摘要
目的：探讨缺血缺氧性心肌损伤过程中血管紧张素－Ⅱ（Ａｎｇ－Ⅱ）与心肌胶原代谢的关系。方法：用异丙基肾上腺素（ＩＳＰ）注射大鼠，造成心肌缺血缺氧和心肌坏死模型，检测血清内ＧＯＴ、ＣＫ、ＬＤＨ、ＨＢＤＨ（羟丁酸脱氢酶）的活性，并检测心肌组织内血管紧张素－Ⅰ转换酶（ＡＣＥ）、血管紧张素－Ⅱ（Ａｎｇ－Ⅱ）和心肌胶原含量变化，观察细胞外间质效应细胞增殖情况。结果：注射ＩＳＰ后，血清ＧＯＴ、ＣＫ、ＬＤＨ、ＨＢＤＨ活性增加，心肌匀浆内ＡＣＥ、Ａｎｇ－Ⅱ含量上升，并发现在ＡＣＥ、Ａｎｇ－Ⅱ升高的同时有成纤维细胞的增生，以后心肌胶原含量明显升高。结论：心肌缺血缺氧后，心肌局部合成释放ＡＣＥ、Ａｎｇ－Ⅱ增加，使心肌成纤维细胞增殖和合成胶原能力增强，出现心肌胶原含量的增加。
AIM:To investigate the relationship between collagen metabolism and local renin angiotensin systems in injured myocardium. METHODS:Isoproterenol (ISP) was injected into Wistar rats to make a myocardial ischemia and necrotic model.The activities of GOT,CK,LDH and hydroxybutyrate dehydrogenase in serum and contents of local angiotensin-converting enzyme (ACE)content,angiotensin-Ⅱ(Ang-Ⅱ),and collagen in injured myocardium were determined,the fibroblasts in myocardium were observed by immunohistochemical method 3,7,14 and 21 days after injected ISP, respectively.RESULTS:Local ACE and Ang-Ⅱ contents were significantly increased with proliferation of the fibroblasts and increase of collagen content after ISP injection.CONCLUSION:Accumulation of collagen in injured myocardium is all related to the release of ACE and Ang-Ⅱ.Ang-Ⅱ might be a signal molecule for collagen accumulation in relatively high concentration in injured myocardium.
出处
《中国病理生理杂志》
CAS
CSCD
北大核心
1999年第2期100-102,共3页
Chinese Journal of Pathophysiology
基金
"八五"攻关课题
