Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Halothane”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,315 records · Page 73Linked to original sources
PubMed1997

The effects of halothane and isoflurane on the phosphoenergetic state of the liver during hemorrhagic shock in rats: an in vivo 31P nuclear magnetic resonance spectroscopic study.

We studied the effects of halothane versus isoflurane on the phosphoenergetic state and intracellular pH (pHi) of the rat liver using in vivo 31P nuclear magnetic resonance (NMR) spectroscopy during and after hemorrhagic shock. Seventeen rats were anesthetized with 1 minimum alveolar anesthetic concentration of halothane or isoflurane. The mean arterial blood pressure was reduced to 40 mm Hg and maintained at this level for 45 min by withdrawing blood from the common carotid artery. The shed blood was then returned slowly. In vivo 31P NMR spectra were consecutively collected throughout the study. The phosphoenergetic state of the liver was evaluated from the changes in adenosine triphosphate (ATP) and inorganic phosphate (P(i)) levels. pHi was calculated from the chemical shifts of P(i) and alpha-ATP peaks. During hemorrhagic shock, beta-ATP decreased to 35% and 45%, and P(i) increased to 300% and 230% of their initial values in the halothane and isoflurane groups, respectively. Intracellular acidosis was more severe in the halothane group. The recoveries of beta-ATP and P(i) were better in the isoflurane group. Halothane showed a more detrimental effect than isoflurane on the hepatic phosphoenergetic level during and after hemorrhagic shock.

Acidosis↗
PubMed1998

Comparative myocardial depression of sevoflurane, isoflurane, and halothane in cultured neonatal rat ventricular myocytes.

UNLABELLED: In this study, we compared the direct myocardial depressant effects of sevoflurane, isoflurane, and halothane and determined whether an L-type Ca2+ channel agonist, Bay K 8644, could attenuate the myocardial depression induced by these anesthetics in cultured neonatal rat ventricular myocytes. Ventricular myocytes were obtained from neonatal rats by enzymatic digestion with collagenase and then cultured for 6-7 days. The myocytes were stabilized in serum-free medium, and the spontaneous beating rate and contractile amplitude were measured by using a fiberoptic sensor. Each anesthetic decreased the beating rate and amplitude in a concentration-dependent manner (1%-4% vol/vol) (P < 0.001), with halothane decreasing the beating rate and amplitude the most (P < 0.01). Isoflurane caused larger decreases in the beating rate than sevoflurane at 3% and 4% (P < 0.05). Potency for suppression of contractile amplitude was in the order of halothane > > isoflurane > sevoflurane. However, the myocardial depressant effects of the anesthetics were not different when their concentrations were corrected for minimum alveolar anesthetic concentration values. Bay K 8644 significantly prevented the anesthetic-depressed amplitude (P < 0.05). We conclude that sevoflurane, isoflurane, and halothane have direct myocardial depressant effects on cultured neonatal rat ventricular myocytes and that the reduction of sarcolemmal L-type Ca2+ channel current levels mediates the myocardial depression observed in these immature hearts. IMPLICATIONS: Sevoflurane, isoflurane, and halothane have a direct cardiodepressant effect on cardiac excitation-contraction coupling in the immature heart, which is mediated by an interaction with the L-type Ca2+ channel.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1999

Recovery characteristics of sevoflurane and halothane in preschool-aged children undergoing bilateral myringotomy and pressure equalization tube insertion.

UNLABELLED: This double-blinded study was undertaken to prospectively evaluate the role of halothane and sevoflurane and the use of IV ketorolac on the anesthetic emergence in a group of children undergoing bilateral myringotomy with pressure equalization tube procedures. Two-hundred ASA physical status I and II patients were premedicated with nasal midazolam (0.2 mg/kg) and randomized to one of four groups (Group 1 - halothane and ketorolac; Group 2 - halothane and placebo; Group 3 - sevoflurane and ketorolac; Group 4 - sevoflurane and placebo). A blinded nurse observer characterized the quality of the anesthetic emergence and recorded the incidence of emesis and the use of pain medications in the recovery room. There were no differences in age, weight, previous anesthetic experience, or duration of anesthesia among the four groups. There was no difference in the incidence of emergence agitation for patients anesthetized with sevoflurane compared with halothane, regardless of whether they received ketorolac or placebo. Regardless of the anesthetic, the incidence of emergence agitation was significantly less in patients who received ketorolac compared with patients who received placebo. The incidence of emesis in the recovery room, the total 24-h incidence of emesis, and the use of at-home pain medications were similar in all four groups. IMPLICATIONS: We conclude that the incidence of emergence agitation in children undergoing ultrashort anesthetic procedures is similar for sevoflurane and halothane and that ketorolac markedly diminishes emergence agitation and/or pain behavior.

