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PubMed1980

Halothane-induced hepatic necrosis in triiodothyronine-pretreated rats.

Hepatic centrilobular necrosis developed in rats pretreated with triiodothyronine (T3) and then anesthetized with halothane, 1 per cent, for two hours at an ambient oxygen concentration. Increasing oxygen concentrations decreased the severity of the lesion, there being a significantly (P less than 0.05) less severe lesion with oxygen, 99 per cent, as compared with 21 per cent. Pretreatment with phenobarbital alone resulted in hepatic necrosis only when hypoxia (FIO2 0.14) was also present, and there was no significant worsening of the T3-induced lesion when phenobarbital was added at any oxygen concentration studied. However, the lesion produced by T3 and oxygen, 14 per cent, was significantly worse than the lesion produced by phenobarbital and oxygen, 14 per cent. Glutamic pyruvic transaminase (SGPT) was significantly elevated to 776 (+/- 226) U/1 in the T3-treated rats (10 mg/kg/day, orally) immediately after halothane anesthesia. There was a significant decrease in glutathione to 1.48 (+/- 0.06) mg/g liver 24 hours after T3 administration (1 mg/kg subcutaneously for five days), but no further decrease with continued T3 pretreatment or with halothane anesthesia. Pretreatment with T3 caused a significant decrease in cytochrome P-450 to 0.41 (+/- 0.01) nmol/mg microsomal protein, and halothane anesthesia caused a further significant decrease to 0.27 (+/- 0.04) nmol/mg microsomal protein. The mechanism for the hepatic toxicity of halothane in this model remains to be determined.

Alanine Transaminase↗
PubMed1980

Respiratory waveform and rebreathing in T-piece circuits: a comparison of enflurane and halothane waveforms.

The effects of respiratory waveform on rebreathing in a modified Mapleson D circuit were studied in 18 healthy adult patients anesthetized with either enflurane or halothane. At high fresh gas flow (FGF) rate, when no rebreathing of CO2 occurred, the duration of inspiration (Ti) with enflurane was 41 per cent greater than that with halothane. With enflurane there was a characteristic long end-expiratory pause, 0.69 s, whereas with halothane it was only 0.196 s. The mean inspiratory flow rate (Vt/Ti) was higher (224 ml/s) when halothane was used than with enflurane (187 ml/s). When the FGF rate was reduced to 100 ml/kg/min in the modified Mapleson D circuit, patients breathing halothane had increases in minute volumes (VE) in response to increases of 53-75 per cent in inspired volumes of CO2. The increases in VE resulted fro increases in Vt/Ti of 34-38 per cent. The volume of CO2 inspired when enflurane was used did not increase until FGF rate was as low as 70 ml/kg/min. The reduced rebreathing was related to the respiratory waveform. The advantage of reduced rebreathing with enflurane is counter-balanced by the more profound respiratory depression it causes. The FGF needed to abolish rebreathing of CO2 is highly variable, and is dependent on respiratory waveform.

Adult↗
PubMed1981

Factors affecting the formation of chlorotrifluoroethane and chlorodifluoroethylene from halothane.

Since CF3CH2Cl and CF2CHCl are probably the products of reactive intermediates formed during the reductive metabolism of halothane (CF3CHClBr), factors affecting their in vitro and in vivo formation were investigated. In vitro studies with rat hepatic microsomes showed that CF3CH2Cl and CF2CHCl are produced by cytochrome P-450 mediated reductive pathways which were inhibited by the presence of CO. Under conditions of exposure known to promote halothane hepatotoxicity in phenobarbital treated rats (1 per cent halothane, 14 per cent oxygen), the hepatic and blood concentrations of the volatile metabolites were enhanced. Central venous levels of the volatile metabolites were much higher than he concentration in peripheral vessels. The CF3CH2Cl/CF2CHCl ratio in blood was approximately three, whereas the ratio in vitro was almost unity. Liver levels of the two volatile metabolites greatly exceeded the blood levels, but interestingly they were present in equivalent concentrations. The differences in the ratio of CF3CH2Cl to CF2CHCl may be explained by the fact that CF2CHCl is further degraded under oxidative conditions, whereas CF3CH2Cl appears relatively stable. Measurement of these metabolic products in patients undergoing halothane anesthesia may permit rapid detection of an unusually high level of halothane biotransformation along its hepatotoxic pathway.

Animals↗
PubMed1981

Regional ischemic ventricular dysfunction in myocardium supplied by a narrowed coronary artery with increasing halothane concentration in the dog.

