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

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Abstract
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 an EEG pattern of slow-wave polyspikes, 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 polyspike period 1-CBF was increased in most 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. After glucose injection (5 min) the hyperemia persisted in only some 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 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. Like hypoxia and ischemia, substrate deficiency due to hypoglycemia is accompanied by vasodilatation in the brain. Like long-lasting ischemia, severe hypoglycemia is followed by a delayed hypoperfusion syndrome that, by restricting O2 supply, may contribute to the final cell damage incurred.