Analgesia↗
PubMed2000

Cardiovascular criteria for epidural test dosing in sevoflurane- and halothane-anesthetized children.

UNLABELLED: This study was designed to determine the detectability of a simulated IV test dose in children during administration of general anesthesia by using heart rate (HR), systolic blood pressure (SBP), and T wave criterion. Forty-two children (0.5-8 yr old) received an IV injection containing epinephrine 0.5 microg/kg and another IV injection containing saline during either halothane or sevoflurane anesthesia administration at 1.0 minimum alveolar concentration in nitrous oxide. A positive test response was defined as a change in T wave amplitude >/=25%, SBP increase >/=15 mm Hg, and HR increase >/=10 bpm. By using the T wave, SBP, and HR criteria, a positive response rate to epinephrine was 100%, 95%, and 71%, respectively, during sevoflurane, and 90%, 71%, and 71%, respectively, during halothane anesthesia administration. These data suggest that the T wave criterion is superior to conventional hemodynamic criteria, and that sevoflurane attenuates T wave and SBP responses less than halothane; however, chronotropic responses are similar to halothane. IMPLICATIONS: We found a greater reliability of the T wave criterion over conventional hemodynamic criteria for detecting intravascular injection of a simulated epidural test dose. Sevoflurane may increase the likelihood of recognition of an accidental intravascular injection of epinephrine-containing solutions in clinical practice compared with halothane.

Anesthesia, Conduction↗
PubMed2002

The differential effect of halothane and 1,2-dichlorohexafluorocyclobutane on in vitro muscle contractures of patients susceptible to malignant hyperthermia.

UNLABELLED: Malignant hyperthermia (MH) is an autosomal dominant, potentially fatal pharmacogenetic disorder of skeletal muscle. Approximately half of all known MH families show a linkage to the ryanodine receptor type 1 (RY1) gene. Although our knowledge of the diagnosis, genetics, and therapy of MH has improved, the exact pathogenesis and the role of volatile anesthetics as trigger substances for an MH crisis remain unknown. Compounds that do not obey the Meyer-Overton hypothesis (i.e., nonimmobilizers) are today an important part of research on anesthetic mechanisms. We designed this study to test the hypothesis that the nonimmobilizer 1,2-dichlorohexafluorocyclobutane (2N) compared with halothane has different effects on in vitro muscle contractures of muscle bundles from MH-susceptible (MHS) individuals. In vitro muscle contracture tests were performed with either halothane (approximately 660 microM, equivalent to approximately 4 minimum alveolar anesthetic concentration [MAC]) or 2N ( approximately 100 microM, equivalent to approximately 5 times predicted MAC). MAC is defined as the anesthetic concentration that prevents nocifensive movements after a surgical stimulus in 50% of subjects. In contrast to halothane, 2N caused only minimal muscle contractures in muscle bundles from six MHS patients (0.13 g [0.04-0.31 g] vs 1.95 g [1.60-4.70 g], median values and ranges; P = 0.004). Halothane and 2N differ in their effects on muscle contractures of MHS individuals, possibly because of a differing action on MH RY1. IMPLICATIONS: Using in vitro contracture tests, we showed that halothane and the nonimmobilizer 1,2-dichlorohexafluorocyclobutane differ in their effects on contractures of muscle bundles from individuals susceptible to malignant hyperthermia (MH) as a result of their differing action on MH ryanodine receptors. These findings render this receptor a possible molecular target for volatile anesthetic action.

Adult↗
PubMed2002

Halothane, isoflurane, and fentanyl increase the minimally effective defibrillation threshold of an implantable cardioverter defibrillator: first report in humans.

