CAJ | 학술논문

目的观察硫化氢对哇巴因诱发触发性心律失常的作用, 并进一步探讨其可能的作用机制. 方法采用SD大鼠, 建立离体心脏Langendorff主动脉逆行灌流系统. 应用1μmol/L哇巴因灌流心脏诱发室性心律失常, 分别观察50, 100, 200 μmol/L硫氢化钠 ( H2 S的供体) 对心律失常的影响, 全程记录心电图的变化. 按照Na+-K+-ATP酶、 Ca2+-Mg2+-ATP酶活性测定试剂盒检测各组心肌细胞Na+-K+-ATP酶、 Ca2+-Mg2+-ATP酶活性. 结果哇巴因可诱发出稳定的室性心律失常, 硫氢化钠可浓度依赖性抑制哇巴因诱发的期前收缩, 降低室速和室颤的发生率 ( P<0. 05 ) , 哇巴因抑制Na+-K+-ATP酶、 Ca2+-Mg2+-ATP酶活性, 硫氢化钠增加其活性. 结论硫化氢有抗心律失常的作用, 其机制可能与增强Na+-K+-ATP酶、 Ca2+-Mg2+-ATP酶的活性有关.
목적 관찰류화경대왜파인유발촉발성심률실상적작용, 병진일보탐토기가능적작용궤제. 방법 채용SD대서, 건립리체심장Langendorff주동맥역행관류계통. 응용1μmol/L왜파인관류심장유발실성심률실상, 분별관찰50, 100, 200 μmol/L류경화납 ( H2 S적공체) 대심률실상적영향, 전정기록심전도적변화. 안조Na+-K+-ATP매、 Ca2+-Mg2+-ATP매활성측정시제합검측각조심기세포Na+-K+-ATP매、 Ca2+-Mg2+-ATP매활성. 결과 왜파인가유발출은정적실성심률실상, 류경화납가농도의뢰성억제왜파인유발적기전수축, 강저실속화실전적발생솔 ( P<0. 05 ) , 왜파인억제Na+-K+-ATP매、 Ca2+-Mg2+-ATP매활성, 류경화납증가기활성. 결론 류화경유항심률실상적작용, 기궤제가능여증강Na+-K+-ATP매、 Ca2+-Mg2+-ATP매적활성유관.
Objective To observe hydrogen sulfide′s effect on ouabain-induced arrhythmias and further explore its possible mech-anism. Methods Healthy Sprague-Dawley rats were used to establish a Langen-dorff retrograde perfusion system. Arrhythmia was e-licited in isolated rat hearts by the perfusion of 1 μmol/L Ouabain, sodium hydrosulfide (50, 100, 200 μmol/L) was given immedi-ately after the development of first sinus arrhythmia respectively. The arrhythmias were monitored and compared by simultaneous ECG recording, and the Na+-K+-ATP and Ca2+-Mg2+-ATP of myocardial cell in each group were examined. Results Ouabain could in-duce stable ventricular arrhythmias. Sodium hydrosulfide inhibited ouabain-induced premature ventricular beats ( PVB) in a concen-tration-dependent manner, and decreased the incidents of ventricular tachycardia (VT) and ventricular fibrillation (VF) (P<0. 05). Ouabain inhibited the activity of Na+-K+-ATP and Ca2+-Mg2+-ATP, while sodium hydrosulfide increased the activity. Conclusion Hydrogen Sulfide can perform anti-arrhythmic function and its mechanism may be related to the increasing activity of Na+-K+-ATP and Ca2+-Mg2+-ATP.