In vitro buffer value of brain tissue during prolonged hypercapnia

Abstract

Ventilatory adaptation to CO 2 has been related to a return toward normal pH via an increase in CSF and arterial [HCO 3 −]. To examine whether the overall brain tissue can contribute HCO 3 − to surrounding fluids, we measured the in vitro CO 2 buffer value ( β CO 2 ) of control and hypercapnic rat brain homogenates and compared values with reported in vivo data. Hypercapnic rats were exposed to 7% CO 2 for 3 days or 1 week. Brain homogenate was continuously tonometered for 3 h at 37°C with 2%, 5% and 15% CO 2 in O 2. In addition, we used KOH to determine the brain buffering in the pH range 6.8–10.25. During CO 2 titration, [HCO 3 −] increased gradually with time up to 90 min by about 10–15%,but the increase was blocked by a metabolic inhibitor, NaF. β CO 2 , estimated per kg brain tissue from the dilute homogenate, ranged between 23.4 ± 2.7 (SD) in controls and 26.0 ± 1.3 meq/pH in the 7 day group, which were not significantly different. Over the same 7 days, CO 2 dissociation curves were shifted upwards with similar slopes by about 6 ml/100 g tissue in association with a rise in pH of about 0.06, consistent with an accumulation of HCO 3 − without any change in buffers. No significant differences between groups were found from KOH titration curves, either in slope or position, consistent with lack of alteration in buffers as well. In vitro brain tissue β CO 2 (about 25) was less than reported in vivo values in the literature (around 40), possibly because H + adjustments by whole body occur so rapidly in vivo. In addition, other investigators demonstrated that a major part of the increased brain cell [HCO 3 −] in prolonged hypercapnia could not be accounted for by the fixed acid production ( Acta Physiol. Scand. 83: 344, 1971). By assuming the in vitro β CO 2 measures the available non-carbonic buffers, the data may be interpreted as showing that the overall brain tissue accumulates HCO 3 − from surrounding fluid during hypercapnia.