Journal of neurotrauma
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Journal of neurotrauma · Jan 1993
Lactated Ringer's solution alleviates brain trauma-precipitated lactic acidosis in hemorrhagic shock.
To determine the influence of brain trauma on blood acid-base and lactate-pyruvate responses to hemorrhage, and the effect of lactated Ringer's solution on these responses, 30 anesthetized rats were assigned to four groups: hemorrhage (n = 7), hemorrhage following fluid percussion brain trauma (trauma-hemorrhage group) (n = 7), hemorrhage treated with lactated Ringer's solution (hemorrhage-resuscitation group) (n = 8), and hemorrhage following brain trauma treated with lactated Ringer's solution (trauma-hemorrhage-resuscitation group) (n = 8). The hemorrhage group showed no significant changes in pH, HCO3, and base excess after hemorrhage. Base excess and pH were significantly reduced after the hemorrhage in the trauma-hemorrhage group but were raised after resuscitation in the hemorrhage-resuscitation group. ⋯ Lactate rose significantly after hemorrhage in the hemorrhage group and was even higher in the trauma-hemorrhage group, but there were no differences between the hemorrhage versus hemorrhage-resuscitation or trauma-hemorrhage-resuscitation groups. Both brain trauma and lactated Ringer's solution increased pyruvate with marked reduction in the ratio of lactate to pyruvate. These data indicate that brain trauma precipitates blood lactate accumulation and metabolic acidosis after hemorrhage, and infusion of lactated Ringer's solution can relieve these disturbances.
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Journal of neurotrauma · Jan 1993
Mild experimental brain injury in the rat induces cognitive deficits associated with regional neuronal loss in the hippocampus.
Memory dysfunction following mild human traumatic brain injury (TBI) is a common clinical observation, but the pathologic substrate underlying this loss of function has not been well-characterized. In the present study, we examined the effects of a mild lateral fluid percussion (FP) brain injury on memory dysfunction, neuronal cell loss in specific regions of the hippocampus, and breakdown of the blood-brain barrier (BBB). A Morris Water Maze (MWM) memory paradigm was used to assess memory retention in rats 42 h after lateral FP brain injury (n = 11) or sham injury (n = 10). ⋯ Immunoreactivity to anti-rat IgG was used to evaluate the extent of BBB disruption. A significant correlation was observed between posttraumatic memory scores and neuronal loss in the hilus of the dentate gyrus (p < 0.005). To our knowledge, these observations are the first to suggest an association between cognitive deficits following a mild experimental brain injury and neuropathological changes in the hippocampus.
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The recent finding that small variations in brain temperature can critically determine the extent of histopathological injury in animal models of brain injury has generated renewed interest in hypothermic brain protection. Whereas mild hypothermia protects the brain from ischemic and traumatic brain injury, mild hyperthermia worsens ischemic outcome. ⋯ The purpose of this article is to review and discuss recent findings demonstrating the importance of brain temperature in ischemic and traumatic brain injury. Potential mechanisms by which mild hypothermia may attenuate and mild hyperthermia accentuate the detrimental consequences of brain injury are reviewed.