Effect of cAMP on myocardial apoptosis induced by ischemia/ reperfusion injury in rat
- VernacularTitle:环磷酸腺苷对大鼠心肌缺血/再灌注细胞凋亡的影响
- Author:
Yanlin WANG
;
Said ALI
;
Chengyao WANG
- Publication Type:Journal Article
- Keywords:
Cyclic AMP;
Myocardial reperfusion injury;
Apoptosis
- From:
Chinese Journal of Anesthesiology
1994;0(04):-
- CountryChina
- Language:Chinese
-
Abstract:
ve To investigate the effect of intravenous cAMP on the myocardial infarct size, the ultrastructure of myocardium and myocardial cell apoptosis and the possible mechanism of myocardial protection affected by cAMP against ischemia /reperfusion (I/R) injury. Methods Forty SD rats of either sex weighing 250-280g were anesthetized with abdominal sodium pentobarbital 4.5mg/100g, tracheotomized and mechanically ventilated (VT = 2ml/100g, RR = 60bpm) . Myocardial I/R was produced by tying and untying of left anterior descending coronary artery. Ischemia lasted 30 min and reperfusion 2h. Rats were randomly divided into 3 groups: control group (n = 8) in which left anterior descending coronary artery was exposed and a piece of silk thread was placed around the artery but not tied; I/R group (n = 16) in which normal saline 1ml was injected into sublingual vein before I/R; cAMP group (n = 16) received intravenous cAMP 1mg/kg 5min before I/R. The animals were then sacrificed and heart was harvested for determination of myocardial infarct size (by TTC) and ultrastructure examination (electron microscope) . Apoptosis was identified by TUNEL and apoptosis index (AI) was obtained. The expression of Fas, Bcl-2 protein was measured by immunohistochemical technique. Results The infarct size was smaller in cAMP group than that in I/R group . Myocardial apoptosis and necrosis were quite obvious in I/R group whereas in cAMP group the ultrastructure of myocardium was fairly normal. The AI in I/R group was significantly higher than that in cAMP group (P 0.05 ) . Conclusions cAMP can protect myocardium from I/R injury by modulating the expression of Fas and Bcl-2 protein and inhibit apoptosis following myocardial I/R.
