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Cerebrovascular response during and following severe insulin-induced hypoglycemia: CO2-sensitivity, autoregulation, and influence of prostaglandin synthesis inhibition

Nilsson, B; Agardh, Carl-David LU ; Ingvar, M and Siesjö, Bo LU (1981) In Acta Physiologica Scandinavica 111(4). p.455-463
Abstract
The objective of the present experiments was to study mechanisms governing cerebrovascular responses during severe hypoglycemia, and in the posthypoglycemic recovery period. To that end, lightly anesthetized (70% N2O) and artificially ventilated rats were injected with insulin so as to abolish spontaneous EEG activity for 15 or 30 min ("coma"). In separate animals, recovery was induced by glucose administration. Previous experiments have shown that in normo- or moderately hypertensive animals hypoglycemic coma is accompanied by a relatively marked increase in cerebral blood flow (CBF), and that a delayed hypoperfusion develops in the recovery period. The present results demonstrate that oxygen supply is in excess of the demands during... (More)
The objective of the present experiments was to study mechanisms governing cerebrovascular responses during severe hypoglycemia, and in the posthypoglycemic recovery period. To that end, lightly anesthetized (70% N2O) and artificially ventilated rats were injected with insulin so as to abolish spontaneous EEG activity for 15 or 30 min ("coma"). In separate animals, recovery was induced by glucose administration. Previous experiments have shown that in normo- or moderately hypertensive animals hypoglycemic coma is accompanied by a relatively marked increase in cerebral blood flow (CBF), and that a delayed hypoperfusion develops in the recovery period. The present results demonstrate that oxygen supply is in excess of the demands during coma, and falls below control during recovery. During hypoglycemic coma, the CO2 response of the circulation was retained but autoregulation was lost. In the recovery period, both CO2 response and autoregulation were lost. Pretreatment with indomethacin was introduced in order to evaluate the possible influence of fatty acid cyclo-oxygenase products on the pattern of CBF changes. Measurements of local cerebral blood flow (1-CBF) showed that, in the majority of structures analysed, indomethacin failed to modulate the changes in CBF. It is concluded that alterations in cerebrovascular tone and loss of autoregulation induce flow changes that may influence substrate and oxygen availability during hypoglycemia. The pronounced decrease in CBF and the loss of autoregulation and CO2-response in the post-hypoglycemic period may influence functional, metabolic and morphological recovery. The 1-CBF findings indicate that neither the increase in CBF during hypoglycemia nor the reduction in flow in the posthypoglycemic period are mediated by mechanisms related to prostaglandin metabolism. (Less)
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author
organization
publishing date
type
Contribution to journal
publication status
published
subject
in
Acta Physiologica Scandinavica
volume
111
issue
4
pages
455 - 463
publisher
Wiley-Blackwell
external identifiers
  • pmid:6795899
  • scopus:0019473625
ISSN
0001-6772
language
English
LU publication?
yes
id
42cf33bf-caa1-4ea7-89f6-654d090b42a5 (old id 1102831)
date added to LUP
2008-08-13 15:37:37
date last changed
2017-07-09 04:13:46
@article{42cf33bf-caa1-4ea7-89f6-654d090b42a5,
  abstract     = {The objective of the present experiments was to study mechanisms governing cerebrovascular responses during severe hypoglycemia, and in the posthypoglycemic recovery period. To that end, lightly anesthetized (70% N2O) and artificially ventilated rats were injected with insulin so as to abolish spontaneous EEG activity for 15 or 30 min ("coma"). In separate animals, recovery was induced by glucose administration. Previous experiments have shown that in normo- or moderately hypertensive animals hypoglycemic coma is accompanied by a relatively marked increase in cerebral blood flow (CBF), and that a delayed hypoperfusion develops in the recovery period. The present results demonstrate that oxygen supply is in excess of the demands during coma, and falls below control during recovery. During hypoglycemic coma, the CO2 response of the circulation was retained but autoregulation was lost. In the recovery period, both CO2 response and autoregulation were lost. Pretreatment with indomethacin was introduced in order to evaluate the possible influence of fatty acid cyclo-oxygenase products on the pattern of CBF changes. Measurements of local cerebral blood flow (1-CBF) showed that, in the majority of structures analysed, indomethacin failed to modulate the changes in CBF. It is concluded that alterations in cerebrovascular tone and loss of autoregulation induce flow changes that may influence substrate and oxygen availability during hypoglycemia. The pronounced decrease in CBF and the loss of autoregulation and CO2-response in the post-hypoglycemic period may influence functional, metabolic and morphological recovery. The 1-CBF findings indicate that neither the increase in CBF during hypoglycemia nor the reduction in flow in the posthypoglycemic period are mediated by mechanisms related to prostaglandin metabolism.},
  author       = {Nilsson, B and Agardh, Carl-David and Ingvar, M and Siesjö, Bo},
  issn         = {0001-6772},
  language     = {eng},
  number       = {4},
  pages        = {455--463},
  publisher    = {Wiley-Blackwell},
  series       = {Acta Physiologica Scandinavica},
  title        = {Cerebrovascular response during and following severe insulin-induced hypoglycemia: CO2-sensitivity, autoregulation, and influence of prostaglandin synthesis inhibition},
  volume       = {111},
  year         = {1981},
}