UNLABELLED: Placing an implantable cardioverter defibrillator (ICD) involves the induction of ventricular fibrillation, whereupon the minimally effective defibrillation energy threshold (DFT) is determined. We evaluated the effects of 0.7% halothane, 1% isoflurane, or 1.5 micro g/kg of IV fentanyl during N(2)O/oxygen-based general anesthesia (GA) or those of subcutaneous 1.5% lidocaine plus IV 0.35 mg/kg of propofol on the DFT during ICD implantation in humans (n = 20 per group). Thirty minutes after the first set of DFT measurements under such conditions, the inhaled anesthetics were withdrawn, and all three GA groups received fentanyl 1 microg/kg IV (second set). A third set was taken 30 min later, before the GA patients awakened and when only N(2)O/oxygen was delivered for GA. The lidocaine plus propofol patients were given the same IV propofol bolus 1 min before each fibrillation/defibrillation trial and at the same time points as the three GA groups. The first DFTs were 16.1 +/- 2.2 J (halothane), 17.7 +/- 2.7 J (isoflurane), 16.4 +/- 2.9 J (fentanyl), and 12.9 +/- 3.8 J (lidocaine plus propofol) (P = 0.01). The second set of DFTs were significantly lower than the first sets for the halothane (P = 0.01) and isoflurane (P = 0.02), but not the fentanyl or lidocaine plus propofol, regimens. The third DFTs were significantly (P < 0.01) lower than the first ones for the three GA groups, but not for the lidocaine plus propofol patients. Thus, halothane, isoflurane, and fentanyl increased DFT values during ICD implantation in humans, whereas lidocaine plus intermittent small-dose IV propofol minimized these thresholds. IMPLICATIONS: Halothane, isoflurane, and IV fentanyl added to N(2)O/oxygen-based general anesthesia similarly increase minimal defibrillation threshold energy requirements (DFT) during cardioverter defibrillator implantation in humans. Subcutaneous lidocaine plus intermittent small-dose IV propofol minimizes DFT compared with these general anesthetics while providing equal patient satisfaction.

Aged↗
PubMed2002

Pulmonary-to-systemic blood flow ratio effects of sevoflurane, isoflurane, halothane, and fentanyl/midazolam with 100% oxygen in children with congenital heart disease.

UNLABELLED: The cardiovascular effects of volatile anesthetics in children with congenital heart disease have been studied, but there are limited data on the effects of anesthetics on pulmonary-to-systemic blood flow ratio (Qp:Qs) in patients with intracardiac shunting. In this study, we compared the effects of halothane, isoflurane, sevoflurane, and fentanyl/midazolam on Qp:Qs and myocardial contractility in patients with atrial (ASD) or ventricular (VSD) septal defects. Forty patients younger than 14 yr old scheduled to undergo repair of ASD or VSD were randomized to receive halothane, sevoflurane, isoflurane, or fentanyl/midazolam. Cardiovascular and echocardiographic data were recorded at baseline, randomly ordered 1 and 1.5 mean alveolar anesthetic concentration (MAC) levels, or predicted equivalent fentanyl/midazolam plasma levels. Ejection fraction (using the modified Simpson's rule) was calculated. Systemic (Qs) and pulmonary (Qp) blood flow was echocardiographically assessed by the velocity-time integral method. Qp:Qs was not significantly affected by any of the four regimens at either anesthetic level. Left ventricular systolic function was mildly depressed by isoflurane and sevoflurane at 1.5 MAC and depressed by halothane at 1 and 1.5 MAC. Sevoflurane, halothane, isoflurane, or fentanyl/midazolam in 1 or 1.5 MAC concentrations or their equivalent do not change Qp:Qs in patients with isolated ASD or VSD. IMPLICATIONS: Sevoflurane, halothane, isoflurane, and fentanyl/midazolam do not change pulmonary-to-systemic blood flow ratio in children with atrial and ventricular septal defects when administered at standard anesthetic doses with 100% oxygen.

Adolescent↗
PubMed2002

Isoflurane, but not halothane, depresses c-fos expression in rat spinal cord at concentrations that suppress reflex movement after supramaximal noxious stimulation.

