Amelioration by cyclosporin A of brain damage following 5 or 10 min of ischemia in rats subjected to preischemic hyperglycemia
Li, Ping-An ; Uchino, Hiroyuki ; Elmer, Eskil LU
and Siesjö, Bo
LU
(1997)
In Brain Research
753(1).
p.133-140
- Abstract
- It has recently been shown that the immunosuppressant cyclosporin A (CsA) dramatically ameliorates the selective neuronal necrosis which results from 10 min of forebrain ischemia in rats. Since CsA is a virtually specific blocker of the mitochondrial permeability transition (MPT) pore which is assembled under adverse conditions, such as mitochondrial calcium accumulation and oxidative stress, the results suggest that the delayed neuronal death is due to an MPT. In the present study we explored whether CsA can also ameliorate the aggravated brain damage which is observed in hyperglycemic subjects, and which encompasses rapidly evolving neuronal lesions, edema, and postischemic seizures. Anaesthetised rats with a plasma glucose concentration... (More)
- It has recently been shown that the immunosuppressant cyclosporin A (CsA) dramatically ameliorates the selective neuronal necrosis which results from 10 min of forebrain ischemia in rats. Since CsA is a virtually specific blocker of the mitochondrial permeability transition (MPT) pore which is assembled under adverse conditions, such as mitochondrial calcium accumulation and oxidative stress, the results suggest that the delayed neuronal death is due to an MPT. In the present study we explored whether CsA can also ameliorate the aggravated brain damage which is observed in hyperglycemic subjects, and which encompasses rapidly evolving neuronal lesions, edema, and postischemic seizures. Anaesthetised rats with a plasma glucose concentration of approximately 13 mM were subjected to 10 min of forebrain ischemia, and allowed a recovery period of 7 days. In these animals, CsA prevented seizure from occurring and virtually eliminated neuronal necrosis. In order to allow even higher plasma glucose values (approximately 20 mM) to be studied, with long-term recovery, the duration of ischemia had to be reduced to 5 min. Again, CsA suppressed seizure activity and reduced neuronal damage. However, the effects were not as marked or consistent as in the 10 min group, suggesting that excessive tissue acidosis recruits mechanisms of damage which are not sensitive to CsA. (Less)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/1111489
- author
- Li, Ping-An
; Uchino, Hiroyuki
; Elmer, Eskil
LU
and Siesjö, Bo
LU
- organization
- publishing date
- 1997
- type
- Contribution to journal
- publication status
- published
- subject
- keywords
- Brain damage, Ischemia, Hyperglycemia, Cyclosporin A, Mitochondria, Histopathology, Rat
- in
- Brain Research
- volume
- 753
- issue
- 1
- pages
- 133 - 140
- publisher
- Elsevier
- external identifiers
-
- pmid:9125440
- scopus:0030951890
- ISSN
- 1872-6240
- DOI
- 10.1016/S0006-8993(97)00005-X
- 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: Neurology, Lund (013027000), Laboratory for Experimental Brain Research (013041000)
- id
- 1a32708f-92ae-4591-9346-3e7282dc7a5d (old id 1111489)
- date added to LUP
- 2016-04-01 11:57:49
- date last changed
- 2022-01-26 20:49:29
@article{1a32708f-92ae-4591-9346-3e7282dc7a5d,
abstract = {{It has recently been shown that the immunosuppressant cyclosporin A (CsA) dramatically ameliorates the selective neuronal necrosis which results from 10 min of forebrain ischemia in rats. Since CsA is a virtually specific blocker of the mitochondrial permeability transition (MPT) pore which is assembled under adverse conditions, such as mitochondrial calcium accumulation and oxidative stress, the results suggest that the delayed neuronal death is due to an MPT. In the present study we explored whether CsA can also ameliorate the aggravated brain damage which is observed in hyperglycemic subjects, and which encompasses rapidly evolving neuronal lesions, edema, and postischemic seizures. Anaesthetised rats with a plasma glucose concentration of approximately 13 mM were subjected to 10 min of forebrain ischemia, and allowed a recovery period of 7 days. In these animals, CsA prevented seizure from occurring and virtually eliminated neuronal necrosis. In order to allow even higher plasma glucose values (approximately 20 mM) to be studied, with long-term recovery, the duration of ischemia had to be reduced to 5 min. Again, CsA suppressed seizure activity and reduced neuronal damage. However, the effects were not as marked or consistent as in the 10 min group, suggesting that excessive tissue acidosis recruits mechanisms of damage which are not sensitive to CsA.}},
author = {{Li, Ping-An and Uchino, Hiroyuki and Elmer, Eskil and Siesjö, Bo}},
issn = {{1872-6240}},
keywords = {{Brain damage; Ischemia; Hyperglycemia; Cyclosporin A; Mitochondria; Histopathology; Rat}},
language = {{eng}},
number = {{1}},
pages = {{133--140}},
publisher = {{Elsevier}},
series = {{Brain Research}},
title = {{Amelioration by cyclosporin A of brain damage following 5 or 10 min of ischemia in rats subjected to preischemic hyperglycemia}},
url = {{http://dx.doi.org/10.1016/S0006-8993(97)00005-X}},
doi = {{10.1016/S0006-8993(97)00005-X}},
volume = {{753}},
year = {{1997}},
}