Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 1997 Sep;12(3):132-6.
doi: 10.1016/s0883-9441(97)90042-3.

The effects of intravenous anesthetics on intracranial pressure and cerebral perfusion pressure in two feline models of brain edema

Affiliations

The effects of intravenous anesthetics on intracranial pressure and cerebral perfusion pressure in two feline models of brain edema

L Nimkoff et al. J Crit Care. 1997 Sep.

Abstract

Purpose: The 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 methods: Intraparenchymal 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.

Results: In 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.

Conclusions: Our 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.

PubMed Disclaimer

LinkOut - more resources