Cerebral carbohydrate metabolism of man during respiratory and etabolic alkalosis.

Publisher Website
Google Scholar
Abstract
In 18 lightly anesthetized (70% nitrous oxide-30% On) male volunteers cerebral carbohydrate metabolism was studied under conditions of normal acid-base balance, respiratory alkalosis, and combined respiratory and metabolic alkalosis. At PaUO2 19 torr (arterial pH 7.60) the brain metabolic pattern was different from that present during normocarbia; a lesser fraction of brain glucose consumption could be related to O2 uptake and a greater proportion of glucose was converted to lactate. When PaCO2 was decreased to 10 torr (arterial pH 7.76) there was a 10% reduction of CMRO2, a 15% increase in cerebral glucose consumption, and an elevated cerebral venous "excess lactate" level. These changes could have been due to the Bohr effect or to reduced brain perfusion. In an effort to separate the 2 factors, PaCO2 was held at 19 torr while NaHCO2 was given intravenously with the expectation that a change in arterial pH similar to that produced by severe hypocarbia would occur without a change in cerebral blood flow. Additional metabolic changes did not develop with the increase of pH from 7.63 to 7.79. This is attributed to the counterbalancing of the Bohr effect by an unexpected increase in cerebral blood flow. Since the infusion of sodium bicarbonate required an additional 90 min. of hypocarbia, study of the time factor became necessary. When hyperventilation was sustained (without bicarbonate infusion) for an additional 90-min. period, no additional changes occurred in any measure of cerebral metabolism.

This publication has 3 references indexed in Scilit: