CARDIOPROTECTIVE EFFECT AGAINST ISCHEMIA-REPERFUSION INJURY OF AHC-52, A DIHYDROPYRIDINE COMPOUND WITH INHIBITORY EFFECT ON CL- BUT NOT CA2+ CURRENT

We examined the effects of a dihydropyridine compound, AHC-52, on guin ea pig myocardium. In ventricular cardiomyocytes, AHC-52 (1 mu M) had no effect on the basal peak inward and steady state currents, but inhi bited the isoprenaline-induced time independent Cl- current. In corona ry perfused right ventricular preparations, no-flow ischemia induced d ecreases in developed tension which recovered only to about 50% of ini tial values after reperfusion. AHC-52 (0.1 mu M) had no effect on deve loped tension under normal conditions and during ischemia, but signifi cantly improved the recovery of developed tension after reperfusion to about 80% of preischemic values. Thus, AHC-52 inhibits Cl- channels i n cardiac muscle and may have protective effects against ischemia-repe rfusion injury.