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Journal of critical care · Sep 1997
The effects of intravenous anesthetics on intracranial pressure and cerebral perfusion pressure in two feline models of brain edema.
- L Nimkoff, C Quinn, P Silver, and M Sagy.
- Division of Pediatric Critical Care Medicine, Schneider Children's Hospital, Long Island Jewish Medical Center, New Hyde Park, NY 11042, USA.
- J Crit Care. 1997 Sep 1; 12 (3): 132-6.
PurposeThe purpose of this study was to investigate the effects of various intravenous anesthetics on intracranial pressure (ICP) and cerebral perfusion pressure (CPP) in two models of brain edema in a prospective study in a Pediatric critical care animal laboratory in a university hospital.Materials And MethodsIntraparenchymal ICP monitors were inserted in 30 anesthetized adult cats. In 15 cats, an intraparenchymal balloon-tipped catheter was placed and inflated to create a space-occupying lesion (SOL) to mimic vasogenic brain edema (VBE). In the other 15 cats, cytotoxic brain edema (CBE) was created by an acute reduction in blood osmolality. We used continuous hemodiafiltration (CAVH-D) and replaced the ultrafiltrate with hypotonic solution to maintain euvolemia. At predetermined points, each cat in each model received multiple intravenous (i.v.) injections of one of the following medications: methohexital 1.5 mg/kg, propofol 2 mg/kg, or ketamine 2 mg/kg. ICP and mean arterial pressure (MAP) were continuously monitored in all animals.ResultsIn the SOL model, all three anesthetic agents decreased ICP after each administration (P < .05). Ketamine administration also resulted in an increase in CPP in this model (P < .05). In the CBE model, none of these agents resulted in a significant change in either ICP or CPP.ConclusionsOur results indicate that i.v. anesthetics decrease ICP caused by SOL but have no significant effect on ICP due to CBE. We postulate that in the SOL model, and similarly in VBE, some brain tissue is viable and remains responsive to anesthetics. In contrast, in the CBE model, diffuse intracellular damage occurs, the cerebral metabolic rate may be severely depressed, autoregulation of the cerebral vasculature may be impaired, and unresponsiveness to i.v. anesthetics may occur.
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