RONS formation under restrictive reperfusion does not affect organ dysfunction early after hemorrhage and trauma

Abstract

Reactive oxygen species have been implicated in the pathophysiology of early reperfusion. We aimed to determine 1) reactive oxygen and nitrogen species (RONS) formation in organs of rats and 2) its pathophysiological relevance during a phase of restrictive reperfusion after hemorrhagic/traumatic shock (HTS). Fifty-seven male Sprague-Dawley rats were subjected to a clinically relevant HTS model, featuring laparotomy, bleeding, and a phase of restrictive reperfusion. The RONS scavenger 1-hydroxy-3-carboxy-2,2,5,5-tetramethyl-pyrrolidine hydrochloride (continuous i.v. infusion) and electron paramagnetic resonance spectroscopy were applied for RONS (primarily superoxide and peroxynitrite) detection. Compared with sham-operated animals, the organ-specific distribution of RONS changed during restrictive reperfusion after HTS. Reactive oxygen and nitrogen species formation increased during restrictive reperfusion in red blood cells and ileum only but decreased in the kidney and remained unchanged in other organs. Hemorrhagic traumatic shock followed by restrictive reperfusion resulted in metabolic acidosis, dysfunction of liver and kidney, and increased oxidative burst capacity in circulating cells. Plasma RONS correlated with shock severity and organ dysfunction. However, RONS scavenging neither affected organ dysfunction nor oxidative burst capacity nor myeloperoxidase activity in lung when compared with the shock controls. In summary, a phase of restrictive reperfusion does not increase RONS formation in most organs except in intestine and red blood cells. Moreover, scavenging of RONS does not affect the early organ dysfunction manifested at the end of a phase of restrictive reperfusion.