This study was performed to ascertain the acute effects of brain missile wounding on brain-stem and hypothalamic biogenic amines in a group of cats anesthetized with pentobarbital (40 mg/kg). Brain wounding is associated with a concomitant increase in intracranial pressure (ICP); to separate the effects of elevated ICP alone from the effects of wounding, a second group of cats had ICP artificially increased from a normal level of approximately 5 mm Hg to approximately 140 mm Hg by infusion of mock cerebrospinal fluid into the cisterna magna. In both groups, significant epinephrine depletions (47% to 74%) occurred in the nucleus tractus solitarius, area A1C1, locus ceruleus, raphe nuclei, and posterior hypothalamus. Epinephrine levels were also significantly decreased in the anterior hypothalamus in the wounded cats. In addition, both brain wounding and artificially induced ICP increases caused significant decreases of norepinephrine in the posterior hypothalamus, and of serotonin, 5-hydroxyindoleacetic acid, dopamine, and homovanillic acid in the raphe nuclei. Only brain wounding, however, caused significant reductions of norepinephrine, dopamine, and homovanillic acid in the nucleus tractus solitarius and area A1C1. The plasma catecholamine levels resulting from brain wounding or artificially induced ICP increases were dissimilar only in the amount of time required to attain maximum plasma levels, with the wounded animals responding faster. It is concluded that the hypothalamic and brain-stem biogenic amine changes resulting from either brain wounding or increased ICP alone are reflective of a stress response. Brain-stem distortion caused by brain wounding did not appear to be a factor and monoaminergic systems appeared to remain intact despite a severe and eventually lethal brain injury. If the detected depletion of epinephrine and serotonin levels is associated with potentially lethal brain injury, pharmacological intervention may be possible.
