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New perspectives of nitric oxide donors in cardiac arrest and cardiopulmonary resuscitation treatment Kruzliak P; Pechanova O; Kara THeart Fail Rev 2014[May]; 19 (3): 383-90Nitric oxide (NO) is often used to treat heart failure accompanied with pulmonary edema. According to present knowledge, however, NO donors are contraindicated when systolic blood pressure is less than 90 mmHg. Based on recent findings and our own clinical experience, we formulated a hypothesis about the new breakthrough complex lifesaving effects of NO donors in patients with cardiac arrest and cardiopulmonary resuscitation therapy. It includes a direct hemodynamic effect of NO donors mediated through vasodilation of coronary arteries in cooperation with improvement of cardiac function and cardiac output through reversible inhibition of mitochondrial complex I and mitochondrial NO synthase, followed by reduction in reactive oxygen species and correction of myocardial stunning. Simultaneously, an increase in vascular sensitivity to sympathetic stimulation could lead to an increase in diastolic blood pressure. Confirmation of this hypothesis in clinical practice would mean a milestone in the treatment for cardiac arrest and cardiopulmonary resuscitation.|*Blood Pressure/drug effects/physiology[MESH]|*Cardiac Output/drug effects/physiology[MESH]|*Heart Arrest/metabolism/physiopathology/therapy[MESH]|*Hemodynamics/drug effects/physiology[MESH]|*Nitric Oxide Donors/metabolism/pharmacology[MESH]|Cardiopulmonary Resuscitation/*methods[MESH]|Cardiotonic Agents/pharmacology[MESH]|Free Radical Scavengers/pharmacology[MESH]|Humans[MESH]|Mitochondria, Heart/drug effects/metabolism[MESH]|Myocardial Stunning/drug therapy/metabolism/physiopathology[MESH]|Oxidative Stress/drug effects[MESH] |