The effects of increasing inspired halothane concentration (0.5, 1.0, 1.5, 2.0 per cent) upon left ventricular myocardium supplied by a critically narrowed coronary artery and a normal coronary artery were studied in 11 open-chested dogs. Regional ventricular function was measured by continuous recording of ventricular segment length using pairs of implanted miniature ultrasonic length detectors in the left anterior descending coronary artery (LAD) and left circumflex coronary artery (LC) territories before and during critical stenosis of the LAD by a micrometer-controlled snare. Critical narrowing was documented by ischemic regional ventricular function (i.e., post-systolic shortening; systolic lengthening) limited to the LAD territory when FIO2 = 0 for 90 seconds. Hemodynamic variables (aortic, left atrial and left ventricular pressure, and heart rate) were measured, ECG lead II was recorded, and the first derivative of left ventricular pressure (LV dP/dt) and coronary perfusion pressure derived for each halothane concentration before and during LAD narrowing. Increasing halothane was associated with equivalent progressive depression of global ventricular function before and during LAD constriction. Prior to LAD constriction, no ischemic changes in regional function occurred. Regional ventricular function was normal during 0.5 percent halothane in the presence of LAD constriction. With increasing halothane during LAD constriction, ischemic regional ventricular function was observed in the LAD territory in eight of eleven hearts, whereas regional ventricular function remained normal in the LC territory. The epicardial ECG was recorded in three dogs and was insensitive as an indicator of ischemia, becoming abnormal only after severe ischemic changes were established. In these studies, in which heart rate remained constant, arterial blood pressure and LV dP/dt decreased, and left ventricular end-diastolic pressure increased, decrease in blood flow and oxygen delivery due to a lower perfusion pressure distal to the coronary artery narrowing appears to be primarily responsible for the observations. The authors hypothesize that clinically unapparent episodes of regional myocardial ischemia distal to narrowed coronary arteries may be an important cause of perioperative myocardial infarction.

Animals↗
PubMed1981

Electroencephalographic evidence of arousal in dogs from halothane after doxapram, physostigmine, or naloxone.

The clinical impressions of enhanced arousal from halothane anesthesia and improvement of postanesthesia recovery scores after doxapram, physostigmine, or naloxone have not been verified in laboratory studies based on the effect of these drugs on MAC. With induction of anesthesia, a shift in the amplitude of the EEG from low to high occurs at anesthetic concentrations well below MAC and appears to coincide with the loss of consciousness. The authors examined the effect of arousal agents on the end-tidal halothane concentration required to produce this shifting EEG. In 24 unmedicated dogs, the end-tidal halothane concentration was elevated to 20 per cent above the shift point concentration (from 0.61 +/- 0.03 to 0.73 +/- 0.03 per cent) and maintained at this level for 30 min. Doxapram, 1 mg/kg, iv, and physostigmine, 0.03 mg/kg, iv, converted the EEG from a high amplitude to a low amplitude tracing in 22 +/- 3 s in eight of eight, and 225 +/- 37 s in seven of eight dogs, respectively. The end-tidal halothane concentration required to restore the shifting EEG was elevated above control for 50 +/- 7 min and 109 +/- 7 min, respectively. Naloxone, 0.06 mg/kg, iv, produced an awake EEG in two of eight dogs in 233 +/- 18 s which persisted for 22 +/- 4 min, and a transiently shifting EEG in three of eight dogs between 200 and 240 s. Naloxone 0.006, mg/kv, iv, produced an awake EEG in 80 +/- 8 s in four of four dogs who had previously received doxapram 3 h earlier. In this model doxapram and physostigmine paralleled the clinically observed onset and duration of arousal. The inconstant arousal from halothane anesthesia induced by naloxone was interpreted in terms of an opiate receptor independent action.

Anesthesia, Inhalation↗
PubMed1982

Induction of anesthesia with halothane increases plasma norepinephrine concentrations.

In seven unstimulated, unmedicated patients given halothane/O2 via face mask, plasma norepinephrine concentration increased 15 min after induction and returned to control at 45 to 60 min. Changes in plasma norepinephrine levels did not correlate with changes in cardiovascular variables. In 10 additional awake, unpremedicated patients, plasma norepinephrine concentration did not change during 5 min of application of 100 per cent oxygen via face mask, but rose with subsequent administration of halothane and nitrous oxide. Again, changes in plasma norepinephrine did not correlate with changes in cardiovascular variables. The authors perfused seven isolated cat spleens with a Krebs-Ringer's lactate solution. Addition of 0.01 atm halothane to the perfusate initially increased release of norepinephrine into the effluent. The authors conclude that halothane or halothane-nitrous oxide initially increases plasma norepinephrine during induction of anesthesia. This increase is not due to the placement of a face mask, but may relate to an effect of halothane at sympathetic nerve endings.

