The cerebral effects of pancuronium and atracurium in halothane-anesthetized dogs

Pancuronium decreases the minimal alveolar anesthetic concentration (MAC) of halothane in humans, while atracurium has a metabolite, laudanosine, which is a known cerebral stimulant. To determine if these muscle relaxants significantly alter cerebral function, their effects on cerebral metabolic rate (CMRo2), cerebral blood flow (CBF), intracranial pressure (ICP), EEG, and the cerebral energy state were studied in halothane-anesthetized dogs. Group A dogs (n = 6) were maintained at 0.86% end-expired (1.0 MAC) halothane. Thereafter, a sequence of 1) pancuronium 0.1 mg . kg-1; 2) reversal of neuromuscular blockade with neostigmine plus glycopyrrolate; and 3) pancuronium 0.2 mg . kg-1 produced no changes in CMRo2, CBF, ICP, or EEG. Group B dogs (n = 6) also were maintained at 0.86% end-expired halothane and received the following in sequence: 1) atracurium 0.5 mg . kg-1; 2) reversal of neuromuscular blockade with neostigmine plus glycopyrrolate; 3) atracurium 1.0 mg . kg-1; and 4) atracurium 2.5 mg . kg-1. There were no changes in CMRo2, CBF, or ICP; EEG evidence of cerebral arousal occurred in only one dog with the final dose of atracurium. Group C dogs (n = 6) received tetracaine spinal anesthesia and the minimal halothane concentration (mean +/- SE = 0.69 +/- 0.03% end-expired) that would maintain an "anesthetic" EEG pattern. Each Group C dog received the following in sequence: 1) atracurium 1.0 mg . kg-1, and 2) atracurium 2.5 mg . kg-1. EEG evidence of cerebral arousal occurred in all six Group C dogs. Arousal was not accompanied by significant increases in CBF, CMRo2, or ICP.(ABSTRACT TRUNCATED AT 250 WORDS)     

Partial reversal of the cerebral effects of isoflurane in the dog by theophylline

The cerebral effects of adding theophylline to 1.4% isoflurane anaesthesia were studied in five dogs by a sagittal sinus outflow technique with direct measurement of the cerebral blood flow (CBF) and calculation of the cerebral metabolic rate for oxygen (CMRo2). Three 3 mg.kg-1 doses of theophylline were given with intervals of 10 min. Five min after the second and third dose, when the mean theophylline plasma concentration was 41 and 65 mumols.1(-1), respectively, CMRo2 had increased significantly with a mean value varying between 15% and 13%, and the EEG had changed from a sleep pattern to a more awake pattern in the four dogs with evaluable recordings. There were no significant changes in CBF or mean arterial blood pressure (MABP). It is concluded that the adenosine receptor antagonist theophylline in this study partially reversed the cerebral effects of isoflurane.     

The Effect of Nitrous Oxide on Oxygen Consumption and Blood Flow in the Cerebral Cortex of the Rat

The effect of 70% nitrous oxide upon cerebral oxygen consumption (CMRo2) and cerebral blood flow (CBF) was studied in artificially ventilated rats. The control groups consisted of unanaesthetized animals in which a stress-induced increase in CMRo2 and CBF was prevented by previous adrenalectomy, or by administration of a beta blocker (propranolol). There were no significant differences in CMRo2 between animals ventilated with either N2O or N2. It is concluded that if nitrous oxide depresses cerebral metabolism the depression cannot exceed 10%.     

Dexmedetomidine, an alpha 2-adrenergic agonist, decreases cerebral blood flow in the isoflurane-anesthetized dog

The purpose of this study was to examine the effects of dexmedetomidine, an alpha 2-adrenergic agonist, on cerebral blood flow and metabolic rate in dogs anesthetized with 0.64% isoflurane. After intubation and institution of mechanical ventilation, arterial, venous, pulmonary artery, and sagittal sinus catheters were inserted. Measurements of cerebral blood flow (CBF), cerebral metabolic rate for oxygen (CMRo2), mean arterial pressure, cardiac output, and blood gas tensions were made at various levels of isoflurane anesthesia (0.64%, 1.9%, and 2.8%), after the administration of 10 micrograms/kg of dexmedetomidine (a dose that has been shown to reduce anesthetic requirements in dogs by greater than 90%) and finally after 0.3 micrograms/kg of the alpha 2-adrenergic antagonist idazoxan. Despite an increase in arterial pressure, dexmedetomidine caused a marked reduction (greater than 45%, P less than 0.05) in CBF when compared with all preceding concentrations of isoflurane. The administration of dexmedetomidine had no effect on the CMRo2. The electroencephalogram showed a loss of high-frequency activity in a pattern similar to that seen with 1.90% isoflurane. Administration of dexmedetomidine was associated with a 57% decrease in cardiac output (to 0.89 L/min). Administration of idazoxan (an alpha 2-adrenergic antagonist) resulted in an increase in cardiac output and a reversal of the electroencephalogram effects. This experiment indicates that 10 micrograms/kg of dexmedetomidine in isoflurane-anesthetized dogs is associated with a profound decrease in CBF and cardiac output in the face of an unaltered CMRo2. Despite the large reduction in the CBF/CMRo2 ratio, there was no evidence of global cerebral ischemia.     

