Cerebral metabolism and EEG during combination of hypocapnia and isoflurane-induced hypotension in dogs

Abstract

Isoflurane (ISF)-induced hypotension causes equal reductions of cerebral blood flow (CBF) and the cerebral metabolic rate for oxygen (CMR(O2)) so that no disturbance of cerebral energy stores or metabolites occurs. While hypocapnia during ISF-induced hypotension causes a further reduction of CBF, the effects on cerebral energy stores and metabolites produced by combining hypocapnia with ISF-induced hypotension are not known. This study examined the effect of hypocapnia (Pa(CO2) = 20 mmHg) on CMR(O2), the electroencephalogram (EEG), and levels of adenine nucleotides, phosphocreatine, lactate, pyruvate, and glucose in brain tissue in 12 dogs during ISF-induced hypotension. All dogs were examined at: 1) normocapnia with normotension; 2) hypocapnia with normotension; 3) hypocapnia combined with ISF-induced hypotension to cerebral perfusion pressures of 60, 50, and 40 mmHg; and 4) restoration of normocapnia with normotension. In six dogs CMR(O2) was determined, and the EEG was evaluated using compressed spectral analysis. In the other six dogs brain tissue metabolites were determined. Hypocapnia combined with ISF-induced hypotension (all levels) caused a decrease of the power of the beta-2 spectra, an increase of the power of the alpha and beta-1 spectra, but no change in total power of the EEG. There was no change in cerebral energy stores or brain tissue metabolites. CMR(O2) was reduced by approximately 27%. Thirty minutes after restoration of normocapnia with normotension, cerebral metabolites remained unchanged and CMR(O2), and the power of the alpha, beta-1, and beta-2 spectra of the EEG returned to control values. These results suggest no adverse effect on cerebral metabolism or function during hypocapnia combined with ISF-induced hypotension.