Objective To investigate the cardioprotective effects of morphine on ischemic reperfused rat heart in vitro and its mechanism Methods The isolated rat heart was perfused in a Langendorff apparatus Infarct myo...Objective To investigate the cardioprotective effects of morphine on ischemic reperfused rat heart in vitro and its mechanism Methods The isolated rat heart was perfused in a Langendorff apparatus Infarct myocardium was determined by TTC Coronary flow (CF), heart rate (HR), left ventricular pressure (LVP), the first derivative of ventricular pressure (LVP/dtmax) and infarct size after ischemia and reperfusion in rat heart given 0.3 μmol/L morphine were observed The effects of naloxone and glibenclamide on the cardioprotection of morphine were also measured Results After ischemia and reperfusion, CF, HR, LVP and LVP/dtmax of isolated rat hearts decreased significantly ( P <0 01) After morphine preconditioning, HR, LVP and LVP/dtmax increased ( P <0 01) and infarct size was reduced significantly ( P <0 01), while no significant change in CF ( P >0 05) The cardioprotective effects of morphine were abolished by naloxone or glibenclamide completely Conclusions Morphine can reduce ischemia reperfusion injuries in isolated rat heart The cardioprotective effects of morphine are mediated by a local opioid receptor K ATP channel linked mechanism in rat hearts展开更多
Objective To explore protective effects of electroacupuncture at ＂Nèiguān＂ （内关 PC 6） for preconditioning on myocardial ischemia-reperfusion injury （MIRI） and the mechanisms involved. Methods Forty-eight ...Objective To explore protective effects of electroacupuncture at ＂Nèiguān＂ （内关 PC 6） for preconditioning on myocardial ischemia-reperfusion injury （MIRI） and the mechanisms involved. Methods Forty-eight male Wistar rats were randomly divided into a sham operation group （Group N）, a MIRI group （Group M） and an electroacupuncture （EA） group （Group E）. The MIRI model was established by ligating the left anterior descending artery （LAD） for 30 min followed by reperfusion for 120 min. Partition sutures were passed under LAD without ligation for rats in Group N. Rats in Group E were pretreated with electroacupuncture （EA） applied at bilateral ＂Nèiguān＂ （内关 PC 6） for 20 min once a day for 3 consecutive days before ischemia. The infarct size plus the area at risk was evaluated by 2,3,5-triphenyltetrazolium chloride staining, and serum isoenzyme of creatine kinase （CK-MB） and lactate dehydrogenase （LDH） levels were measured by biochemical methods. Myocardium morphological changes were observed under light microscopy. The mRNA expressions of myocardial δ and κ opioid receptors （DOR and KOR） were tested by real-time RT-PCR measurements. Results The myocardial infarct size in Group E was more significantly decreased than that in Group M （P0.05）. The levels of CK-MB [（980？±？92） U/L] and LDH [（2743？±？124） U/L] in Group M were significantly higher than those in Group N [（312？±？41） U/L] and [（530？±？56） U/L], respectively （both P0.01）. The levels of CK-MB [（572？±？70） U/L] and LDH [（1819？±？97） U/L] in Group E were significantly lower than those in Group M （both P0.01）. There were no significant differences in mRNA expressions of DOR and KOR between Group M and Group N （both P0.05）, but DOR expression in Group E was significantly higher than that either in Group M or in Group N （both P0.01 ）. No significant differences were found in KOR expression among the three groups （all P0.05）. Conclusion Up-regulation of expression of δ opioid receptors may be involved in protective effects of EA at Nèiguān （内关 PC 6） for preconditioning on MIRI.展开更多
