[Extracorporeal Membrane Oxygenation in the Therapy of Cardiogenic Shock Due to Fulminant Myocarditis].

This article presents a clinical case of a 40-year-old woman with fulminant myocarditis which progressed rapidly to the development of cardiogenic shock resistant to standard intensive care, but with a positive response to extracorporeal membrane oxygenation.

Myocardial Protection against Ischemic and Reperfusion Injuries (Experimental Study).

The effects of hypoxic, hyperoxic, and hypoxic-hyperoxic preconditioning were examined in the prospective study on narcotized and artificially ventilated rabbits. Under artificial circulation, acute myocardial ischemia was modeled by ligation of anterior descending coronary artery, which was followed by reperfusion. The degree of ventricular arrhythmias was assessed, and the ischemic area was evaluated in percent of the area at risk. Microscopic characterization of the myocardium was employed to assess the cardioprotective effect of hypoxic and/or hyperoxic preconditioning. According to Kruskal-Wallis test, the greatest resistance of the myocardium to ischemic and reperfusion injury was observed after hypoxic-hyperoxic preconditioning (H=42.459; p=0.009). The rabbits subjected to this type of preconditioning demonstrated the least damaged myocardium in comparison with nonconditioned controls.

[PHENOMENON OF REMOTE PRECONDITIONING THE HEART AND ITS MAIN MANIFESTATIONS].

Remote ischemic preconditioning prevents reperfusion cardiomyocyte apoptosis and has the infarct-limiting effect which is maintained in the experiments on the isolated perfused heart. Remote preconditioning promotes to recovery the contractility of the heart during reperfusion, but did not affect the incidence of occlusion and reperfusion of ventricular arrhythmias. Remote preconditioning has a mild anti-inflammatory effect. Presented article is a review and formulated conclusions based on the published literature data.

[SIGNALING MECHANISM OF CARDIOPROTECTIVE EFFECT OF REACTIVE OXYGEN SPECIES].

Protein kinase Cepsilon (PKCepsilon) is a target for reactive oxygen species (ROS). It is activated with reaction products of OH* with phospholipids, which presumably include hydroperoxides of fatty acids or alkylperoxy radicals. Activation of PKCs with reactive oxygen species promotes to mito-K(ATP) channel opening and MPT pore (mitochondrial permeability transition pore) closing thereby it is increasing the resistance of cardiomyocytes to hypoxia-reoxygenation. P38 kinase and tyrosine kinases are targets of ROS. Hydroxyl radical or signaling molecules, resulting from its metabolism, may contribute to the activation of p38-kinase that increases the cardiac tolerance to the impact of ischemia-reperfusion. Src tyrosine kinase and P13-kinase apparently are not targets of ROS. The cardioprotective effect of ROS may be due to the activation of transcription factors NFkappaB and CREB.

Comparative analysis of early and delayed cardioprotective and antiarrhythmic efficacy of hypoxic preconditioning.

Hypoxic preconditioning produces an infarct-limiting effect both in the early and delayed periods. The increase in heart resistance to ischemia-repefusion was more pronounced after early preconditioning. Hypoxic preconditioning did not change heart resistance to the arrhythmogenic effect of coronary occlusion and reperfusion.

Effect of opiate peptide dalargin and des-Tyr-dalargin on cardiac pump function during ischemia-reperfusion.

Experiments on isolated perfused rat heart showed that nonselective micro- and delta-opiate receptor agonist dalargin decreased contractility of the intact heart, but had no effect on pump function of the ischemic myocardium. Dalargin analogue des-Tyr-dalargin not binding to opiate receptors decreased contractility of intact myocardium and isolated heart exposed to 45-min total ischemia. We hypothesize that the influence of dalargin is related to activation of cardiac delta-opiate receptors, while the inotropic effect of des-Tyr-dalargin is mediated by other receptors.