Adolescent↗
PubMed1982

Potentiation by thiopental of halothane--epinephrine-induced arrhythmias in dogs.

Epinephrine-induced arrhythmias were studied in 14 dogs (Group 1) anesthetized with halothane alone (1.09% end-tidal), and on another occasion, at the same halothane concentration following intravenous thiopental (20 mg/kg). Surface (Lead II), catheter His bundle and high right atrial electrocardiograms, and airway and femoral arterial pressures were recorded. Graded doses of epinephrine (EPI-least dose 0.25 microgram . kg-1 . min-1) were infused over five minutes, but terminated sooner if ventricular tachycardia occurred (maximal sensitization). Sensitizing EPI doses (microgram . kg-1) were calculated (dose X time to arrhythmia) for: Shift in or wandering atrial pacemaker (SAP-WAP), atrial ectopy (At Ect), A-V dissociation (AVD), and ventricular ectopy, bigeminy, or tachycardia (V Ect, V Bigem, V Tach). With halothane alone, SAP-WAP occurred at the least dose of EPI followed by At Ect, AVD, V Ect, V Bigem, and V Tach in order of increasing EPI dose. Following thiopental, EPI doses for AVD, V Ect, V Bigem, and V Tach were reduced, as well as EPI dose differences for At Ect, AVD, V Ect, and V Bigem. In an additional seven dogs (Group 2), anesthesia was induced with thiopental (20 mg/kg) followed by halothane (1.09% end-tidal). These animals were observed for arrhythmias during graded EPI infusions at 1-2 h and 3-4 h following thiopental. Sensitizing EPI doses for SAP-WAP and V Tach were similar at each time period. The authors concluded that with halothane and increasing EPI dose, sensitization constitutes a spectrum of arrhythmias, beginning with atrial and progressing to severe ventricular arrhythmias. Thiopental reduces the EPI dose needed for AVD and ventricular, but not atrial, arrhythmias. It also reduces the EPI dose discrepancies for atrial and ventricular arrhythmias.

Animals↗
PubMed1982

A noninvasive in vivo method of assessing the kinetics of halothane metabolism in humans.

The authors describe a noninvasive method of estimating the kinetic constants that characterize metabolism of inhaled anesthetics in humans. Ten healthy male volunteers breathed subanesthetic concentrations of halothane and isoflurane in a fixed inspired ratio of 20:1. Isoflurane served as a marker that identified changes in uptake in nonmetabolizing depots. Each study progressed through nine 30-min levels (numbered 0-8). At each level, inspired concentrations of both halothane and isoflurane were doubled, and alveolar concentrations and uptakes were determined. Clearance (uptake/alveolar concentration) of isoflurane remained constant over a range of concentrations of 0.00006 to 0.008%. In contrast, clearance of halothane decreased as the alveolar concentration increased from 0.0007 to 0.13%. On this basis, the authors assumed that the clearance of halothane was a combination of linear clearance to depots and saturable metabolism, the former proportional to the clearance of isoflurane, and the latter attributable to a Michaelis-Menten process. Applying such a model to halothane, they estimated the mean (+/- SE) Vmax (the composite maximum rate of metabolism) to be 0.79 +/- 0.09 ml . min-1 . individual-1, and the Km (the composite concentration at which half-saturation of enzymes occurs) to be 0.029 +/- 0.003%. This model provides a significantly better data fit than that provided by two simpler submodels, one of which assumes that all clearance is linear, and the other of which allows a part of clearance to be saturable but ignores the isoflurane marker data. The value of 0.029% for Km indicates that a wide range of clinical anesthetic concentrations will produce similar rates of metabolism; that metabolism will proceed at near maximum rates during the first several minutes of recovery; and that most metabolism probably occurs after, rather than during, anesthesia.

Adult↗
PubMed1983

Effects of halothane and enflurane on right ventricular performance in hearts of dogs anesthetized with pentobarbital sodium.

