The effect of isoflurane on neuronal necrosis following near-complete forebrain ischemia in the rat
(1986) In Anesthesiology 64(1). p.19-23- Abstract
The effect of deep isoflurane anesthesia on ischemically induced neuronal damage was evaluated in the rat. Sixteen mechanically ventilated animals were maintained normocapnic and normothermic while subjected to a near complete forebrain ischemia insult induced with systemic hypotension (MAP = 50± mmHg) and bilateral carotid artery occlusion. Prior to ischemia, eight of the rats received isoflurane by inhalation until the EEG demonstrated a burst suppression pattern; the other eight were untreated controls. After 10 min of ischemia, the carotid clamps were removed, blood pressure was restored, and, in the treated group, isoflurane administration discontinued. Following the ischemic insult, the animals were observed over a 7-day period,... (More)
The effect of deep isoflurane anesthesia on ischemically induced neuronal damage was evaluated in the rat. Sixteen mechanically ventilated animals were maintained normocapnic and normothermic while subjected to a near complete forebrain ischemia insult induced with systemic hypotension (MAP = 50± mmHg) and bilateral carotid artery occlusion. Prior to ischemia, eight of the rats received isoflurane by inhalation until the EEG demonstrated a burst suppression pattern; the other eight were untreated controls. After 10 min of ischemia, the carotid clamps were removed, blood pressure was restored, and, in the treated group, isoflurane administration discontinued. Following the ischemic insult, the animals were observed over a 7-day period, at which time they were killed and the brains prepared for histologic study. Severity of damage was assessed by a direct count of irreversibly damaged neurons, which appear bright red when stained with cresyl violet-acid fuchsin. Areas of particular interest were those that characteristically display vulnerability to ischemic damage, i.e., hippocampus, caudate nuclei, and neocortex. The control group revealed severe damage in the hippocampal CA1 sector (70% cells acidophilic) with more variability in the caudate nuclei and neocortex. The treated group showed a similar extent of damage with approximately 74% cells acidophilic in hippocampus (CA1). Clinical appearance was indistinguishable between groups. The authors conclude that pretreatment with isoflurane shows no beneficial effects on delayed neuronal necrosis following near-complete forebrain ischemia.
(Less)
- author
- Warner, D. S. ; Deshpande, J. K. and Wieloch, T. LU
- organization
- publishing date
- 1986-01-01
- type
- Contribution to journal
- publication status
- published
- subject
- in
- Anesthesiology
- volume
- 64
- issue
- 1
- pages
- 5 pages
- publisher
- Lippincott Williams & Wilkins
- external identifiers
-
- scopus:0022645930
- pmid:3942333
- ISSN
- 0003-3022
- DOI
- 10.1097/00000542-198601000-00004
- language
- English
- LU publication?
- yes
- id
- 36372cd1-b8cd-430f-b746-f1f173501635
- date added to LUP
- 2019-06-13 17:45:20
- date last changed
- 2024-01-01 10:34:46
@article{36372cd1-b8cd-430f-b746-f1f173501635,
abstract = {{<p>The effect of deep isoflurane anesthesia on ischemically induced neuronal damage was evaluated in the rat. Sixteen mechanically ventilated animals were maintained normocapnic and normothermic while subjected to a near complete forebrain ischemia insult induced with systemic hypotension (MAP = 50± mmHg) and bilateral carotid artery occlusion. Prior to ischemia, eight of the rats received isoflurane by inhalation until the EEG demonstrated a burst suppression pattern; the other eight were untreated controls. After 10 min of ischemia, the carotid clamps were removed, blood pressure was restored, and, in the treated group, isoflurane administration discontinued. Following the ischemic insult, the animals were observed over a 7-day period, at which time they were killed and the brains prepared for histologic study. Severity of damage was assessed by a direct count of irreversibly damaged neurons, which appear bright red when stained with cresyl violet-acid fuchsin. Areas of particular interest were those that characteristically display vulnerability to ischemic damage, i.e., hippocampus, caudate nuclei, and neocortex. The control group revealed severe damage in the hippocampal CA1 sector (70% cells acidophilic) with more variability in the caudate nuclei and neocortex. The treated group showed a similar extent of damage with approximately 74% cells acidophilic in hippocampus (CA1). Clinical appearance was indistinguishable between groups. The authors conclude that pretreatment with isoflurane shows no beneficial effects on delayed neuronal necrosis following near-complete forebrain ischemia.</p>}},
author = {{Warner, D. S. and Deshpande, J. K. and Wieloch, T.}},
issn = {{0003-3022}},
language = {{eng}},
month = {{01}},
number = {{1}},
pages = {{19--23}},
publisher = {{Lippincott Williams & Wilkins}},
series = {{Anesthesiology}},
title = {{The effect of isoflurane on neuronal necrosis following near-complete forebrain ischemia in the rat}},
url = {{http://dx.doi.org/10.1097/00000542-198601000-00004}},
doi = {{10.1097/00000542-198601000-00004}},
volume = {{64}},
year = {{1986}},
}