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PubMed1994

Influence of halothane and isoflurane on the contractile responses to potassium and prostaglandin F2 alpha in isolated human pial arteries.

Volatile anaesthetics may modulate cerebrovascular resistance, but their direct actions on human cerebral arteries are unknown. In the present study, we have evaluated the effects of halothane and isoflurane at different MAC (0.4, 1.0 and 2.0) on contractions induced by depolarization (potassium) or receptor stimulation (prostaglandin F2 alpha) in isolated ring segments of human pial arteries. Neither halothane nor isoflurane had significant effects on potency (unaffected EC50 value) or the maximum response (Emax) in potassium-contracted arteries, even though there was a general tendency to attenuation of Emax. Similarly, the potency of prostaglandin F2 alpha was unchanged (unaffected EC50 value). However, the Emax value for prostaglandin F2 alpha at normocapnia (mean PCO2 4.3 (SEM 0.1) kPa, pH 7.41 (0.01)) and addition of halothane (0.4, 1.0 and 2.0 MAC) was significantly attenuated to 96 (2)%, 91 (3)% and 84 (4)% at the respective MAC concentrations. Isoflurane at 2 MAC and normocapnia also reduced Emax to 94 (3)%. During hypocapnia (PCO2 2.7 (0.1) kPa, pH 7.64 (0.01)), the vasodilator effect of halothane was reduced, whereas isoflurane at 0.4 and 1.0 MAC enhanced the contraction induced by prostaglandin F2 alpha.

Adult↗
PubMed1994

Functional recovery of stunned myocardium is greater with halothane than fentanyl anaesthesia in dogs.

We have compared the effects of halothane or fentanyl on recovery of regional myocardial function in the postischaemic ventricle in dogs. The animals were followed for 120 min during reperfusion after 15-min of occlusion of the left anterior descending coronary artery. After 120 min of reperfusion, the fentanyl group had recovered only 54% and 50% of regional contractility and systolic shortening (P < 0.05), respectively, compared with halothane (63% and 86%). Intramyocardial tissue pressure was less than baseline 60 min after reperfusion in the fentanyl group (P < 0.05), whereas the halothane group had returned to control values. We conclude that halothane is more effective than fentanyl in attenuating regional myocardial dysfunction associated with transient episodes of ischaemia.

Anesthesia, General↗
PubMed1994

Effect of halothane on cilia beat frequency of ciliated human respiratory epithelium in vitro.

The effect of halothane on human ciliated nasal epithelium was studied in vitro. Samples from 24 healthy adult volunteers were exposed to halothane in varying concentrations and cilia beat frequency was measured using the transmitted light technique. Mean cilia beat frequency was measured at 30-min intervals. There was a significant decrease in cilia beat frequency at 2 h in samples that were exposed to halothane (mean 8.4 (SD 2.5) Hz, 9.18 (2.6) Hz and 6.99 (4.9) Hz) compared with air (10.8 (2.7) Hz, 11.6 (2.1) Hz and 12.1 (2.3) Hz) (P < 0.01). The coefficient of variation of cilia beat frequency measurements increased after exposure to halothane. There was no change in the cilia beat frequency of controls exposed to air over a 3-h period.

Adult↗
PubMed1994

Effects of halothane and isoflurane anaesthesia on microcirculatory blood flow in musculocutaneous flaps.

