中文摘要：

目的 观察苦参碱对病理条件下（缺血、酸中毒）单个心室肌细胞快速延迟整流钾电流（rapid component of delayed rectifier potassium current，IKr）的作用，初步探讨苦参碱治疗缺血性心律失常的作用机制。方法 冠状动脉左前降支结扎建立家兔心肌梗死模型，应用全细胞膜片钳技术记录酶解法分离的心肌梗死模型家兔苦参碱灌胃1mon后右心室心肌细胞 IKr的变化。在pH=7．4和pH=6．5的条件下，应用全细胞膜片钳技术记录苦参碱对酶解法分离的豚鼠心室肌细胞，IKr的作用。结果 在正常细胞外液（pH=7．4）的条件下苦参碱（50μmol·L^-1）降低IKr,在刺激电压为＋60mV时，IKr电流密度由（12．15±0．70）pA／pF降低至（9．22±0．65）pA／pF（n=8，P〈0．05）。在细胞外液酸化（pH=6．5）的条件下苦参碱（50μmol·L^-1）仍表现抑制IKr，电流的作用，在刺激电压为＋60mV时IKr,电流密度由（7．05±0．41）pA／pF降低至（5．76±0．28）pA／pF（n=8，P〈0．05）。家兔冠状动脉结扎1mon后，在刺激电压为＋60mV时，心肌梗死组家兔心室肌细胞IKr，电流密度为（1．17±0．12）pA／pF较正常组（1．70±0．11）pA／pF降低（n=12，P〈0．05）。苦参碱组（8mg·kg～·d^-1）家兔心室肌细胞IKr电流密度为（0．86±0．25）pA／pF较心梗组降低（n=12，P〈0．05）。结论 苦参碱阻断心室肌细胞IKr。可能是其延长有效不应期，降低异位节律的发生率，治疗心律失常的机制之一。苦参碱对酸化条件及长期心肌缺血后心室肌细胞IKr，仍表现出明显的抑制作用，表明其对心肌梗死后心律失常有效。

英文摘要：

Aim To investigate the effects of matrine on the rapid component of delayed rectifier potassium current （IKr） in ischemic or/and acidic ventricular myocytes. Methods In isolated ventricular myocytes of guinea pig, the effects of matrine on IKr were observed by using the whole cell patch clamp technique at pH = 7.4 and pH = 6. 5. After ligation of left anterior descending coronary artery and giving matrine by oral administration for one month, whole cell patch clamp technique was used to record IKr in isolated rabbit ventricular myocytes. Results In ventricular myocytes of guinea pig, matrine （ 50μmol · L^-1 ） inhibited IKr significantly in the nomal extracellular fluid （ pH = 7.4）. At test potential of ＋ 60 mV, the IKr density was decreased from（ 12. 15 ± 0.70）pA/pF to（9.22 ± 0. 65 ） pA/pF （ n = 8, P 〈 0. 05 ）. Matrine could also inhibit IKr significantly in the acidifying extracellular fluid. At test potential of ＋ 60 mV, the lKr density was de-creased from（ 7.05 ±0. 41 ） pA/pF to （ 5.76 ±0. 28 ） pA/pF （ n = 8, P 〈 0. 05 ）. At test potential of ＋ 60 mV, The IKr density of myocardial cells from one month post-infarcted rabbit hearts （1.17 ± 0. 12 ） pA/pF depressed obviously compared with that of nomal group （1.70 ±0. 11） pA/pF （n = 12,P 〈0. 05）. After oral administration of matrine （ 8 mg · kg·^-1·d^-1 ） to the post-infarcted rabbits for one-month period, the IK~ density of matrine group （0. 86 ± 0. 25 ）pA/pF reduced markedly compared with that of MI group （n = 12, P 〈 0. 05）. Conclusions The inhibitory effect of matrine on IKr may contribute to its antiarrhythmic action. Matrine may be useful in treatment of ischemic arrhythmias as it is effective in acidic ventricular myocytes or post-infarcted hearts.