【摘要】 目的观察H2S对大鼠离体心脏心功能的影响,以探讨内源性H2S对心肌活动的调节意义。方法检测大鼠心肌组织中H2S的含量及生成率,并采用RT-PCR方法检测心肌组织CSE(内源性硫化氢合成的关键酶)mRNA的表达;应用Langendorff灌流大鼠离体心脏,用不同浓度NaHS(10-6-10-3mmol/L)灌流心脏,及用生理浓度NaHS(4×10-4mol/L)持续灌流20min,测量心率(HR)、左室内压差(△LVP=左室收缩压-左室舒张压)、左室内压变化速率(±dp/dtmax)、冠脉灌流量(CPF)等指标;应用KATP通道阻断剂格列苯脲预灌流,后给予生理剂量NaHS灌流,观察其是否可以阻断NaHS的效应。结果NaHS可以呈浓度依赖性抑制左心室±dp/dtmax及△LVP(P<005),但对HR、CPF没有影响,生理剂量NaHS持续灌流20min内,可以持续抑制±dp/dtmax及△LVP(P<005),而对HR、CPF几乎没有影响。KATP通道阻断剂格列苯脲可以大部分(857%)阻断生理剂量NaHS对心功能的抑制效应。结论内源性H2S可能通过开放心肌KATP通道,抑制大鼠离体心脏左心室的收缩功能。更多还原

【Abstract】 AIM: To observe the effect of hydrogen sulfide （H₂S） on the rat cardiac function in vitro, to explorer the physiological regulation of endogenous H₂S on myocardial action. METHODS: H₂S concentration and production in the rat myocardial tissues were detected. The expression of CSE （a kind of key enzyme of endogenous H₂S production） mRNA in myocardial tissues was screened by RT-PCR. Langendorff apparatus was used to perfuse the rat heart in vitro. After 20 minutes of stabilization, NaHS （10^-6 -10^-3 mol/L） were added cumulatively in order to the perfusive fluid, and another group applied physiological concentration NaHS （4×10^-4 mol/L）, continuously perfusion for 20 min, heart rate （HR）, difference of left ventricular pressure （△LVP）, left ventricular peak rate of contraction （+LV dp/dt_<sup>max ）, peak rate of relaxation （-LV dp/dt_<sup>max ） and coronary perfusive flow （CPF） were measured at the times. Finally, glibenclamide was applied to block the K_<sup>ATP channel of heart, to observe the effect of NaHS at physiological concentration on cardiac function. RESULTS: NaHS concentration-dependently inhibited left ventricular ±dp/dt_<sup>max and △LVP （P<0.05）, but had little effect on HR and CPF. The left ventricular ±dp/dt_<sup>max and △LVP were inhibited （P<0.05） by physiological concentration of NaHS （4×10^-4 mol/L） continuous perfusion for 20 min, but HR and CPF had not been affected. K_<sup>ATP channel blocker, glibenclamide, most partly （87.5%） blocked the inhibitory effect of NaHS at physiological concentration. CONCLUSION: Endogenous H₂S inhibits the left ventricular systolic function of the rat heart in vitro, at least in part, via opening myocardial K_<sup>ATP channel. [更多还原