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目的定量研究在缺氧情况下,心脏结构和功能改变及其规律。方法W istar大鼠40只,雌雄各半,随机分为对照组和单纯缺氧组,置于本课题组设计并研制的常压低氧舱(氧浓度为10%),采用生化、常规病理、超微病理、分子病理和定量病理等多种技术方法,对缺氧后心脏功能、结构和心肌细胞凋亡进行观察。结果缺氧后大鼠心肌酶谱(LDH、AST和CK)均明显高于正常值,且随实验时间延长而增加;PO2在缺氧1~7 d内呈持续性进行性下降,PCO2于缺氧1 d时显著升高,而于3~7 d内则呈持续性下降。pH值于缺氧1 d时显著低于正常对照组、而于3~7 d内则迅速恢复到对照组的水平。HCT(%)于缺氧1~7 d内呈持续性进行性升高;缺氧后大鼠心肌细胞肿胀、变性、凋亡、坏死;心肌纤维排列紊乱;间质细胞肿胀、退变;心肌细胞凋亡指数增加。结论缺氧引起大鼠心脏功能和结构明显损伤,且随缺氧时间延长呈进行性加重趋势;缺氧后心肌细胞凋亡指数增加,可作为缺氧时心脏损伤的一个重要指标。
Objective To quantitatively study the changes of cardiac structure and function and their regularity under hypoxic conditions. Methods Forty Wistar rats were randomly divided into control group and hypoxia group, and were placed in the normal pressure hypoxic chamber (oxygen concentration was 10%) designed and developed by our research group. The biochemical and routine pathology , Ultrastructural pathology, molecular pathology and quantitative pathology and other techniques to observe the cardiac function, structure and myocardial cell apoptosis after hypoxia. Results The myocardial enzymes (LDH, AST and CK) of rats after hypoxia were significantly higher than normal values and increased with the prolongation of experimental time. The PO2 decreased continuously from 1 to 7 days of hypoxia, Oxygen 1 d significantly increased, while in the 3 ~ 7 d showed a sustained decline. The pH value was significantly lower than that of the normal control group on the 1st day of hypoxia, and rapidly returned to the control level within 3 ~ 7 days. HCT (%) increased continuously from 1 to 7 days of hypoxia; swelling, degeneration, apoptosis and necrosis of rat myocardial cells after hypoxia; disordered myocardial fibers; swelling and degeneration of interstitial cells; Apoptosis index increased. CONCLUSION: Hypoxia causes obvious damage to the heart function and structure of rats, and it tends to aggravate with the prolongation of hypoxia. After hypoxia, the apoptotic index of cardiomyocytes increases, which may be used as an important indicator of cardiac injury during hypoxia.