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出 处:《中国药理学与毒理学杂志》1989年第4期259-263,共5页Chinese Journal of Pharmacology and Toxicology
摘 要:0.5μmol/L Iso作用于大鼠离体工作心脏75min后.使其主动脉流量及左室内压dP/dt_(max)降低,而心肌CPK释放明显增加,0.1μmol/L Bop能拮抗Iso对心脏的这种有害作用。结扎大鼠心脏冠状动脉10 min后再灌注,VF发生率为90%,于结扎前给予Bop,Pro或Pra均能防止VF,若干再灌注开始时给予上述药物,则无明显作用。用Iso拮抗Bop或Pro的β受体阻断作用,并不影响二药抗这种心律失常的效果。此结果提示Bop或Pro主要通过作用于缺血期心肌而抗再灌注性心律失常,其机理可能与其β受体阻断及膜稳定作用关系不大。Isoprcnaline 0.5μmol/L caused a decrease in aortic flow and-LVdP/dtmax and a marked increase in crcatinc phosphokinase(CPK)release in the isolated working rat hearts 75 min after administration of the drug.Bopindolol 0.1****umol/L could reduce the deleterious effects of isoprcnalinc on the hearts.Ventricular fibrillation(VF)oc-curcd in 90% of the hearts on rcpcrfusion following 10 min of coronary artery ligation(CAL).Bopindolol,(dl)-propranolol or prazosin,when administered before CAL,was effective in preventing the rcpcrfusion-induced arrhythmia,but ineffective when usedjust before rcpcrfusion.The antiarrhythmic effects of bopindolol or propranolol were not affected by the use of isoprenaline.It was suggested that neither beta-antagonist activity nor membrane stabilizing activity can explain the antiarrhythmic effects of the two drugs and the antiarrhythmic effects during repcrfusion may be related to their protective effects on the myocardium during the ischemic period.
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