ABSTRACT
Objective To investigate the effects of adenosine postconditioning (AP) on serum IL-10 and TNF-α concentrations following myocardial ischemia-reperfusion(VR)in rats.Methods Twenty-four SD ratsweighing 180-250 g were randomly divided into 4 groups(n=6 each):group I sham operation (group S);group Ⅱ myocardial I/R;group Ⅲ ischemic postconditioning(group IP)and group Ⅳ AP.Myocardial I/R was induced by 30 rain occlusion of anterior descending branch of left coronary artery followed by 120 min reperfnsion.IP was induced by 3 cycles of 30 s myocardial ischemia followed by 30 s reperfusion at the end of ischemia.In AP group adenosine 1.5 mg/kg was infused at 40μg·kg-1·min-1 before the onset of reperfusion.SP,DP and HR were recorded before ischemia (baseline) at 30 min of ischemia and 30 and 120 min of reperfusion.Arterial bloodsarnples were collected at 120 min of repednsion for determination of serum TNF-α and IL-10 concentrations.Theanimals were then killed.Their hearts were removed for microscopic examination.Myocardial infarct size wasmeasured and myocardial MDA content was determined.Results BP and HR were signilicandy decreased duringreperfusion while myocardial infarct size.MDA content and serum concentrations of IL-10 and TNF-α weresignificantly increased in I/R group compared with group S.Ischemic and adenosine postconditioning significantlyattenuated hypotension,reduced infarct size,myocardial MDA content and serum TNF-α concentration and increased serum IL-10 concentration in group AP and IP as compared with I/R group.There was no significant difference in the above changes between group AP and IP. Myocardial injury was ameliorated in group AP and IP as compared with I/R group. Conclusion Adenosine postconditioning can protect myocardium from I/R injury by increasing IL-10 production and inhibiting TNF-a release.
ABSTRACT
Objective To investigate the effect of morphine postconditioning on myocardial ischemiarepedusion(I/R)injury and the role of PI3K/Akt signaling pathway in the effect.Methods Seventy male SD rats weighing 280-330 g aged 16-17 weeks Were randomly divided into 5 groups(n=14 each):group Ⅰ sham operation(S);group Ⅱ I/R;group Ⅲ morphine postconditioning(M);group Ⅳ morphine postconditioning+ wortmannin(W+M);groupV wortmannin(W).Myocardial I/R injury wa.g produced by occlusion of anterior descending branch of left coronary artery for 45 min followed by 120 min reperfusion.In group M and W+M (groupⅢ,Ⅳ)morphine 1.25 mCkg was given iv at 3 min before and 2 min after reperfusion.In group W+M and W(groupⅣ,Ⅴ)wortmannin(a specific PDK inhibitor)15μ/gkg Was given iv at 20 min before ischemia. The animals were sacrificed at the end of 120 min repedusion for assessment of ischemic and infarct area and determination of total and phosphorylated Akt expression in myocardium by Western blot.Results There were no significant differences in the size of ischemic area and total Akt expression among the 5 groups. The infarct area was significantly smaller in group M than in group I/R. The were no significant differenees in the size of infarct area between group 1/R, W + M and W (group Ⅱ , Ⅳ,Ⅴ ). The phosphorylated Akt expression was significantly upregulated in group I/R and M as compared with group S, and was significantly higher in group M than in group I/R.Conclusion The PI3K/Akt signaling pathway activation is involved in the protective effect of morphine posteondifioning on myocardium against I/R injury.