Restoration of Oxygen Uptake and Blood Flow in the Rat Cerebral Cortex after Halothane Anaesthesia

Halothane decreases both the certal blooi Row (CBF) and the cerebral metabolic rate for oxygen (CMRo₂) when given in anaesthetic doses. A recent report (G jedde & H indfelt 1975) suggests that when halothane is administered to rats for 1 hour, CBF and CMRo₂ are depressed by about 30 and 40%, respectively, for as long as 4 hours after discontinuation of the halothane anaesthesia. In the present study rats were anaesthetized with 1% halothane for 1 hour, and CBF and CMRo₂ were measured at the end of a 30 min recovery period, during which 70% N₂O was administered. Comparison with animals maintained on 70% N₂O throughout the entire 90 min period showed that previous halothane anaesthesia had no effects on CBF or CMRo₂.     

The effects of prolonged isoflurane anaesthesia on cerebral blood flow and metabolism in the dog

To determine whether cerebral blood flow (CBF) changed with time under isoflurane anaesthesia, as has been reported for halothane, CBF and cerebral metabolic rate for oxygen (CMRO2) were studied in five dogs under prolonged isoflurane anaesthesia. CBF was measured with a modified sagittal sinus technique and CMRO2 was calculated as the product of CBF and the arteriovenous O2 difference. Maintaining this experimental dog model with 1% isoflurane in oxygen and nitrogen for 3 h in five dogs and for 4 h in three dogs did not cause any significant changes in CMRO2 or CBF. Cerebral metabolite levels were consistent with earlier reports from short-time studies and the EEG recordings showed a continuous sleep pattern with no pathological changes. It is concluded that there is no change in CBF or CMRO2 in our modified sagittal outflow model during 3-4 h of 1% isoflurane anaesthesia.     

Reduction of Cerebral Blood Flow and Oxygen Consumption with a Combination of Barbiturate Anaesthesia and Induced Hypothermia in the Rat

The influence of phenobarbitone anaesthesia on cerebral blood flow (CBF) and cerebral metabolic rate for oxygen (CMRo₂) during hypothermia (23°C & 27°C) was studied in the rat, using a modification of the K ety & S chmidt (1948) technique and arterio-venous differences for oxygen. Phenobarbitone (150 mg/kg) was found to decrease CMRo₂ by 40–60% during hypothermia, when compared to N₂O anaesthesia. At a body temperature of 23°C, and during phenobarbitone anaesthesia, CMRo₂ was reduced to about 15% of normal control value (about 10.3 ml.100g^-l. min^-l). CBF was reduced to about 50% of the phenobarbitone control value but was similar to the value obtained with N₂O anaesthesia at 22°C. It is concluded that the combination of phenobarbitone anaesthesia and hypothermia results in a more pronounced reduction in cerebral metabolic rate for oxygen than can be achieved by administration of barbiturates to normothermic animals, or by reducing body temperature by 15°C during superficial anaesthesia.     

