• J K Muir, M Tynan, R Caldwell, and E F Ellis.
• Department of Pharmacology and Toxicology, Medical College of Virginia, Virginia Commonwealth University, Richmond, USA.
• J. Neurotrauma. 1995 Apr 1;12(2):179-88.

AbstractOxygen free radicals, such as the superoxide anion, are known to mediate damage to the cerebral microcirculation following traumatic brain injury. The purpose of this study was to determine if superoxide dismutase (SOD), a scavenger of superoxide anion, could alter posttraumatic cortical blood flow. Following barbiturate anesthesia, rats were surgically prepared for moderate fluid percussion brain injury. Cortical blood flow contralateral to the site of injury was measured using laser-Doppler flowmetry. Laser-Doppler flowmetry assesses flow by measuring cell volume and velocity, which are multiplied electronically to give flow. Starting 10 min before injury, animals received either superoxide dismutase (24,000 U/kg bolus, followed by continuous infusion of 1600 U/kg/min) or an equal volume of saline. Blood pressure, heart rate, and cortical blood flow were measured up to 1 h posttrauma. Rats receiving superoxide dismutase had significantly higher cortical blood flow posttrauma (F = 6.91, p < 0.02). One hour posttrauma, the blood flow in SOD-treated rats was 89 +/- 8% of preinjury baseline, whereas this value was only 66 +/- 6% of control in saline-treated rats. SOD caused not only greater blood velocity but also less reduction in cortical blood volume after injury. There were no significant differences between the groups with respect to blood pressure or heart rate. This study further supports the role of oxygen radical-mediated cerebrovascular dysfunction following traumatic brain injury and is the first to show the beneficial effect of SOD on cortical blood flow following fluid percussion brain injury.

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