Toxic Oxygen Metabolites and Ischemia-Reperfusion Increase Histamine Synthesis and Release in the Isolated Rat Heart

Histamine is synthetized in the heart, and released by ischemia-reperfusion injury in several species. Histamine has arrhythmogenic, chronotropic, inotropic and vasoactive effects. Cardiac histamine release during ischemia-reperfusion may be mediated by toxic oxygen metabolites. We studied the effect of ischemia-reperfusion and toxic oxygen metabolites on release and synthesis of histamine in the isolated rat heart (Langendorff model). The following groups were included: I, (n=10) control perfusion for 60 min; II, (n=7) H2O2 (200 μM) was given for 10 min followed by 50 min recovery; III, (n=7) thiourea (15 mM) was given in addition to H2O2; IV, (n=7) thiourea given alone; V, (n=7) catalase (150 U/ml) plus H2O2); VI, (n=7) 20 min ischemia followed by 40 min reperfusion. The contents of histamine in the coronary effluent and in cardiac tissue were measured repeatedly (radioenzymatic method). Ischemia-reperfusion and toxic oxygen metabolites increased release of histamine in the coronary effluent. Concomitantly the histamine contents in cardiac tissue increased, indicating increased synthesis of histamine.