| Objectives Observe the effects of ischemic postconditioning on connexin43 of myocardial gap junction after ischemia-reperfusion in rats in vivo, to study the protective mechanism against Ischemia-Reperfusion.Methods Male Wistar rats were randomly divided into 4 groups: sham operation group, ischemia-reperfusion group, ischemic preconditioning group, ischemic postconditioning group, 8 rats in each group. The myocardial ischemia-reperfusion model was established by ligation of the left anterior descending coronary artery for 30 minutes, followed by 120 minutes of reperfusion. ECG monitoring the entire process. After reperfusion, the expression of connexin43 of the ischemia-reperfusion myocardium was studied by immunohistochemistry technique; the expression level of the mRNA of Cx43 were measured by reverse transcription-PCR; with ventricular arrhythmia score(VAS) to evaluate the occurrence of ventricular arrhythmias rate; application of xanthine oxidase method and thiobarbituric acid test in each group animal serum malondialdehyde (MDA) levels and superoxide dismutase (SOD) activity; monitoring left ventricular systolic blood pressure, left ventricular end-diastolic pressure, and other indicators of changes in cardiac function by BL-410 biological function of the artery catheter system.Results1. Compared with the sham-operated group, the expression of Cx43 is envidently decreased (P <0.01) and the distribution is disturbed, the Cx43 expression of the mRNA level was significantly decreased (P <0.01), ventricular arrhythmia score and serum MDA were significantly increased (P <0.01), serum SOD activity and left ventricular systolic and diastolic function were decreased (P <0.01).2. Ischemic preconditioning group compared with ischemia-reperfusion group , the Cx43 expression of the mRNA level was significantly increased (P <0.01), ventricular arrhythmia score and serum MDA were significantly decreased (P <0.01), serum SOD activity and left ventricular systolic and diastolic function were decreased (P <0.05).3. Ischemic postconditioning group compared with ischemia-reperfusion group , the Cx43 expression of the mRNA level was significantly increased (P <0.01), ventricular arrhythmia score and serum MDA were significantly decreased (P <0.01), serum SOD activity was decreased ( P <0.01), left ventricular systolic and diastolic function was decreased (P <0.05).4. Ischemic postconditioning group compared with ischemic preconditioning group, the Cx43 expression of the mRNA level, ventricular arrhythmias score, serum MDA, serum SOD activity and left ventricular systolic and diastolic function had no statistical significance differences(P> 0.05).Conclusions1. Myocardial ischemia-reperfusion can degrade the mRNA of Cx43 and decrease the expression level of Cx43, induce oxidative damages to myocardium and decrease the systolic and diastolic function of myocardium.2. Ischemic preconditioning can effectively reduce the degradation Cx43 mRNA of ventricular myocyte caused by ischemia-reperfusion, retain the normal number and distribution of Cx43, decrease oxidative damages to myocardium and elevate the systolic and diastolic function of myocardium.3. Ischemic postconditioning can also effectively reduce the degradation Cx43 mRNA of ventricular myocyte caused by ischemia-reperfusion, retain the normal number and distribution of Cx43, decrease oxidative damages to myocardium and elevate the systolic and diastolic function of myocardium.4. There is a similar myocardial protective effection between Ischemic postconditioning and ischemic preconditioning, they may influence the expression of Cx43 and protect myocardium through the common signal transduction path. Ischemic postconditioning has a better workability and is easy to clinical application. |