The effects of enflurane and halothane on contractile force of the right ventricle were compared using the Walton-Brodie strain gage arch and pulmonary artery catheter data in dogs anesthetized with pentobarbital. Twenty mongrel dogs were studied to determine the effects of the two anesthetics on contractile force during a 30-minute exposure to four approximate multiples of MAC: 0.75, 1.0, 1.25, and 2.0, and during a 2-h exposure to 1.0 MAC of each agent. Both anesthetics caused a dose-dependent reduction in contractile force, cardiac output, and mean arterial blood pressure. Enflurane caused greater depression of all variables at all concentrations tested. After a 30-min exposure to 0.75, 1.0, 1.25, and 2.0 MAC, halothane depressed contractile force 33.9%, 37.9%, 46.1%, and 73.4%, respectively, and enflurane depressed contractile force 48.4%, 53.5%, 66.6%, and 81.3%, respectively. The depression produced by enflurane at 1.0 and 1.25 MAC was significantly greater (P less than 0.05) than the depression produced by halothane at equal MAC. The reduction of cardiac output by enflurane at 1.25 and 2.0 MAC was significantly greater than that observed with halothane (P less than 0.05). The decrease in mean blood pressure produced by enflurane was significantly greater (P less than 0.05) than the decrease produced by halothane at 1.0, 1.25, and 2.0 MAC. No significant differences between groups were found in temperature, arterial PCO2, PO2, pH, or hematocrit levels. No diminution of the differences in effect on contractility between the two agents was observed when the exposure period was lengthened to two hours at 1.0 MAC.

Anesthesia, General↗
PubMed1983

Anesthetic requirements for halothane in young children 0-1 month and 1-6 months of age.

In a previous study, the authors found that infants, in the first 6 months of life, required the highest minimum alveolar concentration (MAC) of any age group (1.09% halothane). Because only two neonates (0-31 days of age) were included in the original study and because profound depression of blood pressure and heart rate have been reported in neonates, the authors determined 1) whether the MAC of halothane in neonates (n = 12) differs from that in infants (1-6 months of age) (n = 12) and 2) whether the blood pressure and heart rate responses in neonates differ from those in infants at approximately 1 MAC. The authors found that the MAC of halothane in neonates, 0.87% +/- 0.03 SEM, was significantly lower (P less than 0.01) than that in infants, 1.20% +/- 0.06 SEM. With induction of anesthesia, the systolic blood pressure decreased 23% in neonates (P less than 0.05) and 34% in infants (P less than 0.005) from awake values. Similarly, the heart rate decreased 12% in neonates and 22% in infants (P less than 0.05). The incidence of hypotension (greater than 30% decrease in systolic blood pressure from awake) in neonates, 33%, was not significantly different from that in infants, 44%. The authors conclude that the MAC of halothane in neonates is 25% less than that in infants and significantly less than was thought previously. The MAC in infants is the highest of any age group. The decrease in blood pressure and the incidence of hypotension in neonates are similar to those in infants at approximately 1 MAC of halothane.

Age Factors↗
PubMed1984

Oxygen drive to breathing during halothane anesthesia: effects of almitrine bismesilate.

The changes in ventilation and breathing pattern induced by the substitution of pure oxygen for room air were tested in patients during stable halothane anesthesia before and after the administration of almitrine bismesilate, a specific stimulant of the peripheral chemoreceptors. Ventilation was monitored in 25 patients for 15 min while breathing an air-halothane (1.5%) mixture and while breathing then for 10 min an O2-halothane (1.5%) mixture. The maneuver was repeated in 11 of these patients after the infusion of 0.5 mg/kg of almitrine bismesilate. Before almitrine administration, O2 inhalation caused a progressive decrease of minute-ventilation (VE) reaching 94.5 +/- 1.4% (mean +/- SEM) of the initial value at the tenth minute (P less than 0.01). This decrease was secondary to a progressive increase of inspiratory and expiratory times. Almitrine bismesilate caused a significant increase in VE (+11.6%), tidal volume (+14.0%), and mean inspiratory flow (+10.0%) when breathing the air-halothane mixture. Ten minutes after O2 administration, these variables were not different from those observed before almitrine infusion. This study shows that during halothane anesthesia, hypoxic ventilatory drive is not abolished but is depressed severely. Almitrine bismesilate can restore the hypoxic ventilatory drive.

Adult↗
PubMed1984

A comparison of the cerebrovascular and metabolic effects of halothane and isoflurane in the cat.

