The influence of hypothermia on hypoglycemia-induced brain damage in the rat
(1992) In Acta Neuropathologica 83(4). p.379-385- Abstract
- The effects of hypothermia on hypoglycemic brain damage were studied in rats after a 30-min period of hypoglycemic coma, defined as cessation of spontaneous EEG activity. The rats were either normothermic (37 degrees C) or moderately hypothermic (33 degrees C). Morphological brain damage was evaluated after various periods of recovery. Hypothermic animals with halothane anesthesia never resumed spontaneous respiration, thus requiring artificial ventilation during recovery (maximally 8 h). In contrast, when isoflurane was used as the anesthetic agent, all animals survived and were examined after 1 week of recovery. There was a tendency towards gradually higher arterial plasma glucose levels during hypoglycemia with lower body temperature.... (More)
- The effects of hypothermia on hypoglycemic brain damage were studied in rats after a 30-min period of hypoglycemic coma, defined as cessation of spontaneous EEG activity. The rats were either normothermic (37 degrees C) or moderately hypothermic (33 degrees C). Morphological brain damage was evaluated after various periods of recovery. Hypothermic animals with halothane anesthesia never resumed spontaneous respiration, thus requiring artificial ventilation during recovery (maximally 8 h). In contrast, when isoflurane was used as the anesthetic agent, all animals survived and were examined after 1 week of recovery. There was a tendency towards gradually higher arterial plasma glucose levels during hypoglycemia with lower body temperature. The time period from insulin injection until isoelectric EEG appeared was gradually prolonged by hypothermia, and was shorter when isoflurane was used for anesthesia. Brain damage was examined within the neocortex, caudoputamen and hippocampus (CA1, subiculum and the tip of the dentate gyrus). Damage to neurons was found to be of two types, namely condensed dark purple neurons (pre-acidophilic) and shrunken bright red-staining neurons (acidophilic). In the neocortex, no clear influence of temperature on the degree of injury was seen. In the caudoputamen, the number of injured neurons clearly decreased at lower temperature (33 degrees C, P less than 0.001) when halothane was used, while no such difference was seen when isoflurane was used as the anesthetic agent. Likewise, a protective effect of hypothermia was seen in subiculum (P less than 0.01) when halothane, but not isoflurane was used.(ABSTRACT TRUNCATED AT 250 WORDS) (Less)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/1106517
- author
- Agardh, Carl-David LU ; Smith, M L and Siesjo, B K
- organization
- publishing date
- 1992
- type
- Contribution to journal
- publication status
- published
- subject
- keywords
- Hypoglycemia, Hypothermia, Neuronal damage, Rat
- in
- Acta Neuropathologica
- volume
- 83
- issue
- 4
- pages
- 379 - 385
- publisher
- Springer
- external identifiers
-
- pmid:1575015
- scopus:0026519441
- ISSN
- 1432-0533
- DOI
- 10.1007/BF00713529
- language
- English
- LU publication?
- yes
- additional info
- The information about affiliations in this record was updated in December 2015. The record was previously connected to the following departments: Unit on Vascular Diabetic Complications (013241510)
- id
- b8e6a547-bef1-48f4-9aef-e2581f727e34 (old id 1106517)
- date added to LUP
- 2016-04-01 15:49:27
- date last changed
- 2021-01-03 11:19:05
@article{b8e6a547-bef1-48f4-9aef-e2581f727e34,
abstract = {{The effects of hypothermia on hypoglycemic brain damage were studied in rats after a 30-min period of hypoglycemic coma, defined as cessation of spontaneous EEG activity. The rats were either normothermic (37 degrees C) or moderately hypothermic (33 degrees C). Morphological brain damage was evaluated after various periods of recovery. Hypothermic animals with halothane anesthesia never resumed spontaneous respiration, thus requiring artificial ventilation during recovery (maximally 8 h). In contrast, when isoflurane was used as the anesthetic agent, all animals survived and were examined after 1 week of recovery. There was a tendency towards gradually higher arterial plasma glucose levels during hypoglycemia with lower body temperature. The time period from insulin injection until isoelectric EEG appeared was gradually prolonged by hypothermia, and was shorter when isoflurane was used for anesthesia. Brain damage was examined within the neocortex, caudoputamen and hippocampus (CA1, subiculum and the tip of the dentate gyrus). Damage to neurons was found to be of two types, namely condensed dark purple neurons (pre-acidophilic) and shrunken bright red-staining neurons (acidophilic). In the neocortex, no clear influence of temperature on the degree of injury was seen. In the caudoputamen, the number of injured neurons clearly decreased at lower temperature (33 degrees C, P less than 0.001) when halothane was used, while no such difference was seen when isoflurane was used as the anesthetic agent. Likewise, a protective effect of hypothermia was seen in subiculum (P less than 0.01) when halothane, but not isoflurane was used.(ABSTRACT TRUNCATED AT 250 WORDS)}},
author = {{Agardh, Carl-David and Smith, M L and Siesjo, B K}},
issn = {{1432-0533}},
keywords = {{Hypoglycemia; Hypothermia; Neuronal damage; Rat}},
language = {{eng}},
number = {{4}},
pages = {{379--385}},
publisher = {{Springer}},
series = {{Acta Neuropathologica}},
title = {{The influence of hypothermia on hypoglycemia-induced brain damage in the rat}},
url = {{http://dx.doi.org/10.1007/BF00713529}},
doi = {{10.1007/BF00713529}},
volume = {{83}},
year = {{1992}},
}