Phospholipase C activation is required for cardioprotection by ethanol consumption.

摘要: Regular alcohol consumption decreases the incidence of myocardial infarction (MI) and improves post-MI survival. It has previously been reported that chronic ethanol exposure induces long-term protection against cardiac ischemia/reperfusion injury, which recovery after MI. Chronic cardioprotection by requires activation myocyte adenosine A1 receptors sustained intramyocyte translocation epsilon protein kinase C. activate phospholipase C (PLC). In present paper, role PLC in mediating ethanol’s protective effect injury is investigated. Isolated hearts from guinea pigs fed 2.5% their water for four months were subjected to ischemia/reperfusion. Hearts ethanol-treated animals showed improved left ventricular developed pressure compared with controls (61% versus 38% baseline, respectively; P<0.05) decreased necrosis, assessed release creatine (263±18 U/mL × g dry weight 360±24 weight, P<0.05). Ethanol was abolished antagonist, U-73122 (50 nM). These findings suggest required injury.