Abstract
Effects of phosphocreatine on the neurohumoral mechanisms controlling the heart under conditions of a local immune injury were studied in acute experiments on anesthetized dogs using electrophysiological, biochemical, and electron microscopy techniques. After the development of heart injury, cardiogenic depressor reflexes evoked by an intracoronary injection of veratrine and mediated by vagus mechanisms disappeared, while pressor reflexes became dominating. This phenomenon correlated with an increase in concentration of a vasoconstrictor agent, leucotriene LTC4, in the blood and with a considerable ultrastructural impairment of nerve terminals in the myocardium. Preliminary injection of phosphocreatine prevented the development of structural impairments, favored the preservation of vagosympathetic depressor reflex, and not only prevented the increase in LTC4 concentration, but even dramatically decreased its level (by 82%, as compared with the initial level). We concluded that complex protective effect of phosphocreatine provides structural and functional preservation of the receptor apparatus in the heart and can play a considerable role in normalization of neurohumoral mechanisms controlling the heart under conditions of pathological impairment.
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Neirofiziologiya/Neurophysiology, Vol. 27, No. 2, pp. 140–146, March–April, 1995.
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Pavlyuchenko, V.B., Popovich, L.F., Kotsyuruba, V.N. et al. Effects of phosphocreatine on the heart nerve structures under conditions of local immune impairment (electrophysiological and neurochemical aspects). Neurophysiology 27, 110–114 (1995). https://doi.org/10.1007/BF01305381
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DOI: https://doi.org/10.1007/BF01305381