Проблеми екології та медицини (Jul 2024)
COMBINED EFFECT OF LAPAROTOMY AND EXPERIMENTAL POST-TRAUMATIC STRESS DISORDER ON THE SOURCES OF SUPEROXIDE ANION RADICAL IN THE RAT HEART
Abstract
The aim of this study was to determine the sources of superoxide anion radical (O₂⁻•) in rat heart homogenate under conditions of surgical trauma inflicted against the background of an experimental model of posttraumatic stress disorder (PTSD). Materials and methods. The experiments were conducted on 42 white Wistar rats weighing (220±10) g, divided into 6 groups: Group 1 – intact animals; Group 2 – rodents with PTSD modeled by reproducing single prolonged stress (SPS); Group 3 – rats that underwent a sham operation; Group 4 – animals that underwent laparotomy; Group 5 – rats that underwent a sham operation after SPS modeling; Group 6 – animals that underwent laparotomy after reproducing SPS. The rate of O₂⁻• generation in the heart homogenate was studied using a spectrophotometric test with nitroblue tetrazolium. Results. The modeling of PTSD (SPS) and surgical trauma leads to a significant increase in oxidative stress in the rat heart, evidenced by an elevated rate of O₂⁻• generation involving NADPH-dependent electron transport chains (ETC) in microsomes, NO synthase, the mitochondrial respiratory chain, and leukocyte NADPH oxidase. In the post-laparotomy period following SPS, the oxidative stress enhanced significantly and was manifested through increased O₂⁻• generation by NADPH-dependent microsomal and NO synthase ETC by 72.3%, by NADH-dependent mitochondrial ETC by 72.9%, and leukocyte NADPH oxidase by 80.9% compared to intact control. When compared to group 2, these indicators rose by 29.6%, 24.4%, and 26.8%, respectively. Group 4 demonstrated an even more pronounced increase in O₂⁻• generation, reaching 54.0%, 54.6%, and 62.9% respectively. Furthermore, O₂⁻• production rates from all sources in group 4 were likely higher than those in group 5 by 29.8%, 21.2%, and 21.5% , respectively. Conclusions. The combined effect of laparotomy and experimental PTSD synergistically enhances O₂⁻• production in the heart homogenate from various sources, significantly exceeding the levels observed with either laparotomy or SPS alone.
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