Endocardial endothelium (EE) is a barrier which controls the passage of macromolecules and fluids between the blood and the adjacent miocardial interstitium. At the same time it is the place of synthesis of numerous endothelial mediators. Histamine as an inflammation mediator increases the permeability of the endothelium, but also has a positive inotropic and chronotropic effects on the heart through the activation of histamine H1 and H2 receptors. The aim of this study was to determine the importance of the role of endocardial endothelium in the effect of histamine on myocardial contraction in the conditions of histamine receptors blockade. The study was carried out on the samples of the right ventricle of the albino Wistar rats (n = 42, age 8 weeks, body mass 180-200g) presented in two experimental models. The first experimental model presented the right ventricle of the rat heart with an intact endocardial endothelium and the second with the endothelium chemically removed by immersion of the chamber in a 1% solution of Triton X-100. Histamine (1x10-4 mol/l) increases the contraction of the right ventricle of the heart with intact endocardial endothelium but also with the removed endocardial endothelium. The effect of the histamine on the contraction was significantly increased in the absence of endocardial endothelium (p<0.05). H1 receptor antagonist, pyrilamine (1x10-6 mol/l) significantly inhibites the positive inotropic effect of histamine on the heart in both groups, with or without endocardial endothelium. Modulatory role of endocardial endothelium in the effect of histamine after the receptors blockade by pyrilamine is not significant. H2 receptor antagonist, cimetidine (1x10-4 mol/l), blocks the positive inotropic effect of histamine on the heart reagardless of the preservation of the endocardial endothelium. Our results indicate the undoubted importance of the modulatory role of endocardial endothelial in the effect of histamine on myocardial contraction.
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