Experiments were carried out to provide further information on the biochemical and morphological changes occurring in the guinea-pig heart after multiple ligature and reopening of the left anterior descending (LAD) coronary artery. In isolated perfused guinea-pig heart the reopening of LAD coronary artery leads to a release of histamine related to a loss of metachromasia by cardiac mast cells. The process is associated with malonyldialdehyde (MDA) production, cellular overload of calcium and ventricular arrhythmias which can be modulated by pharmacological interventions.
Coincubation of rat serosal mast cells with human platelets leads to a significant release of histamine. which dose-dependently increases when platelet aggregation is induced by various concentrations of arachidonic acid. In turn, histamine enhances platelet aggregation induced by different agonists, this effect being mimicked by pyridyl-ethyl-amine (PEA), blocked by mepyramine and amplified by ranitidine. The data suggest the existence of a platelet-derived histamine releasing factor (PDHRF) and indicate the presence of platelet H1 and H2 receptors, capable of modulating platelet aggregation.
Free radicals produced by the occlusion and opening of the left anterior descending coronary artery and/or by perfusion of isolated guinea-pig heart with FeCl3/ADP (10 microM/100 microM) induce a differential release of histamine and lactate dehydrogenase (LDH) in the perfusates with a preferential liberation of histamine in the reperfusion phase, associated with an increase of ventricular arrhythmias. The release of histamine has been correlated with malonyldialdehyde (MDA) production and tissue calcium content in left ventricular tissue. MDA increased during ischemia, while the calcium content increased when the tissue was reperfused. Under these conditions, N-t-butyl-alpha-phenylnitrone (BPN), a molecule capable of forming spin adducts with free radicals, and D-mannitol are active in preventing reperfusion-induced arrhythmias.
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