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。
AIM: To observe the effect of hydrogen sulfide (H_2S) on the rat cardiac function in vitro, to explorer the physiological regulation of endogenous H_2S on myocardial action. METHODS: H_2S concentration and production in the rat myocardial tissues were detected. The expression of CSE (a kind of key enzyme of endogenous H_2S 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_~max ), peak rate of relaxation (-LV dp/dt_~max ) and coronary perfusive flow (CPF) were measured at the times. Finally, glibenclamide was applied to block the K_~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_~max and △LVP (P<0.05), but had little effect on HR and CPF. The left ventricular ±dp/dt_~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_~ATP channel blocker, glibenclamide, most partly (87.5%) blocked the inhibitory effect of NaHS at physiological concentration. CONCLUSION: Endogenous H_2S inhibits the left ventricular systolic function of the rat heart in vitro, at least in part, via opening myocardial K_~ATP channel. [
出处
《中国病理生理杂志》
CAS
CSCD
北大核心
2005年第1期1-5,共5页
Chinese Journal of Pathophysiology
基金
国家重点基础发展规划项目(No.G2000056905)
国家自然科学基金资助项目(No.30271373)
