Ischaemia-reperfusion and toxic oxygen metabolites do not induce release of immunoreactive atrial natriuretic factor from isolated rat hearts

Abstract

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 (200μmoll⁻¹) as a TOM-generating agent for lOmin, followed by recovery for 30min; 1.3., thiourea (10mmoll⁻¹), a hydroxyl radical scavenger, was given together with H₂O₂; 2.1., control perfusion; 2.2., ischaemia (37 °C) for 20min followed by reperfusion for 40min. 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±0.02pmolmin⁻¹ (mean±SEM), and did not change significantly wtih time in any group. In conclusion, ischaemia-reperfusion and TOM do not influence secretion of immunoreactive ANF.

Key Words:

• ANF
• ischaemia
• oxygen free radicals
• reperfusion