Inhaled nitric oxide in the prevention of ischemic and reperfusion injuries of the heart during operations with cardiopulmonary bypass

Abstract

Currently, much attention is paid to the study of the role of nitric oxide, as a universal transmitter, in the development of various pathological conditions. NO causes relaxation of vascular smooth muscle, is involved in protection from ischemic and reperfusion injuries, is a neurotransmitter, regulates programmed cell death and proliferation, plays an important role in the secretory and reproductive system. New data indicate that inhalation of nitric oxide leads to the formation of new compounds that can be transported as thiol groups associated with protein in the blood, or act indirectly through nitrites and nitrates, the metabolites of which, as has been shown, increase over time during exposure to inhalation NO. This fact explains the extrapulmonary effects of inhaled nitric oxide. Experimental and clinical studies have convincingly shown the effectiveness of inhaled nitric oxide in the prevention and treatment of: ischemic and reperfusion injury to organs and tissues, shock, damage to the central nervous system and kidneys. For cardiac surgery, the effect of pharmacological preconditioning of the myocardium, caused by inhalation of nitric oxide, is of undoubted interest. How exactly NO has a protective effect on the heart is currently unknown, but it is possible that direct cGMP/PKG-mediated and cGMP-independent effects on the myocardium with additional relaxation of smooth muscles, inhibiting effects on platelets, anti-apoptotic, anti-inflammatory and antioxidant effectors. The number of clinical studies on the protective effect on the heart of inhaled nitric oxide is currently extremely limited, although all the work carried out confirms its additional cardioprotective effect. Most of the work is devoted to the supply of gaseous nitric oxide to the oxygenator of the heart-lung machine and does not consider other possible options for the implementation of its protective mechanism.