Preconditioning with one-time hydrogen gas does not attenuate skin flap ischemia-reperfusion injury in rat models

Abstract

Hydrogen gas exists in the atmosphere and was previously considered an inert gas. It has been reported to have protective effects on tissue ischemia-reperfusion (IR) injuries in animal models. The protective mechanism of hydrogen molecules is based on selectively reducing highly strong oxidants in cells, thereby reducing inflammation and decreasing the contents of MDA, FOXO3a, and other pathways that result in flap necrosis. Previous studies were conducted with postconditioning with hydrogen. In this article, we want to investigate whether inhalation of hydrogen has a preventive effect on IR injury. Forty-five adult male Sprague Dawley rats (body weight 220-250 g) were randomly divided into three groups: (1) Sham operation group (SH), (2) Ischemia-reperfusion injury group (IR), and (3) Ischemia-reperfusion injury with preconditioning hydrogen group (PRH). IR injury was induced by clamping the right superficial epigastric artery for 3h. Before undergoing 3h of IR management, the PRH group was treated with hydrogen inhalation for 1 h. On the third postoperative day, survival area and blood perfusion of the flap were assessed using laser Doppler flowmetry. RIP1 and RIP3 were examined by immunological detection and western blot analysis. Both the IR and PRH groups had less skin flap survival area and less blood perfusion than the sham group (P<0.05). RIP1 and RIP3 were highly expressed in the IR and PRH groups when compared with those in the SH group (P<0.05). There were no significant differences in flap survival rate (32.34±2.19% and 33.09±1.64%), average blood perfusion (41.66±3.53pu, 48.57±2.83pu), and expression of RIP1 and RIP3 (0.5167±0.1409 and 0.4693±0.1454) between the IR and PRH groups. Preconditioning with one-time inhaled hydrogen does not attenuate skin flap IR injuries in rat models.