Calcium has been demonstrated to play an important role in hepatocyte damag
e during ischemia/reperfusion phases. Calcium influx was determined in prim
ary cultured rat hepatocytes submitted to a succession of warm hypoxia and
reoxygenation phases in the presence of diltiazem, gallopamil and a Na+/ H antiport inhibitor, HOE-694:. Only diltiazem significantly inhibited calci
um influx with higher potency after reoxygenation than after hypoxia only,
suggesting a complex mechanism of action of diltiazem which could act on di
fferent physiological functions involved in Ca2+ invasion of hepatocytes af
ter hypoxic insult.