Articles: brain-injuries.
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Movement of water between the brain and the intravascular space is dependent on osmotic gradients, which may be established by the acute administration of either hyper- or hypo-osmolar solutions. Mannitol, a hypertonic crystalloid solution, is commonly used to decrease brain water content and reduce intracranial pressure (ICP). Hypertonic saline solutions also decrease brain water and ICP while temporarily increasing systolic blood pressure and cardiac output. ⋯ Colloid solutions exert little influence on either variable. Fluid restriction minimally affects cerebral edema and, if pursued to excess, may result in episodes of hypotension, which may increase ICP and are associated with worse neurologic outcome. Although there is no single best fluid for patients with traumatic brain injury, isotonic crystalloids are widely used and can be justified on a scientific basis.
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Head-injured patients require maintenance of systemic hemodynamics as well as attention to cerebral hemodynamics. Most head-injured patients have increased metabolic oxygen consumption, mild hypertension, and increased cardiac indices. Assessment of regional perfusion, difficult in many patients, includes monitoring of urinary output. In head-injured patients, especially those with multiple injuries, the two most important goals are preservation of cerebral perfusion pressure (mean arterial pressure minus intracranial pressure) and maintenance of systemic oxygen availability (cardiac index times arterial oxygen content).
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An important feature of traumatic brain injury is that much of the ultimate damage appears to occur in a delayed or secondary fashion. Although the exact timing of these secondary sequelae has yet to be elucidated, recent experimental evidence suggests that an extended window of opportunity exists during which various forms of therapy appear to be efficacious. Moreover, new therapies have been developed which can be targeted at distinct pathophysiologic aspects of brain trauma. This article summarizes recent efforts to define secondary mechanisms of brain trauma and review the development of therapeutic strategies for reversing these deleterious events.
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Mild to moderate traumatic brain injury (TBI) is associated with enduring impairments of cognitive function in both humans and animals. However, few experiments have investigated the role of post-injury pharmacologic strategies for attenuating the observed cognitive impairment after TBI. This investigation examined the effects of selective blockade of the presynaptic muscarinic M2 autoreceptor with BIBN 99 on cognitive recovery following rodent TBI. ⋯ Sham-injured animals injected (s.c.) with vehicle (n = 9) or 1.0 (n = 8) mg/kg of BIBN 99 were included for comparison. On days 11-15 after injury, cognitive performance was assessed with the MWM procedure. Results of the second experiment indicated that both doses of BIBN 99 were effective in attenuating cognitive deficits in the MWM as compared to the injured-vehicle treated animals (P < 0.05 for both comparisons).(ABSTRACT TRUNCATED AT 250 WORDS)