急性缺氧型肺动脉高压兔左心室功能变化及其与心肌细胞凋亡关系的实验研究  

Experimental study on the effects of acute hypoxia pulmonary artery hypertension on left ventricular function and cardiomyocyte apoptosis

作　　者：崔华[1] 范利[1] 俞森洋[2] 

机构地区：[1]解放军总医院南楼心肾科,北京100853 [2]解放军总医院南楼呼吸科,北京100853

出　　处：《中国呼吸与危重监护杂志》2005年第1期62-64,i001,共4页Chinese Journal of Respiratory and Critical Care Medicine

摘　　要：目的探讨急性缺氧型肺动脉高压(PAH)对左心室功能的影响及其分子生物学机制。方法在建立急性缺氧型PAH兔模型的基础上,采用血流动力学、HE染色、原位细胞凋亡、免疫组化和原位杂交技术对急性缺氧型PAH的左室功能和心肌细胞凋亡进行研究。结果急性缺氧型PAH可致左心室舒张功能不全,对左心室收缩功能无明显影响(P>005);缺氧型PAH组的左室心肌细胞凋亡指数(170±30)高于对照组(20±03,P<001),缺氧型PAH组左室心肌Bax蛋白和mRNA表达明显上调,Bcl2蛋白和mRNA呈弱阳性表达,与对照组相比有显著性差异(P<001)。结论急性缺氧型PAH可以上调凋亡基因的表达,使促凋亡基因和抑凋亡基因的表达失衡。心肌细胞凋亡可能与左心室舒张功能不全有关。Objective To explore the celluar and molecular mechanisms of congestive heart failure due to acute hypoxia pulmonary hypertension.Methods A rabbit model of acute hypoxia pulmonary hypertension was established.The function of left ventricle was studied dynamically while light microscope,TUNEL,immune histochemistry and in situ hybridization were employed to detect cardiomyocyte apoptosis.Results Pulmonary artery hypertension diastolic dysfunction of ventricle was observed in the rabbits with acute hypoxia.Cardiomyocyte apoptosis index in the model was higher than that in the control.The expression of Bcl-2,Bax mRNA and proteins in left ventricular myocardium were up-regulated significantly.Conclusion Acute hypoxia pulmonary hypertension could induce up-expression of pro-apoptosis gene resulting in excessive cardiomyocyte apoptosis that may contribute to left ventricular dysfunction.

关 键 词：急性缺氧 心肌细胞凋亡 PAH 左心室功能 肺动脉高压 表达 对照组 左室心肌 左心室舒张功能不全 上调 

分 类 号：R543.2[医药卫生—心血管疾病]