摘要
目的：探讨压力超负荷致心肌自分泌生长因子（血管紧张素Ⅱ）的机制。方法：联合应用心肌缺氧性损伤特殊染色、心肌酶组织化学染色和透射电镜观察急性压力超负荷后大鼠心肌形态学的动态变化。结果：急性压力超负荷可引起心肌明显的缺氧性损伤。结论：这种缺氧性损伤可能与急性压力超负荷后心肌局部内分泌活化有关。
Objective: To explore the mechanism of the activation of cardiac autocrine or paracrine growth factor induced by pressure overload. Methods: After the myocardium was injured by acute pressure overload in rats, the morphological changes of the myocardium were dynamically observed with special staining for myocardial hypoxic injury, enzyme histochemical staining and electron microscopy. Results: Acute pressure overload caused myocardial hypoxic injury. Conclusion: The hypoxic injury might be related to the activation of cardiac autocrine or paracrine growth factor after acute pressure overload.
出处
《第三军医大学学报》
CAS
CSCD
北大核心
1998年第5期404-407,共4页
Journal of Third Military Medical University
基金
国家自然科学基金