UNLABELLED: We investigated the effects of isoflurane and halothane on the induction of fos-like immunoreactivity (FLI) in the rat lumbosacral spinal cord after supramaximal noxious mechanical stimulation of the hindpaw. Compared with unstimulated controls (0.9% isoflurane), noxious stimulation at 0.9%-1.5% elicited significant (0.9%-1.5% isoflurane) increases in FLI bilaterally. FLI was distributed mainly in the superficial dorsal horn (laminae I-III) and, to a lesser extent, in the deep dorsal horn (laminae IV-VI) and intermediate zone (lamina VII), with three- to fivefold greater labeling ipsilaterally. At 1.8% isoflurane, mean FLI counts in all laminar regions were significantly smaller (1.7 +/- 1.3 per section) compared with the other concentrations (11.4 +/- 9.5, 7.5 +/- 6.8, and 9.7 +/- 6.6 at 0.9%, 1.2%, and 1.5%, respectively) but were not different from unstimulated controls. At sacral levels, we observed a bilateral distribution of FLI primarily in superficial laminae in unstimulated controls that was not significantly different at any isoflurane concentration. FLI counts were not significantly different across groups receiving halothane (0.9%-1.5%). FLI was reduced only at isoflurane concentrations that depressed both gross, purposeful movement and reflex withdrawal, whereas halothane did not cause depression even at concentrations that depressed withdrawal reflexes. Isoflurane and halothane may have differing effects on neuronal function and responses to noxious stimulation. IMPLICATIONS: Isoflurane depressed neuronal activity in the spinal cord as measured with fos-like immunoreactivity (FLI), but this occurred only when reflex withdrawal responses were abolished. Halothane, however, did not depress FLI, even at concentrations sufficient to block reflex withdrawal. These two anesthetics may have differing effects on neuronal function and responses.

Anesthetics, Inhalation↗
PubMed1976

Inhibition of cell-mediated cytotoxicity by halothane and nitrous oxide.

Killing of tumor cells by lymphoid cells is important in cell-mediated immunity and defense against cancer. The authors determined that halothane, in vitro, inhibits the killing of YAAC-1 ascites tumor cells from A/jax mice by sensitized peritoneal exudate cells from C57/Black/6 mice. Lysis of tumor cells was quantitated by release of 51Cr into the culture medium. Inhibition of cell-mediated cytotoxicity ranged from 5 per cent in 0.5 per cent halothane to 44.7 per cent in 2.5 per cent halothane exposure. A 12 per cent inhibition of cytotoxicity by 80 per cent nitrous oxide was not statistically significant, but was of a magnitude near that of an equipotent concentration of halothane. The inhibition of cytotoxicity by halothane and nitrous oxide observed in vitro may partially account for the inhibition of cytotoxicity observed when patients undergo surgical operation.

Anesthesia, Inhalation↗
PubMed1976

Halothane and calcium interaction in isolated pregnant and postpartum rat myometrium.

Isolated strips of mid-pregnant and postpartum rat myometrium were rendered functionally Ca2+-free by exposure to a Ca2+-free modified Krebs-bicarbonate solution containing 1 mM EGTA. The muscle strips were then exposed to 2.25 mM Ca2+ for periods of 15 to 600 seconds for the mid-pregnant tissues and one 120-second period for the postpartum tissues. At the end of each exposure, Ca2+ was removed and simultaneously each muscle was depolarized with 125 mM K2SO4. Isometric tension changes in the muscles were measured with and without 0.5 per cent halothane. In the mid-pregnant muscles, halothane diminished the initial tension development in response to Ca2+ by approximately 50 per cent, regardless of the duration of Ca2+ exposure. The contractile response of these muscles to depolarization with K2SO4 was reduced 10 per cent by 0.5 per cent halothane; this was probably due to reduction in transmembrane influx of Ca2+. In the postpartum muscles, the initial tension development in response to Ca2+ was threefold greater than in mid-pregnant muscles and was reduced 25 per cent by halothane. These tissues failed to develop by any tension in response to K2SO4. The most likely explanation for the effect of halothane is that it reduces the transmembrane influx of Ca2+ in both types of tissues, but that the postpartum sarcoplasmic reticulum present less competition for intracellular Ca2+ than pregnant sarcoplasmic reticulum.

Animals↗
PubMed1976

Mutagenicity of volatile anesthetics: halothane.

The mutagenicity of halothane was tested in an in-vitro microbial assay system employing two histidine-dependent mutants of Salmonella typhimurium, TA98 and TA100, Halothane in concentrations ranging from 0.1 to 30 per cent was incubated with bacteria in the presence or absence of a metabolic activation system prepared from either rat liver treated with Aroclor 1254 or human liver. Trifluoroacetic acid, a major metabolite of halothane, and urine from patients anesthetized with halothane also were tested. Halothane, trifluoroacetic acid, and patients' urines were not mutagenic.

