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The cerebral metabolic rate of oxygen (CMRO2) has been functionally compartmentalized using the barbiturate thiopental into active CMRO2, associated with electroencephalographic (EEG) activity, and the balance, basal CMRO2, associated with the maintenance of neuronal viability. Previous measurements of these CMRO2 compartments were made in anesthetized animals. Our aim was to determine whether the same proportions for these compartments applied in unanesthetized monkeys. The active: basal distribution of the cerebral metabolic rate of glucose (CMRG) and cerebral flood flow (CBF) were also determined. Three measurements of whole-brain CBF (H2 clearance), CMRO2, and CMRG were made in six unanesthetized rhesus monkeys (Macaca mulatta). Thereafter, thiopental anesthesia was induced and maintained until an isoelectric EEG was obtained. Three additional measurements of CBF, CMRO2, and CMRG were made. Arterial blood pressure, end-tidal CO2, and arterial blood gas were measured with each set of measurements. Thiopental-induced isoelectric EEG resulted in a 47% reduction in CMRO2 from 5.95 +/- 0.54 to 3.10 +/- 0.51 ml/100 g/min (mean +/- SD); a 36% reduction in CBF from 76 +/- 21 to 48 +/- 14 ml/100 g/min; and a 61% reduction in CMRG from 8.09 +/- 2.78 to 3.13 +/- 0.77 mg/100 g/min. The oxygen-glucose index was 0.99 +/- 0.10 for the whole brain, 0.87 +/- 0.15 for the active, and 1.27 +/- 0.25 for the basal compartments. These results indicated an active:basal distribution of approximately 50:50 for CMRO2, 40:60 for CBF, and 60:40 for CMRG. The active:basal CMRO2 distribution corroborates earlier data and shows that relative to CMRO2, the active compartment is underperfused with a lower oxygen-glucose index compared with the basal compartment.

Stable xenon (Xe) gas, at inspired concentrations above 30%, reportedly increased cerebral blood flow (CBF) in animals and humans. An unpredictable Xe-induced elevation of CBF could result in erroneous CBF values being measured by Xe-enhanced computed tomography (Xe-CT). In order to detect a potentially rapid and transient effect of Xe on CBF, estimations of supratentorial CBF were obtained by Doppler flow probes chronically and bilaterally implanted on the internal carotid arteries of five adult monkeys. The unanesthetized monkeys with a clear plastic helmet were equilibrated for 15 min on a control gas (33% N2/67% O2) randomly exposed for 5 min to gas mixtures of either 33% Xe/67% O2 or 10% CO2/23% N2/67% O2. The mean control bilateral internal carotid artery blood flow (ICABF) was 23 +/- 10 ml/min (mean +/- SD), mean arterial pressure (MAP) was 101 +/- 13 mm Hg, and PaCO2 was 34 +/- 6 mm Hg. Inhalation of 33% Xe in O2 did not change the ICABF, MAP, or PaCO2. Inhalation of 10% CO2 in O2 increased the ICABF to 39 +/- 15 ml/min (p

We previously reported that 33% xenon (Xe) did not activate cerebral blood flow (CBF) and metabolism in monkeys as it appears to do in humans. However, monkeys may be less sensitive to Xe than humans are, which would explain the discrepancy in the results, but no one has studied the effects of higher concentrations of Xe on CBF and metabolism in monkeys. Therefore, we studied the effect of 80% Xe on whole-brain CBF, cerebral metabolic rate for oxygen (CMRO2) and glucose (CMRG) in five awake rhesus monkeys. Platinum microelectrodes and catheters inserted into the torcular Herophili were used to measure H2 clearance CBF, and to withdraw cerebral venous blood for O2 and glucose analysis. Cerebral variables were measured after 15 min exposure to 80% N2/20% O2 followed by 80% Xe/20% O2. Eighty percent Xe compared with 80% N2 increased (p

If the efficacy of hypothermia and barbiturates in ameliorating ischemic brain injury lies in reducing the cerebral metabolic rate of oxygen (CMRO2), the greater efficacy of mild hypothermia (34 degrees C) compared with barbiturates is inconsistent with the 15-20% reduction of CMRO2 caused by mild hypothermia compared with 50% caused by barbiturates. This paradox, we hypothesized, derives from the fact that whereas barbiturates lower CMRO2 associated with EEG activity or thiopental (TP)-suppressible CMRO2, not essential for cellular viability, hypothermia lowers CMRO2 associated with providing energy, i.e., adenosine triphosphate, to maintain transmembrane ion gradients or TP-nonsuppressible CMRO2, essential for neuronal viability. To test this hypothesis, we measured whole brain cerebral blood flow (CBF) and CMRO2 in two groups of rats mechanically ventilated with 70% N2O/30% O2 before and after TP-induced isoelectric EEG. In the normothermic group (n = 7), measurements were made at a brain temperature (Tb) of 38 degrees C, while in the hypothermic group (n = 7), they were made at 34 degrees C. In the normothermic group, TP-induced isoelectric EEG reduced CMRO2 by 50%, from 7.92 +/- 1.05 to 3.95 +/- 0.70 ml 100 g-1 min-1 (mean +/- = SD). Thus, at 38 degrees C, TP-suppressible and TP-nonsuppressible CMRO2 were both 50 +/- 4% of total CMRO2. In the hypothermic group, decreasing Tb from 38 to 34 degrees C caused a 17% decline in CMRO2, from 7.62 +/- 1.92 to 6.28 +/- 1.22 ml 100 g-1 min-1 (p > 0.05). AT 34 degrees C, TP infusion lowered CMRO2 to 2.15 = 0.46 ml 100 g-1 min-1. At 34 degrees C, TP-suppressible and TP-nonsuppressible CMRO2 values were 64 +/- 7% and 36 +/- 8% of total CMRO2, respectively. TP lowered CBF by 50% at both 38 and 34 degrees C. In conclusion, mild hypothermia selectively lowers TP-nonsuppressible CMRO2 associated with the maintenance of viability rather than EEG-associated or TP-suppressible CMRO2.

Local cerebral blood flow (LCBF) maps produced by 33% xenon-enhanced computed tomographic scanning (Xe/CT LCBF) are useful in the clinical diagnosis and management of patients with cerebrovascular disorders. However, observations in humans that 25-35% xenon (Xe) inhalation increases cerebral blood flow (CBF) have raised concerns that Xe/CT LCBF measurements may be inaccurate and that Xe inhalation may be hazardous in patients with decreased intracranial compliance. In contrast, 33% Xe does not increase CBF in rhesus monkeys. To determine whether this interspecies difference in the effect of Xe on CBF correlates with an interspecies difference in the anesthetic potency of Xe, we measured the minimum alveolar concentration (MAC) of Xe preventing movement to a tail-clamp stimulus in rhesus monkeys. Using a standard protocol for the determination of MAC in animals, we first measured the MAC of halothane (n = 5), and then used a combination of halothane and Xe to measure the MAC of Xe (n = 7). The halothane MAC was 0.99 +/- 0.12% (M +/- SD), and the Xe MAC was 98 +/- 15%. These results suggest that the MAC of Xe in rhesus monkeys is higher than the reported human Xe MAC value of 71%. Thus the absence of an effect of 33% Xe on CBF in the rhesus monkey may be related to its lower anesthetic potency.