EFFECTS OF FENTANYL, DROPERIDOL, AND INNOVAR ON CANINE CEREBRAL METABOLISM AND BLOOD FLOW

The effects of droperidol and fentanyl given individually andin combination (Innovar) on the rate of cerebral oxygen consumption(CMRo,) and cerebral blood flow (c.b.f.) were studied in dogsanaesthetized with nitrous oxide (70 percent) and oxygen. Fentanyl(0.006 mg/kg) decreased both the CMRo, and the c.b.f. (meandecreases at 15 minutes were 18 per cent and 47 percent, respectively).The duration of effect was approximately 30 minutes. Droperidol(0.3 mg/kg) produced a decrease of 40 per cent in c.b.f. dueprimarily to a 30-40 per cent increase in cerebrovascular resistance,and this effect persisted for the period of observation (60minutes). No significant change in CMRo, occurred after droperidolwas administered. With the combination drug (Innovar), the effectswere partially additive. After 15 minutes, CMRo, had decreased23 per cent; c.b.f. had decreased 50 per cent; and cerebralvascular resistance had increased 85 per cent. After 30 minutes,the effects of Innovar were indistinguishable from those ofdroperidol alone. No significant changes occurred in the rateof cerebral glucose consumption or the oxygen-glucose index.The effect of increased and decreased Paooj on c.bi. after Innovarwas compared widi that observed during halothane anaesthesia.With halothane, hypercapnia (Pacoi=60 tnm Hg) increased c.b.f.40 per cent and hypocapnia (Pace = 20 mm Hg) decreased c.b.f.40 per cent. Innovar at normocapnia reduced the c.b.f. 65 percent. With hypercapnia, the c.bi. doubled, but with hypocapnia,little further reduction in c.b.f. occurred. It is concludedthat droperidol is a potent cerebral vasoconstrictor, that thiseffect dominates when it is given in combination with fentanyl,that hypocapnia causes little further reduction in c.b.f., andthat the reduction in c.bi. produced by Innovar is not accompaniedby alterations in normal cerebral metabolic pathways     

Effect of dexmedetomidine, a selective and potent alpha 2-agonist, on cerebral blood flow and oxygen consumption during halothane anesthesia in dogs

The effect of the alpha 2-agonist dexmedetomidine on the cerebral blood flow (CBF) and the metabolic rate for oxygen was studied by a sagittal sinus outflow technique in dogs during halothane anesthesia. Dexmedetomidine was given in a dose (10 micrograms/kg) reported to reduce the anesthetic requirement of halothane by 90%. During 0.9% halothane anesthesia dexmedetomidine caused a significant reduction in CBF without influencing the metabolic rate for oxygen. Reducing the halothane concentration to 0.1% caused no further change in CBF, but increased the metabolic rate for oxygen 19%. The cerebral vasoconstrictive effect, combined with the 90% reduction in MAC for halothane, indicates that dexmedetomidine might be a useful adjunct to inhalation anesthetics during neurosurgery in situations where an increase in CBF should be avoided.     

Cerebral blood flow, cerebral metabolic rate of oxygen and relative CO2-reactivity during craniotomy for supratentorial cerebral tumours in halothane anaesthesia. A dose-response study

Fourteen patients were studied during craniotomy for small supratentorial cerebral tumours. Cerebral blood flow (CBF) and cerebral metabolic rate of oxygen (CMRO2) were measured twice by a modification of the Kety-Schmidt technique using 133Xe intravenously. Anaesthesia was induced with thiopental 4-6 mg kg-1, fentanyl and pancuronium, and maintained with an inspiratory halothane concentration of 0.45% in nitrous oxide 67% at a moderate hypocapnic level. In one group of patients (n = 7) the inspiratory halothane concentration was maintained at 0.45% throughout anaesthesia. About 1 h after induction of anaesthesia CBF and CMRO2 averaged 35 +/- 2 ml 100 g-1 min-1 and 2.7 +/- 0.3 ml O2 100 g-1 min-1 (mean +/- s.c. mean), respectively. During repeat studies 1 h later CBF and CMRO2 did not change. In another group of patients (n = 7) an increase in halothane concentration from 0.45% to 0.90% was associated with a significant decrease in CMRO2 from 2.3 +/- 0.1 to 2.0 +/- 0.1 ml O2 100 g-1 min-1. The CO2-reactivity measured after the second flow measurement was preserved. It is concluded that halothane in this study induces a dose-dependent decrease in cerebral metabolism, an increase in CBF while CO2-reactivity is maintained.     

Local spinal cord glucose utilization in conscious and halo-thane-anaesthetized rats

The authors used the 2-[14C]deoxyglucose method to study local spinal and cerebral glucose utilization simultaneously during 1.2 per cent halothane anaesthesia in adult Sprague-Dawley rats. In conscious animals (n = 5) the rate of glucose utilization in lumbar spinal gray matter was about 50 per cent lower than that of cerebral cortex. Halothane anaesthesia (n = 6) reduced spinal cord and cerebral metabolic rate. Spinal glucose utilization was reduced 12-35 per cent, but this was less than the 45-70 per cent decrease halothane produced in 8 of 16 cerebral structures examined and was independent of the hypotension produced. These results indicate that halothane is a spinal metabolic depressant but that its effects on this tissue are substantially less than those it has on many cerebral structures.     

