The cardiovascular homeostatic responses to hemorrhage are coordinated in the central nervous system. Coincidental brain injury, which is present in 64% of trauma patients, could impair these responses. Our objective was to test the hypothesis that mild to moderate traumatic brain injury alters cardiovascular reflex responses to acute hemorrhage.
Experimental prospective, randomized study in terminally anesthetized rats.
Experimental laboratory of university.
Twenty-four male Wistar rats weighing 240–260 g.
Brain injury was induced using the lateral fluid percussion injury model in anesthetized rats. The fluid percussion device delivered an applied cortical pressure of 1.2 atm and 1.8 atm, producing mild and moderate injury, respectively. Control animals underwent identical surgical procedures but with no applied cortical pressure. Hemorrhage was carried out 10 mins after brain injury, at a rate of 2% of blood volume per minute until 40% blood volume was withdrawn.
The effects of acute traumatic brain injury on the biphasic heart rate and mean arterial blood pressure response to hemorrhage were studied. Traumatic brain injury attenuated the normal bradycardic response and delayed the hypotensive response to hemorrhage. This effect was graded according to the severity of brain injury. In mild injury, the depressor phase was delayed, but the biphasic pattern of heart rate response was maintained. No mortality was observed in this group. Following moderate brain injury, marked attenuation of the biphasic heart rate and mean arterial blood pressure response (p < .001 and p = .0007) was observed. Fifty percent of this group died within 90 mins of hemorrhage completion. Significant differences in the biphasic response were observed between survivors and nonsurvivors (p = .013, p = .001, respectively). In nonsurvivors, the biphasic response was abolished.
Acute mild and moderate traumatic brain injury disrupts cardiovascular homeostatic responses to extracranial hemorrhage; this disruption is graded according to the severity of traumatic brain injury. Severe disruption is associated with an increase in early mortality.
From Emergency Medicine (CGM), Institute of Neuroscience (RAK), and Department of Pharmacology & Therapeutics (KB), Trinity College, Dublin, Ireland; and Biophysics & Trauma (Surgical Science), Biomedical Sciences (EK), Dstl Porton Down, Salisbury, United Kingdom.
Supported, in part, by the Medical Research Council, United Kingdom, as part of the North West Injury Research Program Grant.
The authors have not disclosed any potential conflicts of interest.
For information regarding this article, E-mail: email@example.com