Atrial natriuretic peptide administered just prior to reperfusion limits infarction in rabbit hearts.

摘要: We investigated whether atrial natriuretic peptide (ANP) given just prior to reperfusion reduces infarction in rabbit hearts and protection is related activation of protein kinase G (PKG). Isolated were subjected a 30-min period regional ischemia; treated received 20-min infusion ANP (0.1 microM) starting 5 min before 2 h reperfusion. decreased from 31.5+/-2.4% the risk zone untreated 12.5+/-2.0% (P<0.001). To explore mechanisms ischemic simultaneously with isatin, blocker receptor, shortly ANP's protective effect was aborted (36.8+/-2.9% infarction). There no acceptable that can be used intact organs. However, 8-(4-chlorophenylthio)-guanosine 3', 5'-cyclic monophosphate (10 microM), cell-permeable cGMP analog directly activates PKG, infused 15 after The PKG activator mimicked only 18.2+/-3.6% 5-Hydroxyde-canoate (5-HD), putative mitochondrial KATP channel (mKATP) inhibitor, abrogated (34.4+/-2.6% Unexpectedly, 1H-[1,2,4]oxadiazole- [4,3-a]quinoxalin-1-one (ODQ), soluble guanylyl cyclase also prevented infarct-sparing effect. It unclear this observation implicated participation mechanism or simply lack selectivity ODQ. Finally injury salvage kinases (RISK), phosphatidylinositol 3-kinase extracellular signal-regulated kinase, since either wortmannin PD98059 at administered protects against infarction, likely by opening mKATP, stimulation downstream kinases.