Ischaemia-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 injury by ischaemia-reperfusion and toxic oxygen metabolites (TOM) was investigated 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 given together with H2O2; 2.1., control perfusion; 2.2., ischaemia (37 degrees C) for 20 min followed by reperfusion for 40 min. Ischaemia-reperfusion and TOM temporarily decreased left ventricular developed pressure and increased left ventricular end-diastolic pressure. The cardiac effects of H2O2 were inhibited by thiourea. Coronary flow (CF) was increased by TOM and decreased by ischaemia-reperfusion. Immunoreactive ANF was measured sequentially in the coronary effluent by radioimmunoassay. Basal secretion of immunoreactive ANF for all groups pooled was 0.45 +/- 0.02 pmol min-1 (mean +/- SEM), and did not change significantly with time in any group. In conclusion, ischaemia-reperfusion and TOM do not influence secretion of immunoreactive ANF.
Department of Surgery, University of Tromsø, Norway.
G
G
Valen
I
I
Lettrem
J
J
Sundsfjord
J
J
Vaage
D000818:Animals; D009320:Atrial Natriuretic Factor / Q000276:immunology / Q000378:metabolism*; D001794:Blood Pressure; D003326:Coronary Circulation; D005609:Free Radicals; D006861:Hydrogen Peroxide / Q000633:toxicity*; D066298:In Vitro Techniques; D008297:Male; D017202:Myocardial Ischemia / Q000378:metabolism*; D015425:Myocardial Reperfusion; D009206:Myocardium / Q000378:metabolism*; D051381:Rats; D017208:Rats, Wistar
D005609:Free Radicals; C472610:atrial natriuretic peptide, rat; D009320:Atrial Natriuretic Factor; D006861:Hydrogen Peroxide