Acute, transient hemorrhagic hypotension does not aggravate structural damage or neurologic motor deficits but delays the long-term cognitive recovery following mild to moderate traumatic brain injury
| Autor: | Melissa Motta, Asenia McMillan, Edmund Neugebauer, Christian Schütz, Diego M. Morales, Kristie Soltesz, Joost Schouten, Zachery Spangler, John F. Stover, Rachel C. Hoover, Tracy K. McIntosh, Hilaire J. Thompson |
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| Jazyk: | angličtina |
| Rok vydání: | 2006 |
| Předmět: |
Male
Time Factors Traumatic brain injury Blood Pressure Critical Care and Intensive Care Medicine Cerebral autoregulation Article Hypoxemia Rats Sprague-Dawley Intensive care Medicine Animals Cerebral perfusion pressure business.industry Head injury Shock Hypoxia (medical) medicine.disease Rats Blood pressure Anesthesia Brain Injuries Fluid Therapy medicine.symptom Blood Gas Analysis Hypotension business Cognition Disorders Psychomotor Performance |
| Popis: | Approximately 50% of severely head-injured patients suffer additional potentially life-threatening extracranial injuries such as multiple fractures, lung contusion, traumatic pneumothorax, and injury to intra-abdominal organs. Despite the high prevalence of multiple trauma in brain-injured patients, only a few studies have investigated the effect of extracranial injuries on the clinical course and outcome of patients with traumatic brain injury (TBI) (1, 2). Nevertheless, the prognosis and outcome have been shown to be worsened when multiple extracranial injuries are involved (1, 3). This exacerbation of injury is believed to be a consequence of secondary insults to the brain resulting from hypoxemia, hypotension, elevated intracranial pressure, insufficient cerebral perfusion pressure, hypercapnia, hyperthermia, hypo/hyperglycemia, hyponatremia, and sepsis (4-6) that can be caused by extracranial traumatic injuries. Although the uninjured brain can normally withstand these secondary insults by activating compensatory mechanisms, the brain is rendered vulnerable to secondary insults due to TBI-induced structural and metabolic deficits. Blood loss and subsequent systemic hypotension are major causes of secondary insult to the brain following TBI and occur more frequently in multiply injured patients (4, 7). Moreover, hypotension in the traumatically injured patient has been shown to be predictive for higher mortality and morbidity rates (8). Under laboratory conditions, experimentally induced hemorrhagic hypotension (HH) when superimposed on a traumatically injured brain has been shown to impair cerebral perfusion (9, 10) and reduce the amount of oxygen carriers contributing to the already reduced brain tissue oxygenation (11, 12). Additionally, secondary hypotension, with and without concomitant hypoxia, following TBI has been reported to impair systemic pressure autoregulation (13-15), impair cerebral autoregulation (15, 16), and aggravate TBI-induced structural damage as reflected by a significant increase in contusion volume (9, 17-19). Secondary hypoxia has also been reported to exacerbate acute sensorimotor and cognitive deficits following moderate fluid percussion (FP) brain injury in rats (20). To date, most preclinical pathophysiologic and pharmacologic studies have been conducted primarily in animals subjected to isolated TBI without HH, and a strong need exists to develop combined injury models to elucidate optimal treatment and management strategies for multiply-injured patients (see the excellent review in Ref. 21). Although several rodent models of combined injury (TBI with hypoxia, with and without HH) have been established (9, 15, 17, 20, 22, 23), experimental studies investigating the impact of superimposed HH have focused primarily on the pharmacologic restitution of mean arterial blood pressure (MABP) and/or cerebral perfusion pressure by infusing catecholamines (15, 24) and the evaluation of various resuscitation fluids (13, 25, 26). To date, the impact of hemorrhagic hypotension on neurologic and cognitive outcome following TBI has not been investigated. The present study was designed to reproduce the clinical scenario in which a TBI patient experiences an acute, transient (≤30 mins) arterial hemorrhage immediately following TBI. In one subgroup of brain-injured animals, lactated Ringer’s solution was infused to reverse the arterial hypotension whereas another subgroup was not fluid resuscitated. The impact of superimposed compensated or uncompensated HH on the acute pathologic response to TBI (brain edema formation at 24 hrs postinjury), long-term (5 month) neurobehavioral outcome variables, and hemispheric tissue loss after TBI was also evaluated in the current study. |
| Databáze: | OpenAIRE |
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