Abstract
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) H 2O 2 (200 μM) was given for 10 min followed by 50 min recovery; III, ( n=7) thiourea (15 mM) was given in addition to H 2O 2; IV, ( n=7) thiourea given alone; V, ( n=7) catalase (150 U/ml) plus H 2O 2); 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.
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