ISCHEMIA-REPERFUSION AND TOXIC OXYGEN METABOLITES DO NOT INDUCE RELEASE OF IMMUNOREACTIVE ATRIAL-NATRIURETIC-FACTOR FROM ISOLATED RAT HEARTS

Secretion of immunoreactive atrial natriuretic factors (ANF) after inj ury by ischaemia-reperfusion and toxic oxygen metabolites (TOM) was in vestigated in the following groups of Langendorff-perfused rat hearts: 1.1., control perfusion; 1.2., hearts perfused with H2O2 (200 mumol l -1) as a TOM-generating agent for 10 min, followed by recovery for 30 min; 1.3., thiourea (10 mmol l-1), a hydroxyl radical scavenger, was g iven together with H2O2; 2.1., control perfusion; 2.2., ischaemia (37- degrees-C) for 20 min followed by reperfusion for 40 min. Ischaemia-re perfusion and TOM temporarily decreased left ventricular developed pre ssure and increased left ventricular end-diastolic pressure. The cardi ac effects of H2O2 were inhibited by thiourea. Coronary flow (CF) was increased by TOM and decreased by ischaemia-reperfusion. Immunoreactiv e ANF was measured sequentially in the coronary effluent by radioimmun oassay. Basal secretion of immunoreactive ANF for all groups pooled wa s 0.45 +/- 0.02 pmol min-1 (mean +/- SEM), and did not change signific antly with time in any group. In conclusion, ischaemia-reperfusion and TOM do not influence secretion of immunoreactive ANF.