Stroke, Vol 17, 442-449, Copyright © 1986 by American Heart Association
RN Auer, P Hall, M Ingvar and BK Siesjo
The hypothesis that arterial hypotension aggravates hypoglycemic brain
damage was tested. Thirty minutes of insulin induced hypoglycemia with a
flat EEG ("isoelectricity") was compared in seven series of rats. In three
series of animals, the energy state of the cerebral cortex was determined
at blood pressures of 140, 100 and 80 mm Hg respectively. Hypotension
during hypoglycemia exacerbated cortical energy failure. In the fourth to
sixth series, blood pressure was adjusted during isoelectricity to 160, 100
and 60 mm Hg, respectively. A seventh series had induced hypotension to 60
mm Hg only in the recovery period. Quantitation of neuronal death was
performed in the fourth to seventh series of rats by direct visual counting
of acidophilic neurons in sub- serially sectioned brains after one week
survival. Although the first three series demonstrated enhanced
deterioration of the cerebral energy state with lower blood pressures
during hypoglycemia, the fourth to seventh series showed no augmentation of
quantitated hypoglycemic neuronal necrosis. The distinct distribution of
hypoglycemic brain damage, suggesting a fluid-borne toxin, was present at
normal and reduced blood pressures, with no tendency toward an ischemic
pattern of pathology. In spite of previously demonstrated reductions of
cerebral blood flow to ischemic levels in regions with pronounced loss of
autoregulation, no regional exacerbation of neuronal necrosis was seen in
these brain areas. It is concluded that hypoglycemic brain damage is
distinct from ischemic brain damage, and that the two insults are not
additive. Furthermore, moderate hypotension to 60 mm Hg does not aggravate
the damage in spite of an enhanced energy failure.
ARTICLES
Hypotension as a complication of hypoglycemia leads to enhanced energy failure but no increase in neuronal necrosis