AJP - Heart and Circulatory Physiology, Vol 258, Issue 6 1714-H1721, Copyright © 1990 by American Physiological Society
Hypoglycemia and cerebral autoregulation in anesthetized dogs
F. E. Sieber, R. C. Koehler, S. A. Derrer, C. D. Saudek and R. J. Traystman
Department of Anesthesiology and Critical Care Medicine, Johns Hopkins Medical Institutions, Baltimore, Maryland 21205.
We examined the effects of moderate hypoglycemia with near-normal cerebral
glucose consumption on cerebral autoregulation during graded hemorrhagic
hypotension in anesthetized dogs. Four groups of animals (n = 8 each) were
studied: normoglycemia, insulin-induced hypoglycemia (1.1 mM),
normoglycemia plus alpha- and beta-adrenergic blockade [propranolol (1
mg/kg loading dose + 1 mg.kg-1.h-1 infusion) plus phentolamine (2 mg/kg
loading dose + 2 mg/min infusion)], and hypoglycemia plus alpha- and
beta-adrenergic blockade. As cerebral perfusion pressure was reduced to
40-50 mmHg, cerebral blood flow and O2 consumption increased in the
hypoglycemic group. These increases were not observed after adrenergic
blockade or in the normoglycemic groups. The perfusion pressure at which
cerebrovascular resistance was minimal was higher during hypoglycemia (40
mmHg) and hypoglycemia plus blockade (50 mmHg) than in either of the
normoglycemic groups (30 mmHg). This study demonstrates that hypoglycemia
increases the lower limit of cerebral autoregulation during hypotension.
Furthermore, adrenergic mechanisms acting during combined hypoglycemia and
hemorrhagic hypotension increase cerebral blood flow and O2 consumption and
attenuate the hypoglycemia-induced increase in the lower limit of
autoregulation.
