丙泊酚对离体大鼠心脏缺血再灌注后心律失常的保护作用

王忠; 陈红; 袁文俊; 徐美英; 朱文忠

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丙泊酚对离体大鼠心脏缺血再灌注后心律失常的保护作用

王忠 , 陈红 , 袁文俊 , 徐美英 , 朱文忠

文章导航 > 蚌埠医学院学报 > 2004, 29 > 5: (385-387)

引用本文:

Citation:

丙泊酚对离体大鼠心脏缺血再灌注后心律失常的保护作用

1. 安徽省黄山市532 医院麻醉科, 安徽黄山 245041;
2. 上海第二医科大学药理学教研室, 上海 200025;
3. 第二军医大学生理学教研室, 上海 200433;
4. 上海市胸科医院麻醉科, 上海 200032;
5. 第二军医大学长海医院麻醉科, 上海 200433

作者简介: 王忠(1968-),男,江西波阳人,硕士,主治医师.

基金项目:
国家973项目基金资助(G200005695)
中图分类号: R619.9;R971.2

The protective effect of propofol on arrhythmia in isolated rat heart after ischemia-reperfusion

Department of Anesthesiology, The 532 th Hospital of PLA, Anhui 245041, China
CLC number: R619.9;R971.2

摘要: 目的: 通过测定离体大鼠工作心脏冠脉流出液儿茶酚胺浓度,研究丙泊酚对离体大鼠心脏缺血再灌注损伤后心律失常及心肌代谢的保护作用。方法: 正常雄性SD大鼠,随机分成两大组,第一大组为正常大鼠组,随机分为对照组、丙泊酚10μmol组(P10组)、50μmol组(P50组)、100μmol组(P100组)四小组(每组10只);第二大组为儿茶酚胺耗竭组,随机分为生理盐水对照组(SC组)、耗竭组(DC组)、耗竭加丙泊酚50μmol组(DP组)(每组10只)。建立大鼠离体工作心脏模型,测定冠脉流出液中儿茶酚胺和肌酸激酶(CK)浓度,测量每组动物离体心脏单发室性期前收缩(VBP)、连发室性期前收缩(SALVO)、室性心动过速(VT)、室性纤维性颤动(VF)的发生频率。结果: 缺血前各组心律失常发生率都很低,各组儿茶酚胺含量测不出,CK值差异无显著性(P>0.05)。再灌注期间,P10、P50、P100、DC和DP组心律失常发生的频率、种类和严重程度均比对照组明显减轻(P<0.01),丙泊酚各组肾上腺素(E)和去甲肾上腺素(NE)显著低于对照组(P<0.01),各组多巴胺含量差异均无显著性(P>0.05)。儿茶酚胺耗竭组中DC组和DP组冠脉流出液未测出儿茶酚胺;丙泊酚各组CK值明显低于对照组(P<0.01)。结论: 丙泊酚对离体心脏缺血再灌注后心律失常有明显的保护作用,其作用机制可能与抑制心肌缺血后儿茶酚胺的释放有关。
- 缺血再灌注 /
- 丙泊酚 /
- 心律失常 /
- 大鼠
Abstract: Objective: To investigate the protective effect of propofol on reperfusion arrhythmia and myocardial metabolism in isolated working rat heart.Methods: The healthy male SD rats were randomly divided into two experiment groups.The first experiment group was divided into 4 subgroups(with 10 animals in each subgroup):control group,propofol 10 μmol/L group(P10),50 μmol(P50) group and 100 μmol(P100) group;and the second experiment group(catecholamine depletion group) was divided into 3 subgroups(in with 10 anilmals in each subgroup):saline control group(SC),catecholamine-depleted group(DC) and catecholamine-depleted plus propofol 50 μmol group(DP).The isolated working heart model was used,and coronary outflow was collected for determination of creatine kinase(CK) and catecholamine(epinephrine,norepinephrine and dopamine) concentrations.Severity of arrhythmias was determinated with single ventricular premature beat(VPB),SALVO,ventricular tachycardia(VT) and ventricular fibrillation(VF).Results: Before ischemia,the frequency of the reperfusion arrhythmia was very low,the CK and catecholamine concentrations were not significantly different(P>0.05) among all the subgroups.During reperfusion,the frequency and severity of arrhythmias in subgroups P10,P50,P100,DC and DP were significantly less than that in the control groups(P<0.05);the epinephrine and norepinephrine concentrations in coronary outflow in subgroups P10,P50,P100 were significantly lower than that in control group,and the dopamine concentration were not significantly different in all subgroups;Catecholamine of group DC and DP was not detectable.The CK concentrations of the coronary outflow in subgroups P10,P50,P100 were significantly lower than that in control group.Conclusions: Propofol may markedly protect isolated heart from reperfusion arrhythmia through suppression of catecholamine release following ischemia-reperfusion.
- ischemia-reperfusion /
- propofol /
- arrhythmia /
- rats

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丙泊酚对离体大鼠心脏缺血再灌注后心律失常的保护作用

作者简介: 王忠(1968-),男,江西波阳人,硕士,主治医师.

