Hypoglycemia and cerebral autoregulation in anesthetized dogs.
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.
Sieber
F E
FE
Department of Anesthesiology and Critical Care Medicine, Johns Hopkins Medical Institutions, Baltimore, Maryland 21205.
Koehler
R C
RC
Derrer
S A
SA
Saudek
C D
CD
Traystman
R J
RJ
D000758:Anesthesia; D000818:Animals; D001921:Brain / Q000378:metabolism / Q000503:physiopathology*; D002560:Cerebrovascular Circulation; D004285:Dogs; D004569:Electroencephalography; D006706:Homeostasis; D007003:Hypoglycemia / Q000378:metabolism / Q000503:physiopathology*; D008297:Male