[Effect of 17beta-estradiol on myocardial inducible NOS and endothelial NOS activities after ischemia-reperfusion in rat heart model].

Objective To study the effect of 17β-estradiol(E_2)on myocardial inducible nitric oxide synthase(iNOS)and endothelial nitric oxide synthase(eNOS)activitivies of ischemia-reperfusion myocardium in rat model.Methods 40 Langendorff perfused hearts isolated from bilateral ovariectomy (OVX)rat were randomly divided into four groups:control group(Group C),in which hearts were reperfused ex vivo for 15 minutes before ischemia in rat;isehemia-reperfusion control(Group I-R),in which modified St.Thomas Ⅱ cardiopiegie solution was perfused to perform the ischemia-reperfusion; dissolvent control group(Group D),in which 0.1% dimethyl sulfoxide(DMSO)was dissolved in cardiopiegic solution;E_2 group(Group E),in which 0.1% DMSO and 5μmol of E_2 were dissolved in cardiopiegie solution.Myocardial iNOS and eNOS activities were detected before and after reperfusion. Creatin phosphokinase(CPK),lactee dehydrogenase(LDH)and nitric oxide(NO)of coronary flow were measured,and heart function was evaluated to observe the effect of E_2 on myocardial ischemia-reperfusion injury(MIRI).Results Myocardial eNOS activity declined(P0.01)and iNOS activity increased after ischemia-reperfusion(8.87±3.74 nmol/min/g in Group C,15.83±2.42 nmol/min/g in Group I-R, 17.60±5.21 nmoL/min/g in Group E;P0.01),moreover,iNOS activity was much higher in Group E (25.85±5.21 nmol/min/g,P0.01).NO production was lower in Group I-R and Group D(P0.05), and higher in Group E(30.96±4.91μmol/L in Group C,33.16±5.57μmol/L in Group E;P0.01). CPK and LDH were lower in Group E(P0.05).Recovery of heart function was better in Group E(P 0.05).Conclusions E_2 can relieve the injury of MIRI and promote heart function recovery by increasing iNOS activity and NO production.