目的观察κ阿片受体选择性激动剂(U50488H)及β肾上腺素受体激动剂(异丙肾上腺素,ISO)对大鼠心脏缺血/再灌注(ischemia and reperfusion,I/R)引起的心律失常的影响,初步探讨U50488H对心肌细胞缝隙连接蛋白Cx43的调节机制。方法实验大鼠...目的观察κ阿片受体选择性激动剂(U50488H)及β肾上腺素受体激动剂(异丙肾上腺素,ISO)对大鼠心脏缺血/再灌注(ischemia and reperfusion,I/R)引起的心律失常的影响,初步探讨U50488H对心肌细胞缝隙连接蛋白Cx43的调节机制。方法实验大鼠随机分为5组即对照组、I/R组、ISO+I/R组、U50488H+ISO+I/R组、Nor-BNI(κ阿片受体阻断剂)+U50488H+ISO+I/R组。观察每组心律失常的发生情况并计算心律失常评分,RT-PCR检测Cx43 mRNA表达及用免疫组化方法显示大鼠心肌Cx43的分布特征,半定量统计分析。结果①心律失常评分:ISO+I/R组高于I/R组(P<0.05),在ISO前给予U50488H则可以降低ISO引起的心律失常(P<0.05),其效应可被Nor-BNI阻断。②Cx43 mRNA水平:ISO+I/R组比I/R组略增高,在ISO前给予U50488H则可使基因表达水平降低(P<0.05),其效应可被Nor-BNI阻断。③Cx43蛋白表达:ISO+I/R组Total-Cx43高于I/R组(P<0.05),P-Cx43降低但与I/R组比较差异无统计学意义,给予U50488H后,可提高总Cx43和P-Cx43表达量(P<0.05),其效应可被Nor-BNI阻断。结论κ阿片受体激动剂可通过抑制β肾上腺素受体对Cx43调节从而发挥抗缺血/再灌注性心律失常的作用。展开更多
目的:探讨κ-阿片受体是否参与缺血后处理的对抗心肌缺血/复灌(I/R)损伤和心肌细胞缺氧/复氧(H/R)损伤的作用及其机制。方法:采用离体大鼠心脏Langendorff灌流模型,全心停灌30 m in、复灌120 m in复制I/R模型,测定心室力学指标和复灌各...目的:探讨κ-阿片受体是否参与缺血后处理的对抗心肌缺血/复灌(I/R)损伤和心肌细胞缺氧/复氧(H/R)损伤的作用及其机制。方法:采用离体大鼠心脏Langendorff灌流模型,全心停灌30 m in、复灌120 m in复制I/R模型,测定心室力学指标和复灌各时点冠脉流出液中乳酸脱氢酶(LDH)含量。实验结束测定心肌组织form azan含量。酶解分离的心肌细胞采用缺氧60 m in、复氧60m in复制H/R模型,测定心肌细胞存活率。结果:在离体心脏模型上,与I/R组相比,缺血后处理组心肌组织的form azan含量明显增高,复灌期间冠脉流出液中LDH含量明显降低,同时缺血后处理明显改善心室力学指标,缓解冠脉流量的减少;在分离心肌细胞模型上,缺氧后处理明显提高心肌细胞存活率。κ-阿片受体阻断剂nor-b inaltorph im ine(nor-BN I)和线粒体ATP敏感性钾通道(m itoKATP)阻断剂5-hydroxydecanoate(5-HD)在离体大鼠心脏模型和分离心肌细胞模型上均能明显减弱缺血后处理的作用。同时在心肌细胞模型上,与H/R组相比,κ-阿片受体激动剂U 50488H明显提高心肌细胞存活率,其作用可被m itoKATP阻断剂5-HD所阻断。结论:缺血后处理具有抗心肌缺血/复灌损伤的作用,这种保护作用可能与其激活κ-阿片受体和m itoKATP有关。展开更多
文摘Objective To investigate the cardioprotective effects of morphine on ischemic reperfused rat heart in vitro and its mechanism Methods The isolated rat heart was perfused in a Langendorff apparatus Infarct myocardium was determined by TTC Coronary flow (CF), heart rate (HR), left ventricular pressure (LVP), the first derivative of ventricular pressure (LVP/dtmax) and infarct size after ischemia and reperfusion in rat heart given 0.3 μmol/L morphine were observed The effects of naloxone and glibenclamide on the cardioprotection of morphine were also measured Results After ischemia and reperfusion, CF, HR, LVP and LVP/dtmax of isolated rat hearts decreased significantly ( P <0 01) After morphine preconditioning, HR, LVP and LVP/dtmax increased ( P <0 01) and infarct size was reduced significantly ( P <0 01), while no significant change in CF ( P >0 05) The cardioprotective effects of morphine were abolished by naloxone or glibenclamide completely Conclusions Morphine can reduce ischemia reperfusion injuries in isolated rat heart The cardioprotective effects of morphine are mediated by a local opioid receptor K ATP channel linked mechanism in rat hearts
基金Supported by Guangdong TCM Bureau Project: 2008115
