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PubMed2005

Monitoring oxygenator expiratory isoflurane concentrations and the bispectral index to guide isoflurane requirements during cardiopulmonary bypass.

OBJECTIVE: The purpose of this study was to measure the changes in isoflurane requirements during the rewarming phase of cardiopulmonary bypass with moderate hypothermia. DESIGN: An observational study. SETTING: University hospital, single center. PARTICIPANTS: Forty patients undergoing elective coronary artery bypass surgery with cardiopulmonary bypass. INTERVENTIONS: Isoflurane requirements were quantified by measuring the concentrations in the oxygenator expiratory gas. Anesthesia was guided by bispectral index monitoring. MEASUREMENTS AND MAIN RESULTS: Isoflurane concentrations required to maintain the bispectral index between 40 and 50 during the rewarming phase of cardiopulmonary bypass were measured. There was a progressive increase in expiratory isoflurane requirements during rewarming from 30 degrees C to 37 degrees C, with a Pearson correlation coefficient of 0.78. There was a significant difference in the concentration required at 30 degrees C (0.41% +/- 0.14%) compared with 37 degrees C (1.00% +/- 0.12%). CONCLUSION: Isoflurane requirements are reduced during hypothermic cardiopulmonary bypass. Monitoring anesthetic concentrations in the oxygenator expiratory gas may be a useful adjunct to monitoring the depth of anesthesia.

Anesthesia, Inhalation↗
PubMed1988

Anaesthetic induction with isoflurane or halothane. Oxygen saturation during induction with isoflurane or halothane in unpremedicated children.

The authors performed a randomised, prospective trial in which one junior anaesthetist administered gaseous induction of anaesthesia to 50 unpremedicated children with either isoflurane or halothane in nitrous oxide and oxygen. Arterial oxygen saturation and the electrocardiogram were monitored and the incidence of complications noted. Desaturation below 85% occurred in six children, but only with isoflurane. The incidences of complications and desaturation events did not alter throughout the 25 isoflurane inductions. Coughing, movement, laryngospasm and sinus tachycardia occurred more frequently with isoflurane. Isoflurane inductions took longer (7.9 as compared with 5.4 minutes, p less than 0.001) and had 4.25 times the number of complications.

Anesthesia, Inhalation↗
PubMedDate not supplied

Anesthetic effects of ketamine or isoflurane induction prior to isoflurane anesthesia in medetomidine-premedicated dogs.

Dogs were given medetomidine (10 microg/kg body weight, intramuscularly) followed in 10 minutes by either ketamine (4 mg/kg body weight, intravenously) or isoflurane mask induction and maintained on isoflurane for 30 minutes. Medetomidine induced lateral recumbency in all dogs. Endotracheal intubation was faster and smoother when dogs were given ketamine than when induced with isoflurane. Analgesia was excellent in all groups. Respiratory depression was more profound when dogs were given ketamine. Recovery quality was smooth and similar among all groups. Medetomidine-premedicated dogs could be induced with either ketamine or isoflurane and maintained on 1.3% isoflurane to achieve good analgesia with smooth recovery from anesthesia.

Anesthesia, Inhalation↗
PubMed2002

Effects of electroacupuncture on minimum alveolar concentration of isoflurane and cardiovascular system in isoflurane anesthetized dogs.

The effects of electroacupuncture (EA) on the minimum alveolar concentration (MAC) and on the cardiovascular system were evaluated with dogs under isoflurane anesthesia. Eight healthy male beagles were randomly assigned to six study groups (five heads/group) with washout intervals of 7 ~ 31 days between experiments for recovery and anesthetic clearance. MAC of isoflurane and cardiovascular parameters were determined after EA at nonacupoint and and at acupoints LI-4, SP-6, ST-36 and TH-8. Electroacupuncture for 30 minutes at LI-4, SP-6, ST-36 and TH-8 acupoints lowered the MAC of isoflurane by 17.5 +/- 3.1%, 21.3 +/- 8.0%, 20.5 +/- 8.2% and 15.6 3.1%, respectively (p < 0.05). However, electrical stimulation of nonacupoint did not induce a significant change in MAC of isoflurane. In the cardiovascular system, the ST-36 group did not induce any significant change in cardiovascular parameters. In the TH-8 group, the mean and diastolic arterial pressure and the systemic vascular resistance were decreased. In the LI-4 group, cardiac output and cardiac index decreased after EA. These results indicate that EA at LI-4, SP-6 and ST-36 have advantages in isoflurane anesthesia in terms of reducing the dose of anesthetics and minimizing cardiovascular side effects.

Anesthesia, Inhalation↗
PubMedDate not supplied

Biological monitoring of occupational exposure to isoflurane by measurement of isoflurane exhaled breath.

The relationship between isoflurane environmental concentrations in operating rooms and the corresponding isoflurane concentration in the exhaled air of the operating personnel at the end of the exposure has been investigated. Isoflurane was retained in an adsorbent cartridge and after thermal desorption the concentration was estimated by gas chromatography. Significant correlation between environmental and exhaled air isoflurane concentrations allowed the establishment of a biological exposure index and biological exposure limits corresponding to proposed atmospheric threshold values.

