Crenesse D, Hugues M, Ferre C, Poiree J C, Benoliel J, Dolisi C, Gugenheim J
Laboratoire de Physiologie, Faculté de Médecine, Nice, France.
Pharmacology. 1999 Mar;58(3):160-70. doi: 10.1159/000028278.
Calcium has been demonstrated to play an important role in hepatocyte damage during ischemia/reperfusion phases. Calcium influx was determined in primary 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 calcium influx with higher potency after reoxygenation than after hypoxia only, suggesting a complex mechanism of action of diltiazem which could act on different physiological functions involved in Ca2+ invasion of hepatocytes after hypoxic insult.
