Hypothermia reduces microvascular permeability and reactive oxygen species expression after hemorrhagic shock

Hypothermia is a frequent manifestation after trauma-induced hemorrhagic shock. Clinical studies have suggested that hypothermia is an independent risk variable predisposing patients to an increase in morbidity. Thus, most of the current goal-directed resuscitation protocols are aimed at the establishment of euthermia. However, recent data suggest that hypothermia may provide protection by attenuating the inflammatory response after hemorrhagic shock. The purpose of this study was twofold: to examine the effects of mild to moderate hypothermia on barrier function after hemorrhagic shock, and to determine the role of reactive oxygen species (ROS) in this process.

After a control period, blood was withdrawn to reduce the mean arterial pressure to 40 mm Hg for 1 hour in urethane-anesthetized rats. Mesenteric postcapillary venules in a transilluminated segment of small intestine were examined to quantitate changes in permeability and ROS expression. Sprague-Dawley rats received an intravenous injection of fluorescein isothiocyanate (FITC)-albumin during the control period. The fluorescent light intensity emitted from the FITC-albumin was recorded with digital microscopy within the lumen of the microvasculature and compared with the intensity of light in the extravascular space. The images were downloaded to a computerized image analysis program that quantitates changes in light intensity. This change in light intensity represents albumin-FITC extravasation.

Our results demonstrated a marked increase in albumin leakage after hemorrhagic shock that was significantly attenuated with mild (34 degrees C) and moderate (30 degrees C) hypothermia. In addition, hypothermia attenuated ROS expression after hemorrhagic shock.

These data suggest that hypothermia may protect barrier integrity after hemorrhagic shock by inhibition of oxygen radical expression.