Air↗
PubMedDate not supplied

Determination of the ED50 of isoflurane and evaluation of the isoflurane-sparing effect of butorphanol in cockatoos (Cacatua spp.).

The use of butorphanol as an analgesic in a psittacine species was evaluated by determining its isoflurane-sparing effects. The Effective Dose 50 (ED50) of isoflurane was determined using a bracketing technique based on the purposeful movement elicited by pressure applied to a digit with a hemostat. The ED50 of isoflurane for 11 cockatoos (four greater sulfur crested, three lesser sulfur crested, and four citron crested) was determined to be 1.44 +/- 0.07%. After the administration of 1 mg/kg of butorphanol tartrate intramuscularly (IM), the ED50 was significantly (P < .05) decreased to 1.08 +/- 0.05%. Physiological variables that changed significantly included decreases in heart rate, tidal volume (Vt), inspiratory (Ti) and expiratory times (Te), and an increase in respiratory rate. No complications resulted because of these changes. Based on the results, butorphanol produces an isoflurane-sparing effect in cockatoos and has the potential to be a useful analgesic in psittacines.

Administration, Inhalation↗
PubMed1987

Isoflurane for anaesthesia in the dental chair. a comparison of the incidence of cardiac dysrhythmias during anaesthesia with halothane and isoflurane.

A randomised single-blind trial was performed to compare the effects on cardiac rhythm of isoflurane and halothane in 100 dental outpatients having extractions under general anaesthesia in the dental chair without tracheal intubation. The incidence of supraventricular dysrhythmias did not differ significantly. No patient in the isoflurane group developed a ventricular dysrhythmia, whilst nine of those who received halothane did so (p = 0.0013). The quality of anaesthesia was acceptable in the isoflurane group, but induction time was longer (p less than 0.05) and the maximum heart rate was faster (p less than 0.01). There was no difference in the maximum end tidal carbon dioxide concentrations measured in a further 20 cases.

Adolescent↗
PubMed2004

Impaired acquisition of spatial memory 2 weeks after isoflurane and isoflurane-nitrous oxide anesthesia in aged rats.

Aged rats are impaired on a spatial memory task for at least 24-48 h after isoflurane-nitrous oxide anesthesia. In this study, we tested how long the impairment lasts and investigated the role of nitrous oxide. Eighteen-month-old rats were randomized to anesthesia for 2 h with 1.2% isoflurane with or without 70% nitrous oxide or a control group (30% oxygen). Two weeks later, rats were tested daily for 14 days on a 12-arm radial maze. The number of correct choices to first error, total errors, and time to complete the maze were recorded. Rats anesthetized with 1.2% isoflurane with 70% nitrous oxide made fewer correct choices before first error (P < or = 0.05). Trends toward similar results were noted for error rate and time to complete the maze, but these did not achieve statistical significance. Post hoc analysis comparing all anesthetized rats to controls demonstrated that anesthetized rats made fewer correct choices to first error (P < or = 0.05) and took longer to complete the maze (P <or = 0.05). There were no differences in total number of errors (P < or = 0.06). Thus, spatial memory is impaired for 2 wk after general anesthesia in aged rats independent of whether nitrous oxide is used.

Aging↗
PubMed2006

Isoflurane tolerance against focal cerebral ischemia is attenuated by adenosine A1 receptor antagonists.

PURPOSE: To investigate the role of the adenosine A1 receptor in the rapid tolerance to cerebral ischemia induced by isoflurane preconditioning. METHODS: Seventy-five rats were randomly assigned into five groups (n = 15 each): Control, 8-cyclopentyl-1,3-dipropulxanthine (DPCPX), Isoflurane, DPCPX+Isoflurane and Vehicle+Isoflurane groups. All animals underwent right middle cerebral artery occlusion (MCAO) for two hours. Isoflurane preconditioning was conducted one hour before MCAO in Isoflurane, DPCPX+Isoflurane and Vehicle+Isoflurane groups by exposing the animals to 1.5% isoflurane in 98% oxygen for one hour. In the Control and DPCPX groups, animals were exposed to 98% oxygen one hour before MCAO for one hour. A selective adenosine A1 receptor antagonist, DPCPX, was administered (0.1 mg x kg(-1)) 15 min before isoflurane/oxygen exposure in the DPCPX and DPCPX+Isoflurane groups to evaluate the effect of adenosine A1 receptor antagonist on isoflurane preconditioning. Dimethyl sulfoxide, the solvent of DPCPX, was administered (1 mL x kg(-1)) 15 min before isoflurane exposure in the Vehicle+Isoflurane group. Neurological deficit scores and brain infarct volumes were evaluated 24 hr after reperfusion. RESULTS: Animals in the Isoflurane and Vehicle+Isoflurane groups developed lower neurological deficit scores and smaller brain infarct volumes than the Control group (P < 0.01). Animals in the DPCPX+Isoflurane group developed higher neurological deficