失代偿的某些生物化学基础。结果表明,5000m中度缺氧4d使左、右心室功能、重量、心肌蛋白含量及Ca~(2+)-ATP酶活性均有不同程度的增高。提示机体在整体、心脏器官及心肌细胞分子各个水平的代偿机制均有加强。8000m重度缺氧4d后,左室重量增加,dp/dt_(max)与蛋白含量均下降,肌原纤维ATP酶活性则保持中度缺氧的代偿水平,提示左心功能似已受到损害。与此同时,右室蛋白含量虽也明显减少,但其ATP酶活性则继续增高,dp/dt_(max)未出现下降,表明右心功能仍具有相当的代偿能力。从而支持我们关于在短期内因供氧严重不足而造成的左室心肌的直接损伤作用大于右室心肌的推论。
The rats were placed in different simulated altitude hypobaric chamber 4d, observed left and right ventricular function compensation and decompensation of some of the biochemical basis. The results showed that left ventricular function, weight, myocardial protein content and Ca ~ (2 +) - ATPase activity were increased to varying degrees in hypoxia for 4 days. Prompt body in the whole, heart organ and cardiomyocyte molecules at all levels of compensatory mechanisms have been strengthened. Left ventricular weight increased, dp / dt max and protein content decreased after 8 000 m severe hypoxia. Myofibril ATPase activity maintained a compensatory level of moderate hypoxia, suggesting that left ventricular function may be impaired. At the same time, the content of right ventricular protein decreased significantly, but its ATPase activity continued to increase, dp / dt_ (max) did not decline, indicating that right heart function still has considerable compensatory ability. Thus supporting our hypothesis that the direct damage of left ventricular myocardium caused by severe oxygen deficiency in a short period of time is greater than that of right ventricular myocardium.