Halothane is a well known cerebral vasodilator that can produce dangerous increases in intracranial pressure (ICP) in certain neurosurgical patients. It has been suggested that isoflurane may be a less potent cerebral vasodilator. The authors therefore undertook a direct comparison of the effects of halothane and isoflurane on cerebral blood flow (CBF), cerebral vascular resistance (CVR), intracranial pressure, and cerebral metabolic rate for oxygen (CMRO2). Studies were carried out in normocarbic mechanically ventilated cats, using the intracarotid 133Xe injection technique to measure CBF. The effects of three doses were examined: 0.5, 1.0, and 1.5 MAC, studied in the continued presence of 75% N2O. Autoregulation also was tested at 1.0 MAC (plus 75% N2O) by recording CBF and CVR before and after elevation of blood pressure with angiotensin. Both agents had similar effects on blood pressure and ICP. However, while halothane produced significant increases in CBF at all doses, with values of 61 +/- 5 ml X 100 g-1 X min-1 (123 +/- 8% of control, mean +/- SE) at 1.0 MAC, isoflurane anesthesia caused no significant changes in CBF at any level, (e.g., 48 +/- 8 ml X 100 g-1 X min-1 or 94 +/- 12% of control at 1.0 MAC). Both drugs produced dose-related decreases in CVR, but the changes were greater with halothane, e.g., CVR at 1.0 MAC halothane = 1.46 +/- 0.20 mmHg X ml-1 X 100 g X min (47 +/- 7% of control) compared with 2.23 +/- 0.40 mmHg X ml-1 X 100 g X min (72 +/- 9% of control).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1984

Morphine-halothane interaction in rats.

The effects of morphine, halothane, and their various combinations on the purposeful movement (PM) response and the heart rate (HR) increase caused by noxious stimulation were studied in 250 rat experiments. Doses that block the PM and HR responses for the single agent and for combinations were determined with a probit procedure and compared with an isobolographic analysis. As was evidenced by the PM response, the combined anesthetic effect of morphine and halothane, with some deviations, may be defined as additive. It also was found that the combined administration of morphine and halothane results in an antagonism for suppression of the HR increase to noxious stimulation. Halothane antagonized morphine to a much greater extent than morphine to halothane.

Animals↗
PubMed1984

Halothane antagonizes effect of morphine on the motor reaction threshold in rats.

The ability of halothane (used in "sub-MAC" concentrations) to modify the effect of morphine on motor response threshold to pressure was studied and compared with pentobarbital in 241 rat experiments. It was found that halothane (0.5-0.7%, insp.) decreased the reaction threshold to pressure, as did pentobarbital. Halothane (0.5%) increased morphine ED50 for the reaction threshold to pressure from 0.21 mg . kg-1 (95% fiducial limits: 0.13-0.29 mg . kg-1) to 0.52 mg . kg-1 (0.28-0.73 mg . kg-1, P less than 0.0001). Pentobarbital in a dose of 3 mg . kg-1 demonstrated a similar antanalgesic effect. Neither halothane nor pentobarbital antagonized the effect of morphine with motor response to the tail clamp. On the contrary, both agents strengthened this effect. It has been suggested that the effect of morphine on the motor response threshold to pressure results primarily from activation of inhibitory control mechanisms concerned with this response; halothane in a subanesthetic concentration depresses the inhibitory control mechanisms and, therefore, weakens the effect of morphine.

Animals↗
PubMed1984

Effect of halothane on cardiac acceleration response to somatic nerve stimulation in dogs.

In six dogs, the authors investigated the effect of halothane on cardiac acceleration response to the electrical stimulation of a cutaneous nerve. It was found that increasing the concentration of halothane was associated with a proportional depression of the cardiac acceleration response to somatic nerve stimulation (y--99.8 - 44.3x; y--delta HR, x--halothane end-tidal concentration). Relationship of the response to end-tidal anesthetic concentration was characterized by a strong correlation (r= -0.93, P less than 0.0001). Complete abolition of the increase in heart rate in response to somatic nerve stimulation was observed at a halothane end-tidal concentration of 2.2 vol% (extrapolation). It is suggested that suppression of heart rate increase to noxious stimulation may be used as a graded index of the depth of anesthesia for halothane.

Animals↗
PubMed1985

Effect of halothane on coronary collateral circulation.