文摘Objective To explore protective effects of electroacupuncture at ＂Nèiguān＂ （内关 PC 6） for preconditioning on myocardial ischemia-reperfusion injury （MIRI） and the mechanisms involved. Methods Forty-eight male Wistar rats were randomly divided into a sham operation group （Group N）, a MIRI group （Group M） and an electroacupuncture （EA） group （Group E）. The MIRI model was established by ligating the left anterior descending artery （LAD） for 30 min followed by reperfusion for 120 min. Partition sutures were passed under LAD without ligation for rats in Group N. Rats in Group E were pretreated with electroacupuncture （EA） applied at bilateral ＂Nèiguān＂ （内关 PC 6） for 20 min once a day for 3 consecutive days before ischemia. The infarct size plus the area at risk was evaluated by 2,3,5-triphenyltetrazolium chloride staining, and serum isoenzyme of creatine kinase （CK-MB） and lactate dehydrogenase （LDH） levels were measured by biochemical methods. Myocardium morphological changes were observed under light microscopy. The mRNA expressions of myocardial δ and κ opioid receptors （DOR and KOR） were tested by real-time RT-PCR measurements. Results The myocardial infarct size in Group E was more significantly decreased than that in Group M （P0.05）. The levels of CK-MB [（980？±？92） U/L] and LDH [（2743？±？124） U/L] in Group M were significantly higher than those in Group N [（312？±？41） U/L] and [（530？±？56） U/L], respectively （both P0.01）. The levels of CK-MB [（572？±？70） U/L] and LDH [（1819？±？97） U/L] in Group E were significantly lower than those in Group M （both P0.01）. There were no significant differences in mRNA expressions of DOR and KOR between Group M and Group N （both P0.05）, but DOR expression in Group E was significantly higher than that either in Group M or in Group N （both P0.01 ）. No significant differences were found in KOR expression among the three groups （all P0.05）. Conclusion Up-regulation of expression of δ opioid receptors may be involved in protective effects of EA at Nèiguān （内关 PC 6） for preconditioning on MIRI.
文摘目的观察κ阿片受体选择性激动剂(U50488H)及β肾上腺素受体激动剂(异丙肾上腺素,ISO)对大鼠心脏缺血/再灌注(ischemia and reperfusion,I/R)引起的心律失常的影响,初步探讨U50488H对心肌细胞缝隙连接蛋白Cx43的调节机制。方法实验大鼠随机分为5组即对照组、I/R组、ISO+I/R组、U50488H+ISO+I/R组、Nor-BNI(κ阿片受体阻断剂)+U50488H+ISO+I/R组。观察每组心律失常的发生情况并计算心律失常评分,RT-PCR检测Cx43 mRNA表达及用免疫组化方法显示大鼠心肌Cx43的分布特征,半定量统计分析。结果①心律失常评分:ISO+I/R组高于I/R组(P<0.05),在ISO前给予U50488H则可以降低ISO引起的心律失常(P<0.05),其效应可被Nor-BNI阻断。②Cx43 mRNA水平:ISO+I/R组比I/R组略增高,在ISO前给予U50488H则可使基因表达水平降低(P<0.05),其效应可被Nor-BNI阻断。③Cx43蛋白表达:ISO+I/R组Total-Cx43高于I/R组(P<0.05),P-Cx43降低但与I/R组比较差异无统计学意义,给予U50488H后,可提高总Cx43和P-Cx43表达量(P<0.05),其效应可被Nor-BNI阻断。结论κ阿片受体激动剂可通过抑制β肾上腺素受体对Cx43调节从而发挥抗缺血/再灌注性心律失常的作用。
文摘目的:探讨κ-阿片受体是否参与缺血后处理的对抗心肌缺血/复灌(I/R)损伤和心肌细胞缺氧/复氧(H/R)损伤的作用及其机制。方法:采用离体大鼠心脏Langendorff灌流模型,全心停灌30 m in、复灌120 m in复制I/R模型,测定心室力学指标和复灌各时点冠脉流出液中乳酸脱氢酶(LDH)含量。实验结束测定心肌组织form azan含量。酶解分离的心肌细胞采用缺氧60 m in、复氧60m in复制H/R模型,测定心肌细胞存活率。结果:在离体心脏模型上,与I/R组相比,缺血后处理组心肌组织的form azan含量明显增高,复灌期间冠脉流出液中LDH含量明显降低,同时缺血后处理明显改善心室力学指标,缓解冠脉流量的减少;在分离心肌细胞模型上,缺氧后处理明显提高心肌细胞存活率。κ-阿片受体阻断剂nor-b inaltorph im ine(nor-BN I)和线粒体ATP敏感性钾通道(m itoKATP)阻断剂5-hydroxydecanoate(5-HD)在离体大鼠心脏模型和分离心肌细胞模型上均能明显减弱缺血后处理的作用。同时在心肌细胞模型上,与H/R组相比,κ-阿片受体激动剂U 50488H明显提高心肌细胞存活率,其作用可被m itoKATP阻断剂5-HD所阻断。结论:缺血后处理具有抗心肌缺血/复灌损伤的作用,这种保护作用可能与其激活κ-阿片受体和m itoKATP有关。
