TITLE: BRAIN TISSUE PH DURING SEVERE METABOLIC ACIDOSIS IN THE DOG

AUTHORS: Guy J. Edelman, MD¹, William E. Hoffman, PhD²
AFFILIATION: ¹University of Illinois, Glenview, IL; ²University of Illinois, Chicago, IL.

INTRODUCTION: Cerebral acid/base milieu and its therapeutic implications are of concern during care of the acutely acidotic patient. The ability of brain tissue to buffer acute changes in pH is incompletely understood. Although the blood/ brain barrier (BBB) is quite permeable to carbon dioxide, charged moieties such as bicarbonate or hydronium ions are known to cross the BBB only sparingly under physiologic conditions. In addition, the brain possesses the ability to modulate interstitial pH by altering CNS bicarbonate secretion. The present study evaluated the pH response of the uninjured brain to an acute systemic metabolic acidosis.
MATERIALS AND METHODS: All investigations were approved by the Animal Care Committee. Five adult mongrel dogs (wt 21-27kg) were anesthetized with sodium pentothal 25mg/kg IV and endotracheally intubated. Anesthesia was maintained with 1 MAC isoflurane in 50% oxygen/air. Minute ventilation was adjusted to maintain normocarbia. Femoral arterial and venous access was obtained and rectal temperature maintained at 38½C. A frontotemporal craniotomy was per- formed. A Neurotrend probe (Diametrics Medical, Minneapolis MN) was inserted intracortically in a suitable frontal lobe gyrus. The Neurotrend device is a multiparameter probe which uses a fiberoptics/electrode array to continuously monitor brain tissue pO2, pCO2 and pH. Each subject received a central venous infusion of 0.1N HCl calculated by body weight to achieve an arterial pH of less than 7.10. At 15 minute intervals, samples of arterial blood were obtained and blood gas analysis performed. Concurrent brain probe measurements of tissue pO2, pCO2 and pH were recorded. Preacidotic control and postacidotic values for arterial and brain tissue measurements were statistically compared by paired t-tests, with statistical significance taken at p<0.05.
RESULTS: The mean final brain tissue pH following HCl infusion was 6.81 +/- 0.21(SD) compared to a control tissue pH of 7.11 +/- 0.11 (p<0.03). Arterial pH decreased during HCl infusion to 6.36 +/- 0.40 (SD) from 7.30 +/- 0.04 (p<0.001). This corresponds to an 1149% versus 110% increase respectively in hydrogen ion concentration between arterial and brain tissue compartments.
CONCLUSIONS: Although this study demonstrates that the noninjured canine brain does become acidotic during an imposed severe systemic acid challenge, it also reveals that cerebral mechanisms attenuate pathologic arterial hydrogen ion increases by tenfold. Such mechanisms may be critical in cerebral homeo- stasis during clinical acid/base disturbances. The response of the injured brain to an acidosis challenge is a topic of future research interest.