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目的:从细胞和分子水平揭示婴幼儿肺炎合并心衰的机制。方法:健康清洁级50日龄Wistar大鼠。经气管注射金黄色葡萄球菌菌液,建立肺炎动物模型;开胸获取心脏,进行双心室灌流,测定心肌酶谱和心功能指标;酶解分离出单个右室心肌细胞后,以Fura-2/AM负载细胞并对静息和收缩状态时细胞内[Ca~(2+)]i进行荧光测定;采用全细胞式膜片钳技术记录右室心肌细胞L型钙电流;采用高效液相色谱仪测定心肌组织腺苷酸含量。均采用气管内注射等量生理盐水的同龄Wistar大鼠作为对照。结果:1、肺炎组动物心肌酶谱显著增高。2、肺炎组和对照组的左、右心室功能均随前负荷升高而增强;在同一负荷下,右心室功能均低于对照组。3、静息状态下肺炎组右室心肌细胞内[Ca~(2+)]i随病程显著增高;收缩时CO~(2+)含量增加比率显著低于对照组。4、接种后24h的肺炎组L型钙通道电流峰值无显著变化;120h时显著高于对照组。5、接种后120h,心肌组织腺苷酸含量显著低于对照组。结论:采用气管内接种的方法所建立肺炎动物模型是有效的;肺炎可以合并心衰.尤其是右心衰竭为主;重症肺炎时心肌细胞出现能量代谢障碍;静息期心肌细胞内[Ca~(2+)]i增高.而收缩状态下Ca~(2+)含量增加比率下降,可能是心肌细胞舒张、收缩功能障碍的重要机制;心衰后期。心肌细胞跨膜钙内流增大。可能是病变发展的重要机制。
Objective: To reveal the mechanism of pneumonia complicated with heart failure in infants and young children at the cellular and molecular level. Methods: Healthy clean grade Wistar rats of 50 days old. The model of pneumonia was established by tracheal injection of Staphylococcus aureus bacteria solution. The heart was obtained by thoracotomy and bifocal ventricular perfusion was performed. The myocardial enzymes and cardiac function were determined. After single ventricular myocytes were isolated by enzymolysis, Fura-2 / AM cells were loaded and the intracellular [Ca ~ (2 +)] i was measured by fluorescence at resting and contractile states. The L-type calcium current of right ventricular myocytes was recorded by whole-cell patch clamp technique. High performance liquid chromatography Determination of myocardial tissue adenylate content. Wistar rats of the same age with the same amount of saline injected intratracheally were used as controls. Results: 1, myocardial enzymes in pneumonia group was significantly higher. Left and right ventricular function in both pneumonia group and control group increased with the increase of the former load. Right ventricular function was lower than that of the control group under the same load. The level of [Ca ~ (2 +)] i in the right ventricular myocardium of patients in pneumonia group increased significantly with the course of disease at rest; the rate of increase of CO ~ (2+) in the contraction group was significantly lower than that in the control group. There was no significant change in the peak of L-type calcium channel in pneumonia group at 24 hours after inoculation, but significantly higher than that in control group at 120 hours. 5, 120h after inoculation, myocardial adenosine content was significantly lower than the control group. Conclusion: The animal model of pneumonia established by intratracheal inoculation is effective. The pneumonia can be combined with heart failure, especially the right heart failure. In severe pneumonia, the energy metabolism of cardiomyocytes is disrupted. (2 +)] i increased, while the contractile state increased the rate of Ca ~ (2+) decreased, may be an important mechanism of myocardial cell diastolic dysfunction; heart failure late. Cardiac transmembrane calcium influx increased. May be an important mechanism for the development of the lesion.