| ObjectiveTo evaluate the effects of atorvastatin on myocardial no reflow atfter ischemiaand reperfusion in rats，and to explore its possible mechanisms.Methods56male SD rats were randomly assigned to the following four groups:①.shamegroup（n=8）,②.ischemia and reperfusion group （n=16）,③.atorvastatin group（n=16）,④.atorvastatin+L-NNA group （n=16）. Atorvastatin20mg/Kg·dpretreatment was administered daily via oral gavage to rats for three days.L-NN，anNon-selective NOS inhibitor, intravenously administered at a dose of15mg/kg15min before ischemia.Rats in the latter three groups were underwent60min of Leftanterior descending artery (LAD) occlusion followed by120min ofreperfusion.Then to detect the level of serum CK-MB and the level of myocardialNO.Thioflavin S fluorescent dye negatively stained the myocardium, indicating theArea of NO Reflow: the myocardium unstained by Evans blue dye is the ischemicregion: the white myocardium, which was stained by triphenyltetrazolium chloride(TTC), identifies the necrosis zone,Then the areas of these were computered. toobserve the capillary endothelial cells in microcirculation and mitochondrial inmyocardial with electron mincroscopy.Results①.Aorvastatin improves the level of myocardial NO, decreased CK-MB activity(P <0.05), relieves the injury in microcirculation and myocardial mitochondrial, andreduces45%the no-reflow area and necrosis size(P <0.05);②Whereas theseeffects of atorvastatin on myocardial ischemia and reperfusion injury are partiallyabolished,and these on myocardial no reflow are completely reversed by L-NNA. Conclusions①.Atorvastatin can reduce the area of myocardial no-reflow after ischaemiaand reperfusion in rats.②.This beneficial effect is dependant on NO byup-regulateing eNOS expression and down--regulateing iNOS expression, whichactivates mitochondaial K-ATP channel and then relieves microvascular andmyocardial lnjury;③. NO may be the key material of prevention and management ofno-reflow with atorvastatin. |
PDF Full Text Request