Effects of 1 MAC desflurane on cerebral metabolism, blood flow and carbon dioxide reactivity in humans

We investigated the cerebral haemodynamic effects of 1 MAC desflurane anaesthesia in nine male patients scheduled for elective coronary bypass grafting. For the measurement of cerebral blood flow (CBF) a modified Kety-Schmidt saturation technique with argon as inert tracer gas was used. Measurements of CBF were made before induction of anaesthesia and 30 min after induction under normocapnic, hypocapnic and hypercapnic conditions in sequence. Changes in mean arterial pressure after induction of anaesthesia and during the course of the study were minimized using norepinephrine infusion. In comparison with the awake state under normocapnic conditions, desflurane reduced mean cerebral metabolic rate of oxygen (CMRO2) by 51% and mean cerebral metabolic rate of glucose (CMRglc) by 35%. Concomitantly, CBF was significantly reduced by 22%; jugular venous oxygen saturation (SjvO2) increased from 58 to 74%. Hypo- and hypercapnia caused a 22% decrease and a 178% increase in CBF, respectively. These findings may be interpreted as the result of two opposing mechanisms: cerebral vasoconstriction induced by a reduction of cerebral metabolism and a direct vasodilator effect of desflurane. CBF alterations under variation of PaCO2 indicate that cerebrovascular carbon dioxide reactivity is not impaired by application of 1 MAC desflurane.      

Cerebral blood flow and oxygen consumption during isoflurane and halothane anesthesia in man

In 13 patients, the effects on cerebral blood flow (CBF) and cerebral metabolic rate of oxygen (CMRO2) of isoflurane and halothane administered in a clinically relevant situation were studied. Measurements were performed during fentanyl/nitrous oxide (65%) anesthesia together with moderate hyperventilation (PaCO2 approx 4.5 kPa), and repeated after addition of 0.65 MAC of isoflurane (n = 6) or halothane (n = 7). CBF was measured after intravenous administration of 133xenon and CMRO2 was calculated from the arterial venous differences of oxygen content (AVDO2) determined in arterial and jugular venous bulb blood. CBF and CMRO2 (means +/- s.e. mean) determined prior to administration of volatile agents were 28 +/- 5 ml x 100(-1) x min-1 and 2.0 +/- 0.3 ml x 100 g-1 x min-1, respectively, in the isoflurane group. In the halothane group, CBF was 25 +/- 0.4 ml x 100 g-1 x min-1 and CMRO2 was 2.0 +/- 0.4 ml x 100 g-1 x ml-1. There were no significant intergroup differences. Isoflurane did not change CBF, whereas halothane produced an increase of 36% (P less than 0.05) compared to values obtained during fentanyl/N2O anesthesia. In addition, isoflurane caused a further decrease in CMRO2 of 12% (P less than 0.01) as compared to a 20% increase (P less than 0.05) with halothane. The cerebral metabolic depression caused by the short-acting anesthetic induction agents would be expected to decrease with time, and could partly explain the observed increase in CMRO2 produced by halothane. The study suggests that the cerebrovascular and metabolic properties of isoflurane differ from those of halothane, also in man.     

Whole-Brain Blood Flow and Oxygen Metabolism in the Rat After Halothane Anesthesia

A recent modification of the Kety-Schmidt wash-out technique for 133xenon was used to measure whole-brain blood flow (CBF) and oxygen consumption (CMRO2) 1 to 4 hours after termination of halothane anesthesia in 15 Wistar rats. In this 3-hour experimental period, mean CBF and CMRO2 were reduced to 29 and 43% of control values, respectively. CBF and CMRO2 determined at the beginning and end of the experimental period were not significantly different from each other. Cerebral venous O2 tension was significantly higher than in the control group, supporting recent suggestions of a primary, intrinsic effect of halothane on the homeostatic control of this variable. It is concluded that halothane is not useful for cerebral metabolic studies in the rat.     

