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Local cerebral blood flow in the rat during severe hypoglycemia, and in the recovery period following glucose injection

Local cerebral blood flow in the rat during severe hypoglycemia, and in the recovery period... In order to assess the influence of severe hypoglycemia on local cerebral blood flow (1‐CBF) artificially ventilated rats, maintained on 70% N2O, were injected with insulin to provide either an EEG pattern of slow‐wave poly spikes, or cessation of spontaneous EEG activity for 5, 15, or 30 min (“coma”). In other animals, glucose was injected at the end of a 30 min period of “coma” and 1‐CBF was measured after recovery periods of 5, 30, 90, or 180 min. Local CBF was measured autoradiographically with 14C‐iodoantipyrine as the diffusible tracer. In the slow‐wave poly spike period 1‐CBF was increased in most of the structures studied, and reached values that were 1.4 to 3.2 times greater than control. In many structures, cessation of EEG activity was accompanied by a further increase in 1‐CBF, with some structures (thalamus, hypothalamus, pontine gray, and cerebellar cortex) showing flow rates of 400–500% of control. The increase in 1‐CBF was unrelated to arterial hypertension, hypercapnia, or hypoxia. 5 min after glucose injection the hyperemia persisted in only some of the structures studied; in others, the 1‐CBF were close to, or below, control values. During the subsequent recovery period 1‐CBF was markedly reduced with some structures (cerebral cortical areas, hippocampus, and caudate‐putamen) showing flow rates of only 20–35% of control. In others, notably pontine gray and cerebellar cortex, secondary hypoperfusion was never observed. The hypoperfusion was unrelated to arterial hypotension, hypocapnia, or increase in intracranial pressure. It is concluded that, like hypoxia and ischemia, substrate deficiency due to hypoglycemia is accompanied by vasodilatation in the brain. Furthermore, like long‐lasting ischemia, severe hypoglycemia is followed by a delayed hypoperfusion syndrome that, by restricting oxygen supply, may well contribute to the final cell damage incurred. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Acta Physiologica Wiley

Local cerebral blood flow in the rat during severe hypoglycemia, and in the recovery period following glucose injection

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References (22)

Publisher
Wiley
Copyright
Copyright © 1980 Wiley Subscription Services, Inc., A Wiley Company
ISSN
1748-1708
eISSN
1748-1716
DOI
10.1111/j.1748-1716.1980.tb06601.x
pmid
7446174
Publisher site
See Article on Publisher Site

Abstract

In order to assess the influence of severe hypoglycemia on local cerebral blood flow (1‐CBF) artificially ventilated rats, maintained on 70% N2O, were injected with insulin to provide either an EEG pattern of slow‐wave poly spikes, or cessation of spontaneous EEG activity for 5, 15, or 30 min (“coma”). In other animals, glucose was injected at the end of a 30 min period of “coma” and 1‐CBF was measured after recovery periods of 5, 30, 90, or 180 min. Local CBF was measured autoradiographically with 14C‐iodoantipyrine as the diffusible tracer. In the slow‐wave poly spike period 1‐CBF was increased in most of the structures studied, and reached values that were 1.4 to 3.2 times greater than control. In many structures, cessation of EEG activity was accompanied by a further increase in 1‐CBF, with some structures (thalamus, hypothalamus, pontine gray, and cerebellar cortex) showing flow rates of 400–500% of control. The increase in 1‐CBF was unrelated to arterial hypertension, hypercapnia, or hypoxia. 5 min after glucose injection the hyperemia persisted in only some of the structures studied; in others, the 1‐CBF were close to, or below, control values. During the subsequent recovery period 1‐CBF was markedly reduced with some structures (cerebral cortical areas, hippocampus, and caudate‐putamen) showing flow rates of only 20–35% of control. In others, notably pontine gray and cerebellar cortex, secondary hypoperfusion was never observed. The hypoperfusion was unrelated to arterial hypotension, hypocapnia, or increase in intracranial pressure. It is concluded that, like hypoxia and ischemia, substrate deficiency due to hypoglycemia is accompanied by vasodilatation in the brain. Furthermore, like long‐lasting ischemia, severe hypoglycemia is followed by a delayed hypoperfusion syndrome that, by restricting oxygen supply, may well contribute to the final cell damage incurred.

Journal

Acta Physiologica – Wiley

Published: Jul 1, 1980

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