Abstract
Background Pyruvate, as an end-product of glycolysis, might influence the electrophysiological parameters of the heart by several mechanisms: Pyruvate enhances the phosphorylating potency of the cytosol; it can facilitate the reduction of inorganic phosphate and finally can influence the cytoplasamatic redox state by decreasing the H+ concentration. According to the literature, pyruvate enhances the amplitude of the action potential (APA) and also reduces the duration of the action potential (APD); hereby, it might be used to enhance the contractility in case of heart failure. Our aim was to determine the electrophysiological and hemodynamical effects of pyruvate on diabetic and control rat hearts.
Highlights
Pyruvate, as an end-product of glycolysis, might influence the electrophysiological parameters of the heart by several mechanisms: Pyruvate enhances the phosphorylating potency of the cytosol; it can facilitate the reduction of inorganic phosphate and can influence the cytoplasamatic redox state by decreasing the H+ concentration
Pyruvate enhances the amplitude of the action potential (APA) and reduces the duration of the action potential (APD); hereby, it might be used to enhance the contractility in case of heart failure
Using conventional microelectrode techniques and the Langendorff system we examined the effects of sodium pyruvate (1, 3, 10 and 30 mmol/L) on electrophysiological and hemodynamic parameters of control (n = 28) and streptozotocin-induced diabetic (n = 29) rat hearts
Summary
As an end-product of glycolysis, might influence the electrophysiological parameters of the heart by several mechanisms: Pyruvate enhances the phosphorylating potency of the cytosol; it can facilitate the reduction of inorganic phosphate and can influence the cytoplasamatic redox state by decreasing the H+ concentration. Pyruvate enhances the amplitude of the action potential (APA) and reduces the duration of the action potential (APD); hereby, it might be used to enhance the contractility in case of heart failure. Our aim was to determine the electrophysiological and hemodynamical effects of pyruvate on diabetic and control rat hearts
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