尼卡的平对哇巴因心脏毒性作用的影响

豚鼠iv尼卡的平(50μg/kg),可显著增加哇巴因引起心律失常的剂量及致死量。尼卡的平(0.1μmol/L)与哇巴因(1μmol/L)合用灌流离体豚鼠心脏,明显推迟和减轻哇巴因中毒时表现的心肌收缩力降低,并明显减弱哇巴因所致心脏静息张力的升高。1μmo/L哇巴因几乎完全抑制心肌Na~+、K~+—ATP酶活性;尼卡的平对该酶活性则无影响。实验结果提示尼卡的平与哇巴因合用可减轻哇巴因引起的心脏毒性作用。

THE EFFECT OF NICARDIPINE ON CARDIAC TOXICITY INDUCED BY OUABAIN

The purpose of our study is to determine whether the slow Ca2 + channel blocker, nicardipiae, could prevent or reduce the cardiac to-xicity induced by ouabain. The guinea pig heart in vivo and vitro perfusion of the isolated heart were used for the study . The results demonstrated that nicardipine ( i .v .50μg· kg-1') could significantly increase the doses of ouabain induced arrhythmias and death(P<0.01 ) . When nicardipine ( 0.1μmol/L ) was used in combination with ouabain ( 1 μmol/L ) in the perfusion medium, it could significantly delay or abolish the decline in contractile force induced by ouabain (P< 0.0l)and could attenuate the increase in resting tension (P<0.0l) induced by ouabain. The activity of membrane Na+, K+-ATPase, which was almost completely inhibited by 1 μmol/L ouabain, was unaffected by 10μmol/L nicardipine. The results metioned above suggest that simultaneous use of nicardipine and ouabain may protect against cardiac toxicity induced by ouabain.