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Am J Physiol Heart Circ Physiol 243: H33-H40, 1982;
0363-6135/82 $5.00
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AJP - Heart and Circulatory Physiology, Vol 243, Issue 1 33-H40, Copyright © 1982 by American Physiological Society


ARTICLES

Bicarbonate ion modulation of cerebral blood flow during hypoxia and hypercapnia

R. C. Koehler and R. J. Traystman

The relative importance of changes in extracellular fluid (ECF) pH in mediating increases in cerebral blood flow (CBF) during hypoxia and hypercapnia was assessed by varying [HCO(-3)]ECF in pentobarbital-anesthetized dogs. Blood flow to one caudate nucleus (CNBF) that was bathed by cerebrospinal fluid (CSF) of varied [HCO(-3)] was compared with CNBF (measured by radiolabeled microspheres) on the contralateral side, which received a normal-[HCO(-3)]CSF perfusate. Raising [HCO(-3)]CSF from 25 to 60 meq/l for 150 min lowered CNBF by 16% and suppressed the slope of cNBF response to hypercapnia by 61% but suppressed the slope of CNBF response to hypoxia significantly less (22%). Lowering [HCO(-3)]CSF to 8 meq/l increased CNBF by 71% and augmented the response to hypercapnia by 126% but did not alter the slope of the response to hypoxia. These data indicate that changes in [H+]ECF can account for the increased CBF during hypercapnia but not for the entire hypoxic response. The increase in lactic acid production that would be necessary to solely account for the increase in CBF during hypoxia is much greater than what has been reported in the literature.





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