急性压力超负荷后大鼠心肌损伤与血管紧张素Ⅱ的关系  

Relationship between angiotensinⅡ and myocardial hypoxic damage in rats after acute pressure overload 1

作　　者：冯兵[1] 陈意生[1] 何作云[1] 黄敏[1] 周晓波[1] 

机构地区：[1]第三军医大学新桥医院心内科

出　　处：《中国药理学与毒理学杂志》1999年第4期273-276,共4页Chinese Journal of Pharmacology and Toxicology

基　　金：国家自然科学基金

摘　　要：观察大鼠腹主动脉狭窄后心肌形态学动态变化及其与心肌血管紧张素Ⅱ（ＡｎｇⅡ）含量的关系． 结果表明腹主动脉狭窄形成急性压力超负荷后，大鼠心肌出现明显的缺氧性损伤，线粒体数密度减小，肿胀变性，心肌中ＡｎｇⅡ含量迅速升高，一氧化氮（ＮＯ）含量迅速降低． 卡托普利（３０ ｍ ｇ·ｋｇ－ １·ｄ－ １，术前ｐｏ ２ ｄ）可明显抑制急性压力超负荷引起的心肌中ＡｎｇⅡ含量升高和ＮＯ 含量降低，减轻心肌缺氧性损伤． 提示急性压力超负荷所致心肌缺氧性损伤可能与心肌血管紧张素系统活化有关．The morphological changes of myo cardium in rats after abdominal aorta constriction were observed to investigate the dynamic morphological changes of myocardium and its relationship with the concentration of angiotensin Ⅱ(AngⅡ) of rat hearts. The results revealed that hypoxic damage of myocardium, mitochondria swelling and decrease in number of mitochondria were obviously observed in rats immediately after acute pressure overload induced by abdominal aorta constriction. Meanwhile, the concentration of AngⅡ elevated and the content of nitrite oxide decreased immediately and markedly. Captopril(30 mg·kg -1 ·d -1 po for 2 d before operation) alleviated the hypoxic damage of myocardium, and inhibited the rise of AngⅡ and the fall of nitrite oxide content in myo cardium induced by acute pressure overload strikingly. It is suggested that myocardial damage through demanding hypoxemia induced by acute pressure overload is related to the activation of renin angiotensin system.

关 键 词：高血压 心肌缺血 血管紧张素Ⅱ 卡托普利 

分 类 号：R972[医药卫生—药品] R541.02[医药卫生—药学]