急性压力超负荷诱导心肌内分泌活化.doc

???? 急性压力超负荷诱导心肌内分泌活化* ???? ????　摘要　目的： 探讨压力超负荷致心肌肥大的跨膜信号传递机制。方法：利用放射免疫法及分光光度法动态观察压力超负荷后大鼠心肌组织血管紧张素转换酶活性，血管紧张素II、内皮素和一氧化氮含量的变化，并观察它们与压力超负荷心肌肥大的关系。结果： 随大鼠动脉血压逐步升高，心肌组织中血管紧张素转换酶活性，血管紧张素II、内皮素含量均迅速升高（P＜0.05）,并持续保持高水平，血管紧张素II升高早于内皮素,而一氧化氮含量迅速降低并持续受抑(P＜0.05)。结论：心肌内分泌活化可能是介导压力超负荷致心肌肥大的重要机制。　　主题词　压力；心肌病，肥大性；心肌；内分泌学 Endocrine activation of rat heart stimulated by pressure overload FENG Bing，CHENG Yi-Sheng，HE Zuo-Yun，HUANG Ming，ZHOU Xiao-BoDepartment of Cardiology,Xinqiao Hospital,The Third Military Medical University,Chongqing(400037) 　　Abstract　AIM：To investigate the mechanism of mechanical signal transmembrane transduction in heart hypertrophy induced by pressure overload. METHODS：Changes of activity of angiotensin converting enzyme(ACE),concentractions of angiotensin II (Ang II) and endothelin-1 (ET) and nitrite oxide (NO) in rat hearts were observed dynamically using radioimmunoassay and colorimetric method,and its role in the pathogenesis of heart hypertrophy induced by pressure overload was also analyzed. RESULTS:Accompanyed gradually elevation of arterial pressure after abdominal aorta constriction,activity of ACE,concentration of Ang Ⅱ and ET increased rapidly,and kept at high level (P＜0.05),the elevation of Ang Ⅱ was earlier than that of ET. However,concentration of NO decreased immediately and kept at low level (P＜0.05). CONCLUSION:Heart hypertrophy induced by pressure overload may be mediated by myocardial endocrine activation.　　MeSH　Pressure; Cardiomyopathy,hypertrophic; Myocardium; Endocrinology 　　大量临床和动物试验均证实压力超负荷是心肌肥大的独立致病因素。但是，对于心肌细胞如何将压力超负荷力学信号转化为细胞内生化反应这一关键信号传递环节至今尚未完全阐明［1，2］。80年代以来研究表明心脏具有内分泌功能，外界因素可刺激心肌分泌多种活性物质，其中含有促生长因子。本研究旨在观察压力超负荷后心肌内分泌活化情况，并探讨内分泌活化与压力超负荷致心肌肥大的关系。 　　材料与方法 　　一、动物模型复制及实验分组：　　选用本校实验动物中心提供的健康、雄性Wistar大鼠56只，体重(150.0±30.7) g，实验前饲养1周，给予常规鼠饲料，自由饮自来水，使其适应。将大鼠随机分为对照组(control group,CG,24只，各时点亚组设3只大鼠)、手术组（operation group,OG,32只，各时点亚组为4只），参照黄生宁［3］法复制腹主动脉缩窄大鼠高血压模型，分别在术后10 min、30 min、1 h、4 h、1 d、5 d、10 d、30 d测定血压（动脉收缩压systolic arterial pressu