The variance of calcium homeostasis is known as a risk factor for the development of heart failure. A study of calcium-regulating hormones is a crucial element to understand underlying pathophysiological mechanisms of heart failure. Pro-inflammatory factors, released during mechanical, hypoxic or bacterial damage of myocardial cells, lead to an imbalance of calcium and disrupt to heart function. The investigation of mentioned factors influence mechanism on the heart, is an urgent solution for preventing the development of heart failure.
Present study aimed to reveal the role of calcium-regulating hormones in heart functional activity and their possible involvement in the development of heart failure. The pharmacological analysis of the action mechanism of bacterial lipopolysaccharides on heart functional activity was carried out using a calcium channel blocker.
The concentrations of calcium-regulating hormones in blood serum in patients suffering from heart failure was determined by immunoassay enzyme method, and ionized calcium and inorganic phosphate concentrations - by spectrophotometric method. The photoelectrical method was used to determine the direct effect of calcium-regulating hormones and possible calciumdependent action mechanism of bacterial lipopolysaccharides on the isolated frog’s heart.
Clinical findings show that chronic heart failure is accompanied by shifts in the calciumregulating hormonal system and blood electrolyte balance. In vitro experiments on isolated frog hearts have shown the potentiating effect of parathyroid hormone, its related protein, calcitonin, and vitamin D3 on myocardial contractility. It has been shown, that bacterial lipopolysaccharides suppress the contractile and rhythmogenic functions of the myocardium, and their action can be mediated through a calcium-dependent mechanism.
The increase of parathyroid hormone in chronic heart failure has a protective significance aimed at maintaining the contractile ability of a weakened myocardium and preserving cardiac output. Bacterial lipopolysaccharides are able to suppress functional activity of the heart by calcium-dependent mechanism.
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