1. 安徽省黄山市532 医院麻醉科, 安徽黄山 245041;
2. 上海第二医科大学药理学教研室, 上海 200025;
3. 第二军医大学生理学教研室, 上海 200433;
4. 上海市胸科医院麻醉科, 上海 200032;
5. 第二军医大学长海医院麻醉科, 上海 200433

收稿日期: 2004-03-10

基金项目: 国家973项目基金资助(G200005695)

关键词:

摘要: 目的: 通过测定离体大鼠工作心脏冠脉流出液儿茶酚胺浓度,研究丙泊酚对离体大鼠心脏缺血再灌注损伤后心律失常及心肌代谢的保护作用。方法: 正常雄性SD大鼠,随机分成两大组,第一大组为正常大鼠组,随机分为对照组、丙泊酚10μmol组(P10组)、50μmol组(P50组)、100μmol组(P100组)四小组(每组10只);第二大组为儿茶酚胺耗竭组,随机分为生理盐水对照组(SC组)、耗竭组(DC组)、耗竭加丙泊酚50μmol组(DP组)(每组10只)。建立大鼠离体工作心脏模型,测定冠脉流出液中儿茶酚胺和肌酸激酶(CK)浓度,测量每组动物离体心脏单发室性期前收缩(VBP)、连发室性期前收缩(SALVO)、室性心动过速(VT)、室性纤维性颤动(VF)的发生频率。结果: 缺血前各组心律失常发生率都很低,各组儿茶酚胺含量测不出,CK值差异无显著性(P>0.05)。再灌注期间,P10、P50、P100、DC和DP组心律失常发生的频率、种类和严重程度均比对照组明显减轻(P<0.01),丙泊酚各组肾上腺素(E)和去甲肾上腺素(NE)显著低于对照组(P<0.01),各组多巴胺含量差异均无显著性(P>0.05)。儿茶酚胺耗竭组中DC组和DP组冠脉流出液未测出儿茶酚胺;丙泊酚各组CK值明显低于对照组(P<0.01)。结论: 丙泊酚对离体心脏缺血再灌注后心律失常有明显的保护作用,其作用机制可能与抑制心肌缺血后儿茶酚胺的释放有关。

English Abstract

The protective effect of propofol on arrhythmia in isolated rat heart after ischemia-reperfusion

Department of Anesthesiology, The 532 th Hospital of PLA, Anhui 245041, China

Received Date: 2004-03-10

Abstract: Objective: To investigate the protective effect of propofol on reperfusion arrhythmia and myocardial metabolism in isolated working rat heart.Methods: The healthy male SD rats were randomly divided into two experiment groups.The first experiment group was divided into 4 subgroups(with 10 animals in each subgroup):control group,propofol 10 μmol/L group(P10),50 μmol(P50) group and 100 μmol(P100) group;and the second experiment group(catecholamine depletion group) was divided into 3 subgroups(in with 10 anilmals in each subgroup):saline control group(SC),catecholamine-depleted group(DC) and catecholamine-depleted plus propofol 50 μmol group(DP).The isolated working heart model was used,and coronary outflow was collected for determination of creatine kinase(CK) and catecholamine(epinephrine,norepinephrine and dopamine) concentrations.Severity of arrhythmias was determinated with single ventricular premature beat(VPB),SALVO,ventricular tachycardia(VT) and ventricular fibrillation(VF).Results: Before ischemia,the frequency of the reperfusion arrhythmia was very low,the CK and catecholamine concentrations were not significantly different(P>0.05) among all the subgroups.During reperfusion,the frequency and severity of arrhythmias in subgroups P10,P50,P100,DC and DP were significantly less than that in the control groups(P<0.05);the epinephrine and norepinephrine concentrations in coronary outflow in subgroups P10,P50,P100 were significantly lower than that in control group,and the dopamine concentration were not significantly different in all subgroups;Catecholamine of group DC and DP was not detectable.The CK concentrations of the coronary outflow in subgroups P10,P50,P100 were significantly lower than that in control group.Conclusions: Propofol may markedly protect isolated heart from reperfusion arrhythmia through suppression of catecholamine release following ischemia-reperfusion.