EXCESSIVE OXYGEN OR GLUCOSE SUPPLY DOES NOT ALTER THE BLOOD-FLOW RESPONSE TO SOMATOSENSORY STIMULATION OR SPREADING DEPRESSION IN RATS

We investigated the influence of hyperoxia (arterial pO(2) 446 +/- 43 mmHg) and hyperglycemia (blood glucose 19.4 mmol/l) on somatosensory s timulation (whisker deflection) employing laser Doppler flowmetry (LDF ). Our aim was to test the hypothesis that a possible substrate-sensin g mechanism for glucose and oxygen contributes to the coupling between cortical activity and regional cerebral blood flow (rCBF) in order to match increased demand with substrates. In addition, we looked at the influence of hyperglycemia (blood glucose 17.9 mmol/l) and hypercapni a (arterial pCO(2) 62 mmHg) on rCBF (LDF) and regional cerebral blood oxygenation changes (rCBO) in the even stronger metabolic stimulus of cortical spreading depression (CSD). For the latter we employed the ne w non-invasive technique of near infrared spectroscopy (NIRS). All exp eriments were done using chloralose/urethane-anesthetized rats. Somato sensory stimulation increased rCBF by about 20% of baseline, in the ca se of both norm- and hyperoxia as well as both normo- and hyperglycemi a. The blood-flow response to CSD consisted of a temporary sharp incre ase in rCBF to more than 400%. At the same time, the concentration of oxyhemoglobin [HbO(2)] increased, while deoxyhemoglobin [Hb] decreased , indicating excessive oxygenation. Hyperglycemia altered neither the rCBF nor the rCBO response. Preexisting hypercapnia, however, produced reductions in both hyperperfusion (rCBF) and hyperoxygenation (rCBO) during CSD. We found that, for experimental hyperglycemia, i.v. may be superior to i.p. application of glucose because of the latter's side effects in connection with blood flow. Our findings cannot support the hypothesis of a substrate sensing mechanism in coupling. (C) 1997 Els evier Science B.V.