Aminobiphenyl Compounds↗
PubMed1977

Coronary vascular resistance during halothane anesthesia.

To study the effect of halothane on the coronary circulation, the circumflex diastolic coronary vascular resistance was measured in the working heart and total mean coronary resistance (TCR) in the isolated nonworking heart of the dog during administration of 100 per cent oxygen and during administration of 2--3 per cent halothane in oxygen. In the working heart, when the diastolic aortic pressure was kept at a nearly control level, halothane induced decreases of 12 per cent in circumflex diastolic coronary vascular resistance and 18 per cent in left ventricular arteriovenous oxygen content difference and no significant change in diastolic coronary blood flow. This effect occurred in spite of the absence of any significant change of myocardial oxygen consumption. In the nonworking beating, arrested or fibrillating heart, halothane induced a decrease of 24 per cent in total mean coronary resistance. Since the decrease in circumflex diastolic coronary vascular resistance in the working heart connot be attributed to myocardial hypoxia and since the results in the isolated nonworking heart eliminate the influences of mechanical and neurohumoral factors on coronary resistance, it is concluded that the observed decrease in resistance is probably due to vasodilation produced by a direct action of halothane on the coronary vessels. This effect was not modified by beta-adrenergic blockade.

Animals↗
PubMed1977

Dose-dependent depression of cardiac function and metabolism by halothane in swine (Sus scrofa).

Halothane depresses myocardial blood flow and metabolism in the dog, but no studies in man have been published. However, the coronary circulation of the pig is remarkably similar to that of man. The authors investigated the effects of halothane-nitrous oxide anesthesia on cardiac function and metabolism in piglets. Thermodilution cardiac output, catheter-tip-manometer measurement of left ventricular function, electro-magnetic flowmeter measurement of coronary blood flow, and blood and tissue measurements of gases and metabolites were made during 0.04 (control), 0.46 (low concentration), and 1.04 (high concentration) per cent halothane vaporized in nitrous oxide, 60 per cent: oxygen, 40 per cent. Compared with control, the low concentration decreased cardiac output (CO) by 10 per cent, left ventricular systolic pressure (LVSP) by 30 per cent, peak contractile element velocity (Vmax by 34 percent, coronary blood flow (CBF) by 36 per cent, and cardiac oxygen uptake (V02) by 55 per cent. Compared with control, the high concentration decreased CO by 32 per cent, LVSP and Vmax by 53 per cent, CBF by 63 per cent and V02 by 62 per cent. This indicates that the dose-related depression in left ventricular function produced by halothane was accompanied by equivalent decreases in coronary blood flow and oxygen comsumption. There was minimal evidence of anaerobic metabolism in these depressed ventricles. Tissue levels of the high-energy phosplates, adenosinetriphosphate and creatine phosphate, and glycogen were unchanged. It is concluded that changes in cardiac oxygenation and metabolism in the pig during halothane anesthesia result from the changes in ventricular function.

Animals↗
PubMed1978

Hemodynamics of increased intra-abdominal pressure: Interaction with hypovolemia and halothane anesthesia.

The hemodynamic interaction of acute hypovolemia and halothane anesthesia in dogs with increased intra-abdominal pressure caused by intraperitoneal instillation of N2, N2O and CO2 was studied. During normovolemia and just basal pentobarbital anesthesia, the response to increase of intra-abdominal pressure to 40 torr consisted of a 35 per cent decrease in cardiac output, which was equal to the decrease in magnitude of inferior vena caval blood flow. During basal pentobarbital anesthesia, the addition of halothane anesthesia (1 MAC) in combination with hypovolemia (15 per cent blood volume loss) depressed the pre-inflation cardiac output more than addition of halothane anesthesia alone or induction of hypovolemia alone. During each of these conditions, superimposition of increased intra-abdominal pressure to 40 torr caused a further 26-43 per cent decrease in cardiac output compared with the pre-inflation value. Therefore, the greatest cardiovascular depression occurred when the animals were both hypovolemic and anesthetized with halothane. There was no difference in the responses to increased intra-abdominal pressure with the different inflating gases at any time. These findings indicate that in the presence of halothane anesthesia or hypovolemia, induction of pneumoperitoneum may cause severe cardiovascular depression.

Abdomen↗
PubMed1978

Ventilatory responses to hypoxia and hypercapnia during halothane sedation and anesthesia in man.

To elucidate the effects of halothane on chemical regulation of ventilation in man, the authors studied the ventilatory responses to isocapnic hypoxia and hyperoxic hypercapnia in 33 human subjects while fully conscious and during sedation or anesthesia with halothane, .1, 1.1, or 2 MAC. In each group, the ventilatory effect of intravenous administration of doxapram, .4 mg/kg, was also measured. Halothane, 1.1 and 2 MAC, totally abolished the hypoxic response and nearly abolished the response to doxapram, while leaving the response to CO2 relatively brisk. Halothane, .1 MAC, decreased the responses to hypoxia and doxapram to less than a third of control, but did not alter the response to CO2. It is concluded that halothane selectivity impairs two ventilatory responses mediated by peripheral chemoreceptors in man.

Adult↗
PubMed1979

Carcinogenicity of halothane in Swiss/ICR mice.

A simplified in-vivo bioassay system was used to test the carcinogenic potential of halothane in Swiss/ICR mice. Halothane was tested only at its maximum tolerated dose, and histologic examination was performed only on tumor masses and other grossly abnormal tissues found at necropsy. Two groups, each of 15 timed pregnant mice, were exposed to either halothane, 500 ppm (0.05 per cent), or compressed air for two hours on days 10--19 of pregnancy. Five days after birth the offspring were similarly exposed, three times weekly, for 78 weeks. After a ten-week, no-treatment, observation period, all remaining mice were examined by necropsy. Mice dying or killed in extremis before final sacrifice at 88 weeks of age also underwent complete gross necropsy unless extensive cannibalism or autolysis precluded examination. The incidences of malignant tumors, hepatomas or modular hyperplasias, and benign tumors in halothane-treated mice were 7, 6, and 20 per cent, respectively; there were similar incidences of these lesions in control animals. It is concluded that under the conditions of this experiment, lifetime administration of halothane at its maximum tolerated dose is not associated with an increased incidence of neoplasia in Swiss/ICR mice.

Adenoma↗
PubMed1979

Halothane biotransformation in anesthetists.

Serum bromide levels were measured in 115 anesthetists by use of x-ray fluorescence spectrometry. Bromide levels peaked at 184 +/- 21 micron in anesthetists regularly exposed to halothane (n = 20), at 58 +/- 4 micron in anesthetists sporadically exposed to halothane (n = 71), and at 46 +/- 3 micron in nonexposed anesthetists (n = 24). Kinetic studies were carried out in five other anesthetists after ten days of exposure to halothane. Average daily halothane concentration was 19.2 +/- 3.2 ppm; duration of exposure was 3.8 +/- 0.2 hours/day. Mean serum bromide level increased from 40 +/- 4 micron before exposure to 220 +/- 36 micron on the last day of exposure. Serum bromide half-life was 14 +/- 1.7 days. The study demonstrates that anesthetists debrominate halothane in a dose-related fashion. Serum bromide levels achieved, however, were far below those reported to result in clinical bromism.

Anesthesiology↗
PubMed1979

Perfusion of naloxone through the fourth cerebral ventricle reverses the circulatory and hypnotic effects of halothane in dogs.

To determine whether naloxone when perfused through the cerebroventricular system would modify the circulatory and hypnotic effects of halothane, the authors studied its effect in six trained dogs. Naloxone, 20 microgram/ml, was perfused through the fourth cerebral ventricle in three and through the third cerebral and lateral ventricles in three other dogs when awake and during halothane anesthesia (0.75--0.82 vol per cent in oxygen). Blood pressure, heart rate, and circulatory responses to bilateral occlusion of the carotid arteries were measured. The state of consciousness was evaluated by the animals behavior and the EEG. Arterial hypotension, bradycardia, depressed baroreceptor responses, and EEG synchronization associated with halothane anesthesia were reversed when naloxone was perfused through the fourth ventricle. To maintain comparable depths of anesthesia the halothane concentration had to be doubled during naloxone perfusion. No change in the circulatory or hypnotic effects of halothane occurred when the third ventricle was perfused with naloxone. It is concluded that opiate receptors in structures bordering the fourth cerebral ventricle may be important modulators of inhalational anesthesia.

Animals↗