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目的观察双苯氟嗪对实验性心律失常的作用及其可能机制。方法采用静脉灌流毒毛花苷G诱发豚鼠心律失常,心肌缺血再灌注诱发大鼠心律失常,观察双苯氟嗪的抗心律失常作用;利用激光共聚焦扫描显微镜观察双苯氟嗪对心室肌细胞内游离钙子浓度([Ca2 +]i)的影响。结果双苯氟嗪20mg·kg-1能提高毒毛花苷G诱发豚鼠室性早搏、室速、室颤和死亡的剂量;10 mg·kg-1提高诱发室性早搏的剂量。双苯氟嗪20 mg·kg-1减少心肌缺血再灌注诱发的大鼠室速、室颤发生率及动物死亡率;10mg·kg-1减少室颤发生率及动物死亡率。双苯氟嗪预先给药可降低豚鼠正常心室肌细胞[Ca2 +]i,并抑制细胞外高钙诱发的细胞[Ca2 +]i升高;在细胞外高钙已诱发细胞[Ca2 +]i升高的条件下,仍可降低[Ca2 +]i升高的程度。结论双苯氟嗪具有抗实验性心律失常作用,这种作用可能与其保持细胞内钙稳态有关。
Objective To observe the effect of dipfluzine on experimental arrhythmia and its possible mechanism. Methods The guinea pig arrhythmia was induced by intravenous injection of ouabain and the arrhythmia was induced by myocardial ischemia reperfusion in rats. The antiarrhythmic effect of dipfluzine was observed. The effects of dipfluzine on ventricular myocytes Effect of intracellular free calcium concentration ([Ca2 +] i). Results Dipfluzine 20 mg · kg-1 can increase the dose of furosemide G-induced premature ventricular premature beats, ventricular tachycardia, ventricular fibrillation and death; 10 mg · kg-1 increase the dose of induced premature ventricular contractions. Dipfluzine 20 mg · kg-1 decreased the incidence of ventricular fibrillation, VF and animal mortality induced by myocardial ischemia-reperfusion in rats; 10 mg · kg-1 decreased the incidence of VF and animal mortality. Preconditioning with dipfluzine decreased [Ca2 +] i in guinea pig ventricular myocytes and inhibited the increase of [Ca2 +] i in cells induced by extracellular high calcium. When extracellular calcium was added, [Ca2 +] i Elevated conditions, can still reduce the degree of [Ca2 +] i increase. Conclusion Dipfluzine has anti-experimental arrhythmia, which may be related to its maintenance of intracellular calcium homeostasis.