The benefit of antiinflammation treatment via IL-10 in diverse experimental models of heart failure

Aim. The in vitro estimation of IL-10 effects in diverse experimental models of heart failure (HF). Material and methods. HF was induced in rats either by Dx administration in cumulative dose of 16 mg/kg or by isoproterenol administration twice in dose of 150 mg/kg. IL-10 was i/p administration daily during 7 days after HF modeling in single dose of 50 mkg/kg. Functional effects were assayed using perfused isolated heart exposed to hemodynamic and neuroendocrine efforts. Results. IL-10 improved in a similar manner in both HF models capacity of the heart regarding its adaptation to effort by volume and resistance, the most important tool being increasing of isovolumic relaxation and contraction velocity by up to 19%. Noteworthy, IL-10 led to appearance of positive inotropic effect on ET-1 action associated with cardiac output enhancement. Likewise, IL-10 augmented myocardium tolerance to ischemia and reperfusion action according to significant lesser levels of the left ventricle end diastolic pressure. Finally, IL-10 increased coronary functional reserve inherent to acetylcholine action, and coronary flow raised by 25-33% during parasympathetic stimulation. Conclusion. IL-10 notably improves analogically the functional performances of the heart in various models of experimental heart failure during hemodynamic and neuroendocrine efforts, underlying that inflammation is an important pathogenic factor of HF regardless of myocardial injury kind.