The Effect of Hypoxemic Resuscitation of Hemorrhagic Shock on Hemodynamic Stabilization and Inflammatory Response: A Pilot Study in a Rat Experimental Model

Abstract

BACKGROUND: Resuscitation of hemorrhagic shock is associated with tissue injury. The effect of hypoxemia during resuscitation was investigated. METHODS: Shock was induced by withdrawing blood to mean arterial pressure (MAP) 40 mm Hg and maintained for 60 minutes in 25 Wistar rats. Animals were randomly divided to receive either normoxemic (controls, FiO2 = 21%, n = 14) or hypoxemic (HypRes, FiO2 = 12%, n = 11) resuscitation by re-infusing their shed blood. Outcome was assessed through hemodynamic and inflammatory parameters. Another nine rats served to correlate different FiO2 to the corresponding PaO2. RESULTS: At 60 minutes of resuscitation HypRes had higher MAP than control animals (p = 0.008). The respective median (range) malondialdehyde and TNF-alpha levels was 1.7 (1-2.1) versus 3.1 (2.4-4.3) micromol/L, (p = 0.02) and 0 versus 5.8 (0-5.8) pg/mL, (p = 0.025). Glutathione, endotoxin, interferon-gamma, and nitric oxide values were similar between groups. FiO2 of 12% induced only a mild hypoxemia (PaO2 approximately 80 mm Hg). CONCLUSIONS: Even mild hypoxemia during resuscitation of shock leads to effective hemodynamic stabilization.