Intracranial and spinal cord hemodynamics in the sitting position in dogs in the presence and absence of increased intracranial pressure

The effect of the sitting position on cerebral blood flow (CBF), spinal cord blood flow (SCBF), and cerebral metabolic rate for oxygen (CMRo2) was studied in anesthetized dogs with and without increased intracranial pressure. Blood flow measurements were made at four time periods: (a) initial supine; (b) after 5 min in the sitting position; (c) after 60 min in the sitting position; and (d) 15 min after resuming the supine position. Six dogs (group 1) served as a control group with a normal intracranial pressure (ICP). In five dogs (group 2) ICP was elevated with a parietal epidural balloon 1 h before the first measurements of blood flows were made. Saline was injected incrementally into the balloon so as to reach a steady-state ICP of 30 mm Hg for 1 h. Elevation of ICP in group 2 resulted in significantly lower CBF, SCBF, and CMRo2 compared with group 1. Postural changes in group 1 did not result in any significant change in blood flow measurements whereas in group 2, after 1 h in the sitting position, there were significant decreases in CBF and SCBF compared with the initial supine measurements. There was, however, no corresponding decrease in CMRo2 in group 2 with change in position. These data suggest that both the brain and spinal cord may be at risk for ischemia during sitting position procedures under general anesthesia in the presence of elevated ICP.     

Cerebral blood flow and metabolism in patients undergoing anesthesia for carotid endarterectomy. A comparison of isoflurane, halothane, and fentanyl

The effects of isoflurane, halothane, and fentanyl on cerebral blood flow (CBF) and cerebral metabolic rate for oxygen (CMRO2) during anesthesia prior to carotid endarterectomy were compared using the intravenous method of 133-Xenon CBF determination. Patients, mean (+/- SE) age 68 +/- 2, received either isoflurane (N = 16), 0.75% in O2 and N2O, 50:50; halothane (N = 11), 0.5% in O2 and N2O, 50:50; or fentanyl (N = 10), 5-6 micrograms/kg bolus and then 1-2 micrograms.kg-1.h-1 infusion in addition to O2 and N2O, 40:60. Measurements were made immediately before carotid occlusion. Mean (+/- SE) CBF (ml.100 g-1.min-1) was 23.9 +/- 2.1 for isoflurane, 33.8 +/- 4.8 for halothane, and 19.3 +/- 2.4 for fentanyl. CMRO2 (ml.100 g-1.min-1) was available from 22 patients and was 1.51 +/- 0.28 for isoflurane (N = 7), 1.45 +/- 0.24 for halothane (N = 6), and 1.49 +/- 0.21 for fentanyl (N = 9). Although CBF was greater during halothane than during isoflurane or fentanyl anesthesia (p less than 0.05), there were no demonstrable differences in CMRO2 among the 3 agents. We conclude that choice of anesthetic agent for cerebrovascular surgery with comparable anesthetic regimens should not be made on the basis of "metabolic suppression." During relatively light levels of anesthesia, vasoactive properties of anesthetics are more important than cerebral metabolic depression with respect to effects on the cerebral circulation.     

Autoregulation of cerebral blood flow in response to adenosine-induced hypotension in dogs

During induced hypotension for surgical procedures, cerebral blood flow (CBF) autoregulation and cerebrovascular responsivity to CO2 may be impaired-changes that appear to be agent-specific. Adenosine is a potent endogenous systemic vasodilator and has been investigated as a hypotensive agent. In this study in dogs we investigated cerebral vascular responses to graded decreases of cerebral perfusion pressure (CPP) (100%, 60%, 45%, and 35% of control CPP) during normocapnia (PaCO2 = 37 mm Hg) and hypocapnia (PaCO2 = 21 mm Hg). CBF was measured using the venous outflow technique. Six mongrel dogs were anesthetized with halothane (0.6% inspired) and nitrous oxide (70%) in oxygen and studied during both normocapnic and hypocapnic hypotension. The entry sequence was randomized with >/= 1 h of recovery between normocapnia and hypocapnia. Hypocapnia reduced control CBF from 60.6 +/- 7.1 to 45.1 +/- 5.4 ml 100 g min (mean +/- SEM, p <0.05) during normotension. CBF was unchanged from control values during both graded normocapnic and hypocapnic hypotension until CPP reached 60% of control CPP (50 and 47 mm Hg for normocapnia and hypocapnia, respectively). Thereafter CBF decreased significantly from control values at 45% (37 mm Hg for both groups) and 35% (29 mm Hg for both groups) of control CPP. The lower limit of CBF autoregulation derived by applying linear regression analysis to the CBF-CPP relationship above and below the inflexion point was similar under both experimental conditions (60 +/- 1% of control CPP during normocapnia and 63 +/- 3% of control CPP during hypocapnia). CBF was significantly greater during normocapnia compared with hypocapnia at all levels of CPP, except at 35% of control when the values were similar. Cerebral metabolic rate was unchanged throughout the study. We conclude that neither CBF nor CO2 responsivity is appreciably altered during adenosine-induced hypotension when GPP remains above the lower limit of autoregulation of CBF.     

