| Background: Myocardial ischemia reperfusion injury(MIRI) is a very complicated pathophysiological course. It has been verified that after the reperfusion there will be endothelial dysfunction as well as activation of neutrophils . This 'reperfusion injury' shares many characteristics with inflammatory responses in the myocardium, leading to the release of different cytokines and chemically active compounds finally inducing myocardial injury. Statins exert a broad spectrum of cholesterol-independent protective effects following chronic treatment, including scavenging of free radicals; antiinflammatory; antiproliferative; plaque stabilization; and preservation of endothelial function. But little is known about the acute effects.Objective: We have observed the acute effects of fluvastatin on nitric oxide and intercellular adhesion molecule-1 in the reperfusion injury after myocardial ischemia in rabbits. To investigate the protective effect of short treatment of fluvastatin during myocardial ischemia reperfusion injury and the protective mechanism.Method: 21 rabbits were randomly divided into 3 groups (n=7) : ①sham group; ②the model myocardial ischemia reperfusion control group; ③flusvastatin pretreatment group. Acute application of fluvastatin was started 3h before ischemia. In the F group 10mg/kg fluvastatin was oral administered. The Sham and the IR group were oral administered with 0.9% saline. Myocardial infarction was induced by ligature of the left anterior desending artery for 40 min followed by reperfusion for 2h. Myocardial function was determined by LVSP, ±dp/dtmax and LVEDP that recorded during the experiment. At the end of reperfusion, infarct size was measured by Evans Blue and triphenyltetrazolium chloride (TTC) staining. The levels of myocardial NO, NOS were measured. The expression of ICAM-1 mRNA in myocardium was measured with RT-PCR.Result: After the reperfusion, the LVSP, ±dp/dtmax decreased and LVEDP increased markedly in the IR group compared with the Sham group( P<0.01). Compared with the IR group, F group had a better recovery of cardiac function withthe LVSP^ ±dp/dtmax increased and LVEDP decreased markedly (P<0.01). The level of myocardial NO decreased and iNOS increased markedly in the IR group than those in the Sham group(P<0.01). The level of myocardial NO increased and iNOS decreased markedly in the F group than those in the IR group(P<0.01). The level of myocardial ICAM-1 mRNA was significantly elevated in IR group compared with the Sham group (P<0.01). The level of myocardial ICAM-1 mRNA was significantly reduced in F group than that in the IR group(P<0.01). Fluvastatin reduced myocardial infarct size(28.13±2.48)% compared with the ischemia reperfusion group(38.61±2.63)% (P<0.001).Conclusion: After the myocardial ischemia reperfusion, the level of NO decreases and the expression of ICAM-1 mRNA increases. Short pretreatment with fluvastatin could increase the level of NO, decrease myocardial ICAM-1 mRNA expression, limit infart size, improve cardiac function and exerted a cardioprotective effect against myocardial ischemia reperfusion injury in rabbits.
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