Perioperative myocardial ischemia(PMI) is mainly caused by increasesin sympathetic nervous system activity due to stress,which results incoronary endothelial dysfunction,hence that it is hypothesized thatcaptopril may improve PMI.In our study,twenty mongrel dogs wererandomized for four groups;group Ⅰ:control,group Ⅱ:myocardialinfarction (MI) model,Group Ⅲ:MI+partial gastrectomy,group Ⅳ:MI+captopril+partial gastrectomy.Myocardial infarction wasproduced by ligation of left anterior descending coronary artery exceptthe group Ⅰ.In the group Ⅲ and Ⅳ,the hemodynamics,plasmaendothelin (ET) and nitric oxide (NO) on baseline,pre-andpostoperation were investigated two weeks after MI All animals werekilled by overdose anesthetic and their cardiac samples of non-infarction area taken for examining nitric oxide synthase (NOS)mRNA expression levels in vascular endothelial cells.Results:ingroup Ⅲ,the operation decreased the maximal rate of left ventricularpressure rise (LV+dP/dtmax),cardiac index (CI) and plasma No level,and increased left ventricular end diastolic pressure (LVEDP),time-course of isovolumic pressure fall (T constant),total peripheralresistance (TPR) and the levels of ET.In group Ⅳ,40 minutes afteradminstration of captopril,the TPR was decresed,and the t constantwas incresed significantly.The operation attenuated the TPR and Tconstant,but didn’t affect the other values.In situ hybridization it wasshowed that the expression levels of NOS mRNA was the highest ingroup Ⅰ,lower in groups Ⅱ and Ⅳ,and the lowest in group Ⅲ.Conclusions:1.Partial gastrectomy performed after myocardialinfarction may induce left ventricular systolic and diastolic dysfunction,and may produce coronary endothelial dysfunction;2.captopril canimprove left ventricular dysfuction and endothelial dysfunctioninduced by noncardiac operation.
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