Nitric oxide and mitochondria injuries in kidney tissue upon a simulation of cardiopulmonary bypass and circulatory arrest: an experimental study

Introduction: Surgical interventions under cardiopulmonary bypass and circulatory arrest are complicated by impaired microcirculation in tissues; during hypoxic period the mitochondria dysfunction becomes the leading pathogenetic factor of ischemia-reperfusion injuries. In this regard, the search for methods of organ protection seems to be an extremely urgent task. The using of nitric oxide can be a promising technique given its pluripotent properties. Objective: The study was aimed to examining of mitochondria injuries in kidney biopsies stipulated by cardiopulmonary bypass and circulatory arrest when simulating cardiac surgery, as well as to assessing the potentials of organ protection with nitric oxide in the experiment. Methods: The study was carried out on Altai breed sheep and included simulating of cardiopulmonary bypass and circulatory arrest. The first group (n = 6) was provided with intraoperative nitric oxide donation. The second group (n = 6) served as a control (without nitric oxide donation). Mitochondria injuries were assessed in kidney biopsies by measuring transmembrane potential and Ca2+-binding capacity of organelles, as well as by determining ATP and lactate concentrations. Results: Nitric oxide therapy was associated with less mitochondria dysfunction in kidney biopsies compared with the control group. There was a steady trend to the amelioration of the energy maintenance in the renal parenchyma in the nitric oxide donation group. Conclusion: A steady trend towards optimizing the energy supply of tissues under cardiopulmonary bypass and circulatory arrest was revealed in an experiment against the background of NO donation at a concentration of 80 ppm.