Abstract

The antifibrillatory actions of HBI‐3000 (sulcardine sulfate) were studied in a conscious canine model of sudden cardiac death (SCD). Female purpose‐bred beagles were anesthetized, and left ventricular anterior wall ischemic injury was induced by a 90 minute occlusion followed by reperfusion of the left anterior descending coronary artery. Three to seven days later, the dogs were randomized into two groups: Group 1 (n = 8) received 0.9% NaCl solution for injection while Group 2 (n = 7) received 15 mg/kg of HBI‐3000 intravenously. The dogs were subjected to anodal current‐induced injury of the circumflex coronary artery, resulting in transient interruptions in coronary artery blood flow and posterolateral myocardial ischemia. The electrocardiogram confirmed the presence of regional myocardial ischemia and ventricular fibrillation (VF). Control animals developed premature ventricular complexes (PVC) followed by ventricular tachycardia, which terminated in VF in four of the eight dogs and one expired overnight. PVC was also observed in HBI‐3000 treated animals, but only one of the seven animals developed VF in SCD (p < 0.05 vs. control). The data indicate that HBI‐3000 is effective in reversing polymorphic ventricular arrhythmias and has favorable antifibrillatory actions in the post‐infarcted canine heart subjected to a remote ischemic event.Supported by HUYA Bioscience International.

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