Effect of fructose-1,6-dephosphate pretreatment on myocardial connexin43 in a rat model of acute myocardial ischemia
10.3760/cma.j.issn.0254-1416.2010.04.033
- VernacularTitle:1,6-二磷酸果糖预先给药对大鼠急性心肌缺血时缝隙连接蛋白43的影响
- Author:
Changsheng LI
;
Mengtao XING
;
Shuaiguo Lü
;
Tingkun LI
;
Gang XU
;
Yanping FENG
- Publication Type:Journal Article
- Keywords:
Fructosediphosphates;
Myocardial ischemia;
Connexins
- From:
Chinese Journal of Anesthesiology
2010;30(4):494-496
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the effect of fructose-1,6-diphosphate (FDP) pretreatment on myocardial connexin43 (Cx43) in a rat model of acute myocardial ischemia.Methods Thirty-six male 8-12 week old SD rata weighing 220-280 g were randomly divided into 3 groups (n=12 each):group Ⅰ sham operation (group S);group Ⅱ ischemia(group Ⅰ)and group Ⅲ FDP+ischemia(group F).The animals were anesthetized with intraperitoneal 10%chloral hydrate 40 mg/100 g,tracheostomized and mechanically ventilated.Acute myocardial ischemia was induced by occlusion of left anterior descending coronary artery for 30 min.Myocardial ischemia was;verified by elevation of S-T segment on ECG.In group F FDP 100 mg/kg was injected iv at 10 min before ischemia.Arrhythmia was recorded within 30 min after occlusion and the severity of arrbythmia was aggesged.The hearts were removed after 30 min myocardial ischemia.The Left ventricle area (LVA),myocardial infarct area (IA) and area at risk (AAR) were measured and AAR/LVA and IA/AAR ratios were calculated.The expression of myocardial Cx43 protein was determined by immuno-histochemestry and analysis of mean optical density.Results The severity of arrhythmia was significantly higher in group F and I than in gropu S.while lower in group F than in group I(P<0.05).The IA,IA/AAR ratio was significantly lower in group F than in group I.The myocardial Cx43 protein expression was down-regulated in group I and F as compared with group S.and was significantly lower in group I than in group F.Conclusion FDP pretreatment can protect myocardium against acute ischemia by up-regulation of myocardial Cx43 expression.
