气体信号分子硫化氢对大鼠心肌缺血再灌注心律失常的影响

目的:研究硫化氢(H2S)对大鼠心肌缺血再灌注室性心律失常的影响及作用机制。方法:以硫化氢钠(NaHS)作为H2S供体,建立心肌缺血再灌注损伤动物模型,将实验大鼠按随机原则分为假手术组、心肌缺血再灌注(I/R)组、H2S+I/R组及H2S+KATP通道阻断剂(格列本脲)+I/R组,监测大鼠心率(HR)、动脉压(ABP)、左心室内压(LVP)及左室内压力最大上升速率(+dp/dtmax)、左室内压力最大下降速率(-dp/dtmax)等血流动力学指标,观察大鼠室性心律失常的发生情况。结果:I/R组ABP(12.6±1.3)kPa∶(14.2±1.3)kPa]、LVP(13.7±1.1)kPa∶(15.6±1.6)kPa]、+dp/dtmax(398±52)kPa/s∶(516±63)kPa/s]、-dp/dtmax(307±27)kPa/s∶(388±52)kPa/s]均较假手术组显著降低(P均0.05);H2S+I/R组HR(309±11)次/min∶(395±12)次/min、(387±10)次/min]、ABP(10.0±1.3)kPa∶(12.6±1.3)kPa、(11.7±1.2)kPa]、LVP(11.0±1.2)kPa∶(13.7±1.1)kPa、(12.6±1.0)kPa]显著低于I/R组及H2S+格列本脲+I/R组(P均0.05),且各项指标均显著低于假手术组;H2S+格列本脲+I/R组各项指标与I/R组相似,无显著差别(P均0.05)。H2S+I/R组室性早搏数(483±136)个∶(765±175)个、(700±167)个]、室性心动过速发生率(51%∶86.5%、86.3%)、室颤(33.5%∶66.5%、60.3%)死亡率(0:27%、23%)以及室性心律失常评分(2.6±0.7)分∶(4.3±0.9)分、(4.1±0.7)分]明显低于I/R组及H2S+格列本脲+I/R组(P均0.05),I/R组及H2S+格列本脲+I/R组间无显著差异(P均0.05)。结论:硫化氢可减少大鼠心肌缺血再灌注室性心律失常的发生,其作用机制可能与开放细胞内KATP通道有关。

Effects of gaseous signal molecule hydrogen sulfide on myocardial ischemia reperfusion arrhythmia in rats

Objective： To explore the effects and mechanism of hydrogen sulfide on myocardial ischemia reperfusion arrhythmia in rats. Methods： The sodium hydrosulfide （NariS） was the donor of H2S. The animal model of myocardial ischemia reperfusion was established. SD rats were randomly divided into sham operation group, myocardial ischemia reperfusion group （I/R group）, H2 S＋ 1/R group, and I/R＋ H2 S＋ KATP, channel blocker （glibenclamide） group. The hemodynamics of the rats, including heart rate （HR）, arterial blood pressure （ABP）, left ventricular pressure （LVP）, ＋dp/dt and --dp/dt were monitored. The incidence of ventricular arrhythmia in each group was also observed. Results： In I/R group, ABP（12.6±1.3）kPa：（14.2±1.3）kPa]、LVP（13.7±1.1）kPa：（15.6±1.6）kPa]、＋dp/dt max（398±52）kPa/s：（516±63）kPa/s] -dp,/dtmax（307±27）kPa/s：（388±52）kPa/s] were significantly decreased compared with those of sham operation group （P〈0.05 all） . in H2S-k I/R group, HR （309±11） times/minvs. （395±12） times/rain, （387±10） times/mini, ABP （10.0±1.3） kPa vs. （12.6_±1.3） kPa, （11.7±1.2） kPa], LVP ]- （11.0!1.2） kPavs. （13.7±1.1） kPa, （12.6±1.0） kPa] were sig- nificantly lower than those of I/R group and I/R-f H2 S-t-glihenclamide group （P〈0.05 all）. The items of I/R＋H2S ＋ glibenclamide group and I/R group showed no significant difference （P〉0.05 all）. In Ha S＋ I/R group, number of ventricular premature （483±136） vs. （765±175）, （700± 167）], incidence of ventricular tachycardia （51% vs. 86.5}4, 86.3%）, ventricular fibrillation （33.5% vs. 66.5%, 60.3%）. mortality （0 vs. 27%, 23%） and the scores of ventricular arrhythmia （2.6±0.7） scores vs. （4.3±0.9） scores, （4. 1±0.7） points] were significantly lower than those of I/R group and I/R＋ HaS-v glibenclamide group （P〈C0.05 all）. There was no significant difference between I/R group and I/R＋ H2 S＋ glibenclamide group （P〉0.05 all）. Conclusion： H2 S can reduce the incidence of ventricular arrhythmia in myocardial ischemia reperfusion rats, its mechanism may be associated with H2S open KATP channel in cells.