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By J. Knoll and K. Kelemen (Eds.)

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Additional resources for Advances in Pharmacological Research and Practice. Proceedings of the 4th Congress of the Hungarian Pharmacological Society, Budapest, 1985

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Kamishiro,T,, Masaki,M. , 1982, Reduction of experimentally produced acute myocardial infarction size by a new synthetic inhibitor, NCO-700, against calcium-activated neutral protease. Heart J. 23:829-834. , Deth,R. , 1985, Effects of nisoldipine, a new calcium antagonist, on myocardial infarct size and cardiac dynamics 30 following acute myocardial infarction. Pharmacol. 7: 361-367. Vassalle,M. , 1984, Caffeine actions on currents induced by calcium-overload in Purkinje fibers. Pharmacol. 106:121-131.

Pharmac. , Hekimian K. : Synthesis of compounds with properties of leukotrienes C4 and D4 in gerbil brain after ischemia and reperfusion. > Di Rosa M.. , Chiara P.. Meli R.. A. Pharmac. , Takáts I. : Actionomycin D suppresses the protective effect of dexamethasone in rats affected by global cerebral ischemia. , Suqio K. : The role of glucocor­ ticoid receptors and gene expression in the anti-inflammatory action of dexamethasone. Nature 257, 680-682, /1979/ Correspondence to:Dr. M. B. 115. Hungary 59 Proc.

Secondly, plaque rupture would only be postponed by attenuating the total and peak mechanical activity of the heart. An additional action of beta-blockers could be to reduce the impact of focal ischaemia subsequent to plaque rupture and thrombosis. The simultaneous effects of focal ischaemia and catecholamine release could create a deleterious feedback loop. Local catecholamine release will promote glycogenolysis, ele­ vate intracellular cyclic AMP, and promote slow inward calcium currents, factors all predisposing to VF.

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