Hypoperfusion and necrosis in musculocutaneous flaps used for reconstruction of tissue defects is still a significant clinical problem. Although the causes of hypoperfusion are frequently surgical in nature, little is known about the effects of anaesthetic management on blood flow in flaps or the outcome of flap surgery. We compared in minipigs the effects of halothane and isoflurane anaesthesia in equipotent doses on microcirculatory blood flow (MBF) in the skin and muscle part of musculocutaneous flaps and also in intact (control) skin and muscle. Measurements were made during stable normovolaemic conditions and during mild to moderate hypovolaemia (withdrawal of 5%, 10% and 15% of total blood volume). Multi-channel laser Doppler flowmetry (LDF) was used to measure MBF and electromagnetic flowmetry (EMF) for total flap blood flow. During normovolaemic conditions there was no significant difference between the two groups in central haemodynamic or respiratory data. After 15% blood loss, however, there was a significant decrease in mean arterial pressure and cardiac output in the halothane group while there was no significant change in the isoflurane group (P < 0.05). MBF in control skin, control muscle and flap muscle remained approximately 10-15% higher in the isoflurane than in the halothane group throughout the study. In the isoflurane group, MBF in flap skin was unchanged during normovolaemia and there was less than 10% decrease during hypovolaemia. In the halothane group hypovolaemia caused a significant decrease in MBF in flap skin: 27% decrease after 5% blood loss, 45% decrease after 10% blood loss and 49% decrease after 15% blood loss compared with 5%, 20% and 21%, respectively, in intact skin.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1996

Effects of 3 MAC of halothane, enflurane and isoflurane on cilia beat frequency of human nasal epithelium in vitro.

We have measured the effects of three times the minimum alveolar concentration (MAC) of halothane, enflurane and isoflurane on cilia beat frequency of human nasal epithelial brushings from 18 healthy adult patients. Using the transmitted light technique and paired perfusion chambers, the cilia were exposed to 2.25% halothane, 5% enflurane or 3.6% isoflurane in air, or air alone, in a controlled and blinded manner. Over a 4-h observation period, cilia beat frequency of the samples exposed to inhalation anaesthetic agents demonstrated a significant reduction in frequency compared with controls exposed to air alone. Mean cilia beat frequency for the samples exposed to halothane was 9.3 (SEM 1.3) compared with its controls of 11.4 (1.0); for the samples exposed to enflurane, 10.9 (1.3) compared with its controls of 11.6 (1.2); and for the samples exposed to isoflurane, 10.8 (1.1) compared with its controls of 11.6 (1.2). There was a statistically significant difference between the samples exposed to all three volatile agents and their associated controls (halothane, P = 0.01; enflurane, P = 0.03; isoflurane, P = 0.01; nested repeated measures analysis of variance utilizing polynomial contrasts).

Adult↗
PubMed1997

Effect of halothane on K+ and carbachol stimulated [3H]noradrenaline release and increased [Ca2+]i in SH-SY5Y human neuroblastoma cells.

We have examined the effects of the volatile general anaesthetic agent, halothane, on K+ and carbachol stimulated [3H]noradrenaline release and associated increases in intracellular Ca2+ in a cultured human neuroblastoma cell line, SH-SY5Y. K+ (but not carbachol) stimulated [3H]noradrenaline release, and the increase in intracellular Ca2+ concentration was entirely extracellular Ca2+ dependent. Halothane produced a dose-dependent reduction in K+ evoked release of [3H]noradrenaline with significant inhibition (17%) occurring from 1.26 atm%. Basal and carbachol evoked release were unaffected. Halothane also produced a dose-dependent reduction in K+ evoked increases (measured at the peak) in intracellular Ca2+ with significant inhibition (29%) occurring from 0.88 atm%. K+ plateau, basal and carbachol evoked increases in intracellular Ca2+ were unaffected. These data suggest that halothane reduced Ca2+ entry through voltage-sensitive Ca2+ channels and implicate this important class of ion channel in the mechanism of anaesthesia.

Anesthetics, Inhalation↗
PubMed1998

Endocrine and metabolic effects of hypotension or halothane inhalation in sheep anaesthetized with pentobarbital.

