Hyperbaric oxygen prevents intestinal ischemia-reperfusion injury in rats after resuscitation from traumatic/hemorrhagic shock

Abstract

Objective To investigate the effects of hyperbaric oxygen (HBO) on ischemia/repeffusion (Ⅰ/R) injury of the small intestine after resuscitation from trauma and hemorrhagic shock (T/HS) in rats in order to elucidate the underlying mechanisms. Method Ninety-six male Wistar rats were randomly divided into four groups with 24 rats in each group. In shock group, rats were operated with induced T/HS. In sham group, rats operated without induced T/HS. In one HBO therapy (HBOT) group, rats with T/HS were treated with HBOT once. In three-HBOT group, rats with T/HS were treated with HBOT thrice. The Animal Care and Use Committee of China Medical University approved all animal protocols. Rats were anesthetized with amobarbital sodium (80 mg/kg, i.p.) at room temperature (25 ℃), the bloed pressure was monitored via polyethylene cannula inserted into the right femoral artery, connecting with the pressure analyzer (Multiparameter Monitor, M3046A, Boebin-gen, Germany). The left jugular vein was cannulated for administering normal saline and for resuscitation. The right carotid artery was cannulated for shedding blood. After operation, the middle part of left thigh of rat was se-lected as a site to be made of trauma by a lump of 2.5 kg iron falling upon from 20 cm height, causing the com-pound fracture of femur and crush injury of muscular tissue, then the damaged thigh was bandaged and fixed. At the same time, the blood was drawing out of fight carotid artery via cannula until the mean arterial was reduced to 30-35 mmHg within 5 minutes. The hypotension was kept constant for 60 minutes by additional drawing small amounts of blood as needed. After 60 minutes of hypotension, the rats were resuscitated by transfusing the shed blood over 5 minutes, followed by 4 -6 mL normal saline in 60 minutes to get the mean artery pressure maintained above 80 mmHg. The resuscitated rats were put into the hyperbaric chamber (10N-750, menoplace chamber, Ningho, China). The pressure inside the chamber was adjusted to 2.5 ATA and the oxygen concentration was higher than 95 %. The set pressure and oxygen concentration were maintained for 60 minutes. When the pressure within the chamber was decreased to 1 ATA, rots were taken out. The rats in one-HBOT group were given one HBO therapy immediately after resuscitation, and the rats in three-HBOT group were given one HBO therapy im-mediately after resuscitation with additional twice HBO therapy within 24 hours ((q 8 h). The one-way ANOVA and Pearson's bivariate methed were used for statistics. Results Twenty-four hours after resuscitation, the levels of lactate, induced nitric oxide synthase (iNOS), nitric oxide (NO), and tumor necrosis factor-α (TNF-α) in in-testinal tissue of rats in both HBOT groups were significantly lower than those in the rats of shock group without HBOT (P 0.05). Conclusions HBO decreases the production of inflammatory factors, inhibits the excessive inflammatory reaction to T/HS, and prevents the mucosal barrier of intestine from I/R injury after resuscitation from T/HS. Key words: Hyperbaric oxygen; Ischemia-reperfusion; Mucosal barrier