The authors studied the effect of halothane in a canine model of coronary collateral circulation secondary to chronic occlusion of a coronary artery. Two sets of experiments were performed. In the first experiments, Ameroid constrictors were placed around the left anterior descending coronary artery to produce complete occlusion in three weeks. An inflatable occluder was placed around the circumflex coronary artery in order to apply a mild stenosis to the artery supplying the collateral vessels to produce vasodilation distal to the stenosis. Regional myocardial blood flows were measured using radioactive microspheres. Blood flows to normal and collateralized myocardium were decreased significantly during halothane anesthesia, but perfusion of the subendocardium in both regions was maintained even in the presence of mild stenosis of the circumflex coronary artery supplying the collateral vessels, as indicated by unchanged endocardial/epicardial blood flow ratios. In the second experiments, chronic occlusions of both circumflex and right coronary arteries were produced using Ameroid constrictors. In these animals, sedated using xylazine, pacing-induced tachycardia produced a marked but reversible decrease in blood flow to the collateralized subendocardium. During halothane anesthesia at normal heart rate, blood flow to the collateralized subendocardium was well maintained, but tachycardia produced marked decrease in blood flow to the collateralized subendocardium, leading to the demise of four of seven dogs. The authors conclude that in this chronic canine model, in which control measurements were made during sedation using xylazine, coronary collateral blood flow is well maintained during halothane anesthesia at normal heart rate, but tachycardia during halothane anesthesia severely limits blood flow to the collateralized subendocardium.

Animals↗
PubMed1985

Effect of halothane on renal hemodynamics during normovolemia and acute hemorrhagic hypovolemia.

The effects of halothane on renal hemodynamics under both normovolemic and hypovolemic conditions were investigated in chronically instrumented conscious dogs whose homeostatic mechanisms were not altered by the presence of preexisting drugs. Renal blood flow and aortic pressure were assessed by prior implantation of Doppler ultrasonic flow probes on the renal artery and a catheter in the descending aorta. Administration of halothane to conscious normovolemic dogs (Group HN) resulted in 11-26% decreases in renal vascular resistance with no significant changes occurring in renal blood flow. In a second group of animals made hypovolemic while awake (Group AH), 30% of the blood volume was removed over one-half hour. In response to hemorrhage, these conscious animals' renal blood flow did not significantly change from the normovolemic control, and renal vascular resistance significantly decreased. With no further intervention, renal vascular resistance and renal blood flow remained unchanged from the level achieved after the 30% hemorrhage. A third group of animals (Group HH) was hemorrhaged in a manner similar to that of Group AH. They also showed no significant changes in renal blood flow and a significant decrease in renal vascular resistance in response to hemorrhage. Thereafter, administration of halothane, as in Group HN, to this group produced 11-23% decreases in renal vascular resistance with no significant decline in renal blood flow from the hypovolemic control levels established after hemorrhage. The author concludes the following: administration of halothane to normovolemic conscious dogs does not decrease renal blood flow; a moderate degree of acute hemorrhagic hypovolemia does not decrease renal blood flow in conscious dogs; and administration of halothane to acutely hypovolemic conscious dogs does not impair renal perfusion.

Anesthesia, Inhalation↗
PubMed1985

Local application of 133Xenon for measurement of regional cerebral blood flow (rCBF) during halothane, enflurane, and isoflurane anesthesia in humans.

It is well known that halothane causes an increase in cerebral blood flow (CBF). In this study the effects of halothane, enflurane, and isoflurane on regional cerebral blood flow (rCBF) in humans were determined in the presence of 70% N2O at a combined MAC concentration of 1.5. CBF was determined in 24 patients from the washout of locally applied 133Xenon with the use of an external scintillation. All 24 patients (control n = 6, halothane n = 6, enflurane n = 6, and isoflurane n = 6) were undergoing neurosurgical procedures. All patients were anesthetized with thiopental, fentanyl, droperidol, and 70% N2O in oxygen and paralyzed with pancuronium. The measurements were performed after the dura had been opened and before definitive surgery. The first measurement was done in the absence of any volatile agent, and the wash-out curve was registered for 6 min. The second measurement was done after one of the volatile agents had been added for at least 20 min and had reached a concentration of 0.58% for halothane, 1.14% for enflurane, or 1.0% for isoflurane in the expiratory gases in order to obtain about 1.5 MAC with each volatile anesthetic. The anesthetic concentrations were measured with the Engström multigas analyzer EMMA. The physiologic variables changed very little throughout the period of observation. Body temperature, heart rate, blood pressure, PaCO2, and PaO2 were stable. Ephedrine was used to maintain a stable arterial pressure. At approximately 1.5 MAC, halothane (plus N2O) increased rCBF to nearly three times (166%) the control value, while enflurane induced only a slight increase (35%) in rCBF.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