心肌肥厚形成过程中肌醇磷脂途径的作用

目的:探讨肌醇磷脂途径在压力超负荷性心肌肥厚形成中的作用。方法:对SD大鼠行腹主动脉部分缩窄术复制心肌肥厚模型,术后10d、30d时处死动物测全心重/体重比值,以免疫印迹法测左室组织Gαq/11蛋白含量,以放免法测左室组织1,4,5-三磷酸肌醇(IP₃)含量。结果:术后10d和30d时腹主动脉部分缩窄(CA)组全心重/体重比值均高于假手术(SO)组(P＜0.01),在术后10d和30d两个时点两组大鼠左室组织Gαq/11蛋白含量均无显著差异(P＞0.05)。术后10d时CA组大鼠左室组织IP₃含量明显高于SO组(P＜0.05),但术后30d时两组IP₃含量无显著差异(P＞0.05)。结论:肌醇磷脂途径过度激活可能参与压力超负荷性心肌肥厚早期病理过程。

Role of phosphoinositide pathway in the formation of cardiac hypertrophy induced by pressure overload in rats

AIM: To investigate the role of phosphoinositide pathway in the formation of pressure-overload cardiac hypertrophy. METHODS: Cardiac hypertrophy was induced in male Sprague-Dawley rats with coarctation of abdominal aorta, whole heart weight/body weight ratio was tested after 10 or 30 days of operation. Content of Gαq/11 protein in left ventricle was detected by immunoblot analysis and concentration of IP₃ was measured by radioimmunoassay. RESULTS: At 10 and 30 days, whole heart weight/body weight ratio of coarctation aorta (CA) group was higher than that of sham-operated (SO) rats (P＜0.01). Protein Gαq/11 contents were not modified after 10 or 30 days of stenosis (P＞0.05). At 10 days, the level of IP₃ significantly increased in left ventricle of CA rats compared with the control animals (P＜0.05), but there was no difference in IP₃ level between CA and SO group after 30 days of operation. CONCLUSION: Phosphoinositide signaling pathway may play a role in the early stage of cardiac hypererophy induced by pressure overload.