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...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.展开更多
Objective To evaluate the effects of BQ-123 on cardiac function and ventricular remodelling after coronary microembolization (CME) in rats. Methods We created a rat model of CME by injecting a suspension of autogenic ...Objective To evaluate the effects of BQ-123 on cardiac function and ventricular remodelling after coronary microembolization (CME) in rats. Methods We created a rat model of CME by injecting a suspension of autogenic microthrombotic particles into left ventricle. Three days after the procedure, the 30 surviving rats were randomly divided into 3 groups, each consisted of 10 rats: sham-operation group(SO), CME model group(CM) and BQ-123 intervention group(BQ). Rats in the BQ group received BQ-123 (400μg/kg per day, intraperitoneally) for 4 weeks. Plasma and myocardial endothelin-1 (ET-1) were measured by radioimmunoassay. And serial echocardiography was performed to monitor alterations of left ventricular end-systolic and end-diastolic diameter (LVESD, LVEED), and left ventricular short-axis fraction shortening(LVFS) and ejection fraction (LVEF), and physiologicography to document the changes of left ventricular systolic pressure (LVSP) and end-diastolic pressure pressure(LVEDP), and left ventricular maximum positive and negative dp/dt (±LVdp/dtmax). Results Compared with sham-operated group, both LVEDD and LVESD were increased (P【0.01), whereas LVFS and LVEF were significantly decreased (P【0.01) in CME group; LVEDP was markedly increased, while LVSP and±LVdp/ dtmax markedly reduced in CME group (P【0.01); plasma and tissue ET-1 levels increased in CME group (P【0.01). BQ-123 intervention significantly decreased both the plasma and tissue ET-1 levels (P【0.01), and markedly increased LVFS and LVEF, with significant improvement of LVSP and±LVdp/ dtmax (P【0.01). Conclusions Treatment with BQ-123 prevents ventricular remodeling after CME due to suppression of the endothelin system.展开更多
文摘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.
文摘Objective To evaluate the effects of BQ-123 on cardiac function and ventricular remodelling after coronary microembolization (CME) in rats. Methods We created a rat model of CME by injecting a suspension of autogenic microthrombotic particles into left ventricle. Three days after the procedure, the 30 surviving rats were randomly divided into 3 groups, each consisted of 10 rats: sham-operation group(SO), CME model group(CM) and BQ-123 intervention group(BQ). Rats in the BQ group received BQ-123 (400μg/kg per day, intraperitoneally) for 4 weeks. Plasma and myocardial endothelin-1 (ET-1) were measured by radioimmunoassay. And serial echocardiography was performed to monitor alterations of left ventricular end-systolic and end-diastolic diameter (LVESD, LVEED), and left ventricular short-axis fraction shortening(LVFS) and ejection fraction (LVEF), and physiologicography to document the changes of left ventricular systolic pressure (LVSP) and end-diastolic pressure pressure(LVEDP), and left ventricular maximum positive and negative dp/dt (±LVdp/dtmax). Results Compared with sham-operated group, both LVEDD and LVESD were increased (P【0.01), whereas LVFS and LVEF were significantly decreased (P【0.01) in CME group; LVEDP was markedly increased, while LVSP and±LVdp/ dtmax markedly reduced in CME group (P【0.01); plasma and tissue ET-1 levels increased in CME group (P【0.01). BQ-123 intervention significantly decreased both the plasma and tissue ET-1 levels (P【0.01), and markedly increased LVFS and LVEF, with significant improvement of LVSP and±LVdp/ dtmax (P【0.01). Conclusions Treatment with BQ-123 prevents ventricular remodeling after CME due to suppression of the endothelin system.