Additive Effects of Hypothermia and Phenobarbitol upon Cerebral Oxygen Consumption in the Rat

The quantitative effects of a combination of hypothermia and phenobarbital on cerebral oxygen uptake (CMRo2) was studied in rats, curarized and artificially ventilated with 70% nitrous oxide in oxygen. Cerebral blood flow (CBF) was measured with a modification of the KETY & SCHMIDT (1948) technique, using 133xenon as a tracer. Arteriovenous difference in oxygen content over the brain was measured and CMRo2 was calculated. Four groups were studied. Group 1 was a control group. The three experimental groups were injected with phenobarbital intraperitoneally: Group 2 with 50 mg/kg body weight; Group 3 with 150 mg/kg; and Group 4 with 50 mg/kg of phenobarbital, and, in addition, body temperature was lowered to 32 degrees C in this group. CMRo2 in groups 2, 3 and 4 was reduced by 22, 37 and 43%, respectively, compared to Group 1. The changes in CBF were of the same magnitude. In a previous study we have found that CMRo2 decreases by 5% per 1 degree C decrease in body temperature. The value for CMRo2 in Group 4 is close to the value obtained if the effect of 50 mg/kg body weight of phenobarbital on CMRo2 is added to the effect of a temperature reduction of 5 degrees C. It is concluded that the effects of barbiturates and hypothermia on CMRo2 are additive.     

The effect of sevoflurane on ciliary motility in rat cultured tracheal epithelial cells: a comparison with isoflurane and halothane

Halothane and isoflurane potently depress airway ciliary motility. We compared the effect of sevoflurane on ciliary beat frequency (CBF) with that of halothane and isoflurane using purified and cultured rat tracheal epithelial cells. Rat tracheal epithelial cells were isolated from adult male Sprague-Dawley rats to establish an air-liquid interface culture. Apical surfaces of the cells were exposed to a fresh gas containing humidified and warmed (25 degrees C) air (vehicle) with or without sevoflurane (0%-4%), halothane (0%-2%), or isoflurane (0%-2%). The images of motile cilia were videotaped and CBF was analyzed using a computer. Baseline CBF (= 100%) and CBF 30 min after the exposure were measured. CBF 30 min after vehicle exposure was 101% +/- 4% (mean +/- sd). Exposures to 0.25%-2% sevoflurane did not change CBF significantly, although exposures to 0.25%-2% halothane or isoflurane decreased CBF dose-dependently. CBFs 30 min after exposures to 2% of sevoflurane, halothane, and isoflurane were 97% +/- 9%, 56% +/- 14%, and 47% +/- 6%, respectively (n = 5 each). Sevoflurane 4% reduced CBF significantly but slightly (84% +/- 2%, n = 5). These results show that sevoflurane has a direct cilioinhibitory action but its action is much weaker than that of halothane and isoflurane in isolated rat tracheal epithelial cells.     

A comparison of the direct cerebral vasodilating potencies of halothane and isoflurane in the New Zealand white rabbit

Halothane is commonly viewed as a more potent cerebral vasodilator than isoflurane. It was speculated that the lesser vasodilation caused by isoflurane might be the result of the greater reduction in cerebral metabolic rate (CMR) that it causes, and that the relative vasodilating potencies of halothane and isoflurane would be similar if the two agents were administered in a situation that precluded volatile-agent-induced depression of CMR. To test this hypothesis, cerebral blood flow (CBF) and the cerebral metabolic rate for oxygen (CMRO2) were measured in two groups of rabbits before and after the administration of 0.75 MAC halothane or isoflurane. One group received a background anesthetic of morphine and N2O, which resulted in an initial CMRO2 of 3.21 +/- 0.17 (SEM) ml X 100 g-1 X min-1; second group received a background anesthetic of high-dose pentobarbital, which resulted in an initial CMRO2 of 1.76 +/- 0.16 ml X 100 g-1 X min-1. In rabbits receiving a background of morphine sulfate/N2O, halothane resulted in a significantly greater CBF (65 +/- 10 ml X 100 g-1 X min-1) than did isoflurane (40 +/- 5 ml X 100 g-1 X min-1). Both agents caused a reduction in CMRO2, but CMRO2 was significantly less during isoflurane administration. By contrast, with a background of pentobarbital anesthesia, CBF increased by significant and similar amounts with both halothane and isoflurane.(ABSTRACT TRUNCATED AT 250 WORDS)