We have studied the mechanism whereby halothane induces adrenocortical activity in eight sheep anaesthetized twice for 2 h with pentobarbital. During the second hour they received infusion of nitroprusside to lower mean arterial pressure by 40 mm Hg (group NP) or on another occasion they inhaled 0.5% halothane (group HAL). Plasma concentrations of cortisol, adrenocorticotrophic hormone (ACTH), arginine vasopressin (AVP), glucose and lactate were measured. Infusion of nitroprusside increased cortisol concentrations from mean 44 (SD 33) to 256 (131) nmol litre-1 (P < 0.05), AVP from 19 (14) to 174 (102) pmol litre-1 (P < 0.05) and ACTH from 30 (17) to 54 (32) pmol litre-1. Glucose and lactate concentrations did not change significantly. After 60 min of halothane administration, there were fewer effects: plasma cortisol increased from 47 (39) to 63 (44) nmol litre-1 (P > 0.05) and AVP from 14 (11) to 32 (29) pmol litre-1 (P > 0.05) while ACTH decreased from 32 (13) to 25 (10) pmol litre-1. The AUC60-120 values for all three hormones were significantly lower in group HAL than in group NP (P < 0.01). Glucose was unchanged but lactate concentration decreased. These results support, but do not prove, the hypothesis that hypotension is the main stimulus to pituitary-adrenocortical activity during halothane anaesthesia in sheep. A direct effect of nitroprusside cannot be ruled out.

Adrenocorticotropic Hormone↗
PubMed1999

Ventilatory compensation for inspiratory resistive loads during anaesthesia with halothane or isoflurane.

We have analysed the ventilatory response to sustained inspiratory resistive loads in 14 patients, while awake and during halothane (n = 7) or isoflurane (n = 7) anaesthesia. Patients breathed halothane or isoflurane in oxygen at 1.2 minimum alveolar concentration (MAC). Inspiratory resistances of 0, 12 and 37 cm H2O litre-1 s were applied. Tidal volume (VT) was maintained with the greater loads. At the greatest resistance, a significant reduction in minute ventilation occurred in both awake (-18.9%) and anaesthetized states, with both halothane (-10.4%) and isoflurane (-14.5%). Ventilatory frequency decreased significantly from mean 14.6 (SD 4.7) to 12.5 (4.3) bpm in the awake state and during anaesthesia, with increasing inspiratory resistance (29.5 (3.6) to 23.7 (7.2) bpm and 25.8 (3.3) to 23.4 (4.0) bpm, respectively, for halothane and isoflurane) because inspiratory time (TI) was significantly longer (P < 0.01). End-tidal PCO2 increased by 0.3 kPa, on average, from baseline to the highest level of resistance (P < 0.01). Inspiratory occlusion pressure at 100 ms increased significantly with increased loading in all situations (P < 0.001). We found a similar pattern of ventilatory adaptation to sustained inspiratory flow resistive loads both in awake and anaesthetized states. VT was maintained at increased loads because of an increase in inspiratory neuromuscular output and inspiratory duration.

Adolescent↗
PubMed1999

Relaxation by sevoflurane, desflurane and halothane in the isolated guinea-pig trachea via inhibition of cholinergic neurotransmission.

We have studied relaxation of airway smooth muscle by sevoflurane, desflurane and halothane in the isolated guinea-pig trachea. Ring preparations were mounted in tissue baths filled with physiological salt solution (PSS), aerated continuously with 5% carbon dioxide in oxygen. Electrical field stimulation (EFS) elicited cholinergic contractions that were abolished by tetrodotoxin, indicating nerve-mediated responses. Anaesthetics were added to the gas aerating the tissue baths. Halothane, sevoflurane and desflurane at 0.5-1.0 MAC markedly attenuated cholinergic contractions to EFS. Initiation of contractile responses to acetylcholine (ACh) were not affected by volatile anaesthetics, suggesting prejunctional inhibition (i.e. inhibition of acetylcholine release). When added to a maintained submaximal contraction to ACh, volatile anaesthetics induced relaxation, indicating postjunctional inhibition. We conclude that sevoflurane, desflurane and halothane inhibited postganglionic cholinergic neuroeffector transmission in the trachea. The effect was probably exerted via pre- and postjunctional mechanisms (i.e. inhibition of acetylcholine release and direct muscle actions). Sevoflurane and desflurane were more potent than halothane both pre- and postjunctionally.

Acetylcholine↗
PubMed2005

The effects of halothane and isoflurane on cardiovascular function in laterally recumbent horses.

BACKGROUND: Experimental studies in adult horses have shown that general anaesthesia maintained with isoflurane is associated with less depression of cardiovascular function compared with halothane anaesthesia. Adverse effects of intermittent positive-pressure ventilation (IPPV) have also been demonstrated. Nevertheless, the haemodynamic effects of these agents and the effects of differing modes of ventilation have not been assessed during clinical anaesthesia in horses undergoing surgery. METHODS: The haemodynamic effects of isoflurane or halothane anaesthesia during spontaneous or IPPV were studied non-invasively in 32 laterally recumbent horses undergoing elective surgery. Indices of cardiac function and measurements of femoral arterial blood flow and resistance were recorded using transoesophageal and transcutaneous Doppler echocardiography, respectively. Arterial pressure was measured directly using a facial artery catheter. RESULTS: Cardiac index (CI) was significantly higher during isoflurane anaesthesia than during halothane anaesthesia and was also higher during spontaneous ventilation with isoflurane. CI decreased significantly over time and an inverse relationship was observed between CI and mean arterial pressure (MAP). Horses with higher MAP had a significantly lower CI. During isoflurane anaesthesia, femoral arterial blood flow was significantly higher in both pelvic limbs compared with halothane anaesthesia, and flow in the lower limb was significantly higher during spontaneous ventilation than during IPPV. No significant change in femoral blood flow was observed over time. CONCLUSION: The effects of anaesthetics and mode of ventilation on cardiovascular function recorded under surgical conditions in horses are similar to those reported under experimental conditions. However, in contrast with previous experimental studies, CI progressively decreased over time regardless of agent used or mode of ventilation employed.

Anesthesia, Inhalation↗
PubMedDate not supplied

Rapid analysis of halothane in biological samples using headspace solid-phase microextraction and gas chromatography-mass spectrometry--a case of a double homicide.

A simple, rapid, and sensitive method for the analysis of halothane in biological samples was developed. The procedure describes the extraction of halothane from blood, liver, kidney, brain, urine, bile, and stomach contents by headspace solid-phase microextraction (HS-SPME) followed by capillary gas chromatography coupled with mass spectrometry (GC-MS). The recovery in blood samples after addition of ammonium sulfate and sulfuric acid was 72% compared to a sample prepared in water (100%). Linearity was established over a concentration range of 0.1-100 mg/kg of spiked blood samples with an excellent coefficient of correlation (0.996) and a limit of detection of 0.004 mg/kg. The time for analysis was approximately 40 min per sample including the extraction step. The procedure was used for quantitation of halothane in various samples in a case of a double homicide. HS-SPME in combination with GC-MS was an effective method for the determination and quantitation of halothane in biological material.

Aged↗
PubMed1996

Effect of halothane and isoflurane on in situ diameter responses of small mesenteric veins to acute graded hypercapnia.

The purpose of the present study was to quantify the inhibitory effect of inhaled halothane and isoflurane on acute hypercapnia-induced responses of capacitance-regulating veins and related cardiovascular variables in response to sequential 40-s periods of 5%, 10%, 15%, and 20% inspired CO2 (FICO2). Measurements were made in normoxic alpha-chloralose-anesthetized rabbits before, during, and after either 0.75 minimum alveolar anesthetic concentration inhaled halothane or isoflurane. The graded hypercapnia caused graded venoconstriction and bradycardia but minimal pressor responses. Hypercapnia-induced venoconstriction was blocked by prior local superfusion of the exposed veins with 3 x 10(-6) M tetrodotoxin. Both the hypercapnia-induced venoconstriction and bradycardia responses were significantly attenuated by halothane or isoflurane and did not fully recover after removal of the anesthetics from the circulation. Both anesthetics produced a significant baseline (i.e., prehypercapnia) hypotension and a tendency toward a resultant tachycardia. The baseline hypotension did not recover completely after elimination of the anesthetic. Neither anesthetic altered baseline vein diameter. These results agree with previous studies demonstrating that hypercapnic acidosis produces mesenteric venoconstriction by elevating excitatory sympathetic efferent neural input via activation of peripheral and central chemoreceptors and that bradycardia results from activation of compensatory baroreflexes. The neural components of these reflexes are possible primary sites for attenuation of these cardiovascular responses by halothane and isoflurane.

Acute Disease↗
PubMed1996

Steady-state myogenic response of rat coronary microvessels is preserved by isoflurane but not by halothane.

The myogenic response of vascular smooth muscle produces vasomotion in response to changes in vessel transmural pressure. While this is an important determinant of coronary blood distribution, the effect of volatile anesthetics on the response has not been previously investigated. In this study, we examined the effect of isoflurane and halothane on this myogenic response. Coronary resistance arteries were isolated from Wistar rats. As the intraluminal pressure was increased from 10 to 120 mm Hg in the presence of either isoflurane (1%, 2%, and 3%), halothane (1% and 2%), or no volatile agent (control), the vessel intraluminal diameter was monitored using a video detection system. Passive changes in vessel diameter were measured after exposure to papaverine 100 microM. Additionally, the myogenic responses of endothelium-intact and endothelium-denuded vessels were compared. Endothelium-intact control vessels demonstrated myogenic constriction above 80 mm Hg of intraluminal pressure. This response was not affected by endothelial denudation. The response was preserved by isoflurane 1%, 2% or 3% but abolished by halothane 1% or 2%. We conclude that, in rat coronary resistance arteries, myogenic constriction can be demonstrated above 80 mm Hg of intraluminal pressure and is endothelium independent. This response is preserved by isoflurane but abolished by halothane. These findings may have implications for the effect of the anesthetics on coronary blood flow distribution.

Anesthetics, Inhalation↗
PubMed1996

Intensity of halothane- and hypercapnia-induced cerebral hyperemia is strain-dependent in rats.

Cerebrovascular responses to physiologic and pharmacologic stimuli vary between laboratories using different strains of the same species. We tested whether the cerebral blood flow (CBF) response to 1% halothane or hypercapnia is strain-dependent in rats. Age-matched adult male (n = 14 of each strain) Wistar, Wistar-Kyoto (WKY), and spontaneously hypertensive rats (SHR) were anesthetized with pentobarbital and mechanically ventilated. Under baseline conditions blood flow to cerebrum (microspheres) in WKY (66 +/- 5 mL.min-1.100 g-1) was less than (P < 0.05) in Wistar (88 +/- 5 mL.min-1.100g-1) and SHR (83 +/- 5 mL.min-1.100 g-1). Blood flow to brainstem was greater (P < 0.05) in Wistar (106 +/- 8 mL. min-1.100 g-1) than in WKY (71 +/- 5 mL.min-1. 100 g-1) and SHR (84 +/- 4 mL.min-1.100 g-1). In the halothane protocol (n = 8 each strain), administration of 1% halothane, during normocapnia, increased blood flow to the cerebrum in WKY (64 +/- 6 to 120 +/- 12 mL.min-1.100 g-1, P < 0.05) and SHR (78 +/- 6 to 115 +/- 8 mL.min-1.100 g-1, P < 0.05) but not Wistar rats (88 +/- 8 to 102 +/- 5 mL.min-1.100 g-1, not significant). Discontinuing halothane caused blood flow to return to baseline values. In the hypercapnia protocol (n = 6 each strain), exposure to 3% CO2 (to achieve a PaCO2 of 50-55 mm Hg) and 6% CO2 (to achieve a PaCO2 of 60-70 mm Hg) caused blood flow to the cerebrum to increase in Wistar (87 +/- 11 to 112 +/- 15 to 162 +/- 23) to similar amount as observed in WKY (69 +/- 7 to 115 +/- 13 to 162 +/- 23 mL.min-1. 100 g-1) but less than that observed in SHR (89 +/- 7 to 174 +/- 24 to 237 +/- 28 mL.min-1.100 g-1). These data demonstrate that the cerebral hyperemic response to vasodilator stimuli is strain-dependent in rats.

Anesthetics, Inhalation↗
PubMed1996

Enflurane decreases the threshold for vasoconstriction more than isoflurane or halothane.

Intraoperative hypothermia results largely from anesthetic-induced inhibition of tonic thermoregulatory vasoconstriction. Sufficient hypothermia, however, triggers peripheral vasoconstriction, which usually prevents further decrease in core temperature. The thermoregulatory effects of all volatile anesthetics have been tested in adults and/or children, but different anesthetics have not been directly compared. We therefore evaluated thermoregulatory responses during enflurane, isoflurane, and halothane administration. Anesthesia was maintained with 1 minimum alveolar anesthetic concentration (MAC) of halothane, isoflurane, or enflurane in 27 patients undergoing intraabdominal surgery. Patients were maintained normovolemic and normocapnic but were allowed to cool passively. A forearm minus fingertip, skin-temperature gradient of 4 degrees C identified significant vasoconstriction; the core temperature triggering vasoconstriction identified the threshold. Morphometric characteristics, initial core temperatures, ambient operating room temperatures, blood pressures, and anesthetic potencies were similar in each group. All eight patients given halothane vasoconstricted at a core temperature of 35.5 +/- 0.6 degrees C. Eight of the patients given isoflurane vasoconstricted at a core temperature of 35.2 +/- 0.5 degrees C. However, two others did not at minimum core temperatures of 34.0 and 33.8 degrees C. Only one patient given enflurane vasoconstricted at a core temperature of 34.6 degrees C. The other six patients never vasoconstricted, at minimum core temperatures of 33.6 +/- 0.4 degrees C. Our data indicate that enflurane profoundly inhibits thermoregulatory responses in children. The mechanism for this extraordinary inhibition remains unknown but does not result from any obvious anesthetic pharmacology or thermoregulatory physiology. We conclude that unwarmed pediatric patients will become colder when anesthetized with enflurane than with halothane or isoflurane.

Anesthetics, Inhalation↗
PubMed1997

Isoflurane and halothane attenuate endothelium-dependent vasodilation in rat coronary microvessels.

Volatile anesthetics attenuate endothelium-dependent vasodilation but the mechanism of attenuation remains controversial. The present study examines the mechanism of isoflurane- and halothane-mediated attenuation of endothelium-dependent vasodilation in Wistar rat coronary microvessels of about 100 microns internal diameter. The vessels were studied in vitro in a pressurized (40 mm Hg), no-flow state using video microscopy. After preconstriction of the vessels with the thromboxane analog U46619 1 microM, concentration response curves to acetylcholine (ACh), the calcium ionophore A23187, sodium nitroprusside (SNP), or the stable cyclic guanosine monophosphate (cGMP) analog 8-bromo-cGMP (Br-cGMP) were obtained in the presence of 0% (control), 1% or 2% isoflurane, or 1% or 2% halothane. Isoflurane 1% and 2% significantly attenuated vasodilation to ACh and A23187. Isoflurane 2%, but not 1%, attenuated vasodilation to SNP. Vasodilation to Br-cGMP was not affected by isoflurane. Halothane attenuated vasodilation to ACh, but had no effect on vasodilation to A23187, SNP, or Br-cGMP. We conclude that isoflurane attenuates endothelium-dependent vasodilation by impairing at least two distinct steps in the nitric oxide (NO)-cGMP pathway, the first being between endothelial increase of calcium and smooth muscle guanylate cyclase and the second being inhibition of soluble guanylate cyclase activity. These two steps appear to have different sensitivities to the effect of isoflurane. Halothane has an effect at the endothelial receptor level, but not any distal steps in the NO-cGMP pathway.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed1997

Laser Doppler skin blood flow and sympathetic nervous responses to surgical incision during halothane and isoflurane anesthesia.

The aim of the present study was to evaluate whether a sudden decrease in skin blood flow measured using a laser Doppler velocimeter reflects sympathetic nervous response to surgical skin incision during halothane (n = 17) and isoflurane (n = 16) anesthesia in 33 ASA physical status I or II patients scheduled for laparotomy. Plasma norepinephrine concentrations in the responding patients who showed a sudden decrease in the skin blood flow after surgical incision increased significantly and continued to increase 1-10 min after skin incision under halothane and isoflurane anesthesia. Although plasma norepinephrine concentrations in the nonresponders did not increase after surgical incision with halothane, the concentrations increased significantly at 1 min, but not at 3 and 10 min, after skin incision with isoflurane. The results indicate that the sudden decrease in laser Doppler flow reflects the sympathetic response to surgical incision. However, these also suggest that the factors that control the skin blood flow may not be simply sympathetic but may reflect other modulators as well. Plasma epinephrine concentration increased during skin incision, but the concentrations did not differ between the patients with and without a sudden decrease in skin blood flow. Increases in systolic blood pressure and rate-pressure product on skin incision were also significantly more in patients with skin blood flow response compared with those without the response. The magnitude of changes in plasma norepinephrine concentration and hemodynamic variables with skin incision was greater with isoflurane than with halothane at the same minimum alveolar anesthetic concentration level.

Adult↗
PubMed1997

The effects of sevoflurane on recovery of brain energy metabolism after cerebral ischemia in the rat: a comparison with isoflurane and halothane.

UNLABELLED: Isoflurane is an appropriate anesthetic for neuroanesthesia. We evaluated whether the effect of sevoflurane is similar to that of isoflurane or halothane on brain energy metabolism after cerebral ischemia followed by reperfusion using 31P-magnetic resonance spectroscopy. Wistar rats (n = 21) were divided into three groups: isoflurane-, sevoflurane-, or halothane-treated. After anesthesia induction and surgical preparation, each anesthetic concentration was adjusted to 1 minimum alveolar anesthetic concentration. Cerebral ischemia was induced with bilateral carotid occlusion and reduction of mean arterial blood pressure to 30-40 mm Hg by blood withdrawal. Magnetic resonance measurements were performed during ischemia and for 120 min of reperfusion. Intracellular pH in the isoflurane-treated, sevoflurane-treated, and halothane-treated groups decreased to 6.180 +/- 0.149, 6.125 +/- 0.134, and 6.027 +/- 0.157, respectively, at the end of ischemia. There were no differences in the change of phosphorous compounds and intracellular pH between the isoflurane-treated and the sevoflurane-treated groups during ischemia and reperfusion. However, in the halothane-treated group, we observed a significant delay in the recovery of adenosine triphosphate and intracellular pH (0.038 +/- 0.013 pH unit/min compared with 0.064 +/- 0.011 in the isoflurane-treated group and 0.058 +/- 0.008 in the sevoflurane-treated group) until 24 min of reperfusion (P < 0.05). We conclude that sevoflurane has effects similar to isoflurane on brain energy metabolism during and after cerebral ischemia. IMPLICATIONS: It is important to know whether anesthetics adversely effect brain metabolism during ischemia and reperfusion. A new anesthetic, sevoflurane, affected the brain in a manner similar to isoflurane, which has been used for many years as an anesthetic.

Adenosine Triphosphate↗