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Mild hypothermia prevents the occurrence of cytotoxic brain edema in rats

Hypothermia maintains the impermeability of the blood-brain barrier to proteins and, therefore, presumably the development of vasogenic brain edema after brain ischemia. We intended to determine whether mild hypothermia would have a protective effect against cytotoxic brain edema, the early stage of... Full description

Journal Title: Acta neurobiologiae experimentalis 1998, Vol.58 (1), p.29-35
Main Author: Schwab, M
Other Authors: Bauer, R , Zwiener, U
Format: Electronic Article Electronic Article
Language: English
Subjects:
Publisher: Poland
ID: ISSN: 0065-1400
Link: https://www.ncbi.nlm.nih.gov/pubmed/9583185
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recordid: cdi_proquest_miscellaneous_79866799
title: Mild hypothermia prevents the occurrence of cytotoxic brain edema in rats
format: Article
creator:
  • Schwab, M
  • Bauer, R
  • Zwiener, U
subjects:
  • Animals
  • Body Water - metabolism
  • Brain Edema - pathology
  • Brain Edema - prevention & control
  • Cell Survival
  • Humans
  • Hypothermia, Induced
  • Rats
  • Rats, Wistar
ispartof: Acta neurobiologiae experimentalis, 1998, Vol.58 (1), p.29-35
description: Hypothermia maintains the impermeability of the blood-brain barrier to proteins and, therefore, presumably the development of vasogenic brain edema after brain ischemia. We intended to determine whether mild hypothermia would have a protective effect against cytotoxic brain edema, the early stage of ischemic brain edema. Two groups of Wistar rats (37 degrees C and 35 degrees C body temperature) were subjected to 6 h of moderate decrease of cerebral blood flow (CBF) by means of permanent bilateral carotid artery ligation, and compared to a third group of unaffected animals. Carotid artery ligation induced a local cerebral blood flow (LCBF) reduction to 50-80% of baseline values. LCBF in the frontal cortex was restored to a higher level in hypothermic animals than in normothermic ones (P < 0.05). In normothermic animals, an increase of brain water content was detected in the frontoparietal and occipital cortex as well as in the hippocampus (P < 0.05), but only in one region of the frontoparietal cortex in hypothermic animals. The impermeability of the blood-brain barrier to proteins was shown by the absence of staining with Evans blue as an indicator of vasogenic brain edema. We conclude that mild hypothermia offers protection against the development of cytotoxic brain edema.
language: eng
source:
identifier: ISSN: 0065-1400
fulltext: no_fulltext
issn:
  • 0065-1400
url: Link


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titleMild hypothermia prevents the occurrence of cytotoxic brain edema in rats
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descriptionHypothermia maintains the impermeability of the blood-brain barrier to proteins and, therefore, presumably the development of vasogenic brain edema after brain ischemia. We intended to determine whether mild hypothermia would have a protective effect against cytotoxic brain edema, the early stage of ischemic brain edema. Two groups of Wistar rats (37 degrees C and 35 degrees C body temperature) were subjected to 6 h of moderate decrease of cerebral blood flow (CBF) by means of permanent bilateral carotid artery ligation, and compared to a third group of unaffected animals. Carotid artery ligation induced a local cerebral blood flow (LCBF) reduction to 50-80% of baseline values. LCBF in the frontal cortex was restored to a higher level in hypothermic animals than in normothermic ones (P < 0.05). In normothermic animals, an increase of brain water content was detected in the frontoparietal and occipital cortex as well as in the hippocampus (P < 0.05), but only in one region of the frontoparietal cortex in hypothermic animals. The impermeability of the blood-brain barrier to proteins was shown by the absence of staining with Evans blue as an indicator of vasogenic brain edema. We conclude that mild hypothermia offers protection against the development of cytotoxic brain edema.
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subjectAnimals ; Body Water - metabolism ; Brain Edema - pathology ; Brain Edema - prevention & control ; Cell Survival ; Humans ; Hypothermia, Induced ; Rats ; Rats, Wistar
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descriptionHypothermia maintains the impermeability of the blood-brain barrier to proteins and, therefore, presumably the development of vasogenic brain edema after brain ischemia. We intended to determine whether mild hypothermia would have a protective effect against cytotoxic brain edema, the early stage of ischemic brain edema. Two groups of Wistar rats (37 degrees C and 35 degrees C body temperature) were subjected to 6 h of moderate decrease of cerebral blood flow (CBF) by means of permanent bilateral carotid artery ligation, and compared to a third group of unaffected animals. Carotid artery ligation induced a local cerebral blood flow (LCBF) reduction to 50-80% of baseline values. LCBF in the frontal cortex was restored to a higher level in hypothermic animals than in normothermic ones (P < 0.05). In normothermic animals, an increase of brain water content was detected in the frontoparietal and occipital cortex as well as in the hippocampus (P < 0.05), but only in one region of the frontoparietal cortex in hypothermic animals. The impermeability of the blood-brain barrier to proteins was shown by the absence of staining with Evans blue as an indicator of vasogenic brain edema. We conclude that mild hypothermia offers protection against the development of cytotoxic brain edema.
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abstractHypothermia maintains the impermeability of the blood-brain barrier to proteins and, therefore, presumably the development of vasogenic brain edema after brain ischemia. We intended to determine whether mild hypothermia would have a protective effect against cytotoxic brain edema, the early stage of ischemic brain edema. Two groups of Wistar rats (37 degrees C and 35 degrees C body temperature) were subjected to 6 h of moderate decrease of cerebral blood flow (CBF) by means of permanent bilateral carotid artery ligation, and compared to a third group of unaffected animals. Carotid artery ligation induced a local cerebral blood flow (LCBF) reduction to 50-80% of baseline values. LCBF in the frontal cortex was restored to a higher level in hypothermic animals than in normothermic ones (P < 0.05). In normothermic animals, an increase of brain water content was detected in the frontoparietal and occipital cortex as well as in the hippocampus (P < 0.05), but only in one region of the frontoparietal cortex in hypothermic animals. The impermeability of the blood-brain barrier to proteins was shown by the absence of staining with Evans blue as an indicator of vasogenic brain edema. We conclude that mild hypothermia offers protection against the development of cytotoxic brain edema.
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