Effect of non-respiratory alkalosis on brain tissue and cerebral blood flow in rats with damaged blood-brain barrier.
Acute alterations in plasma bicarbonate concentration have minimal effects on intracerebral pH and cerebral blood flow, perhaps due to blood-brain barrier mechanisms. To test this hypothesis, the consequences of an acute rise in the plasma bicarbonate concentration were studied in anesthetized rats previously subjected to an acute pressure pulse in the carotid system with unilateral damage to the blood-brain barrier. In rats subjected to a "heavy" hypertensive insult, the hemisphere on the side of the lesion showed a lactic acidosis, edema, and a depression of cerebral blood flow. An increase in the plasma bicarbonate concentrations of 15--20 mEq/1 during 35 minutes provoked a marked rise in the total CO2 content of this hemisphere, and a further increase in the lactate concentration, but did not later the brain edema nor affect further the already very low cerebral blood flow. An increase in the lactate concentration and a decrease of cerebral blood flow in the "reference" hemisphere indicated that the lesion was not completely unilateral. In rats subjected to a "moderate" hypertensive insult the changes were less pronounced and statistically not significant for all the parameters. There results illustrate the importance of an intact blood-brain barrier for the maintenance of intracerebral pH in the face of acute alterations in plasma [HCO3]. The impaired cerebral blood flow after an acute hypertensive insult did not appear to be influenced by the intracerebral [HCO3].
D000471:Alkalosis / Q000378:metabolism*; D000818:Animals; D001639:Bicarbonates / Q000097:blood; D001812:Blood-Brain Barrier; D001921:Brain / Q000378:metabolism*; D002245:Carbon Dioxide / Q000097:blood; D002560:Cerebrovascular Circulation; D006973:Hypertension / Q000097:blood; D007773:Lactates / Q000097:blood; D008297:Male; D051381:Rats
D001639:Bicarbonates; D007773:Lactates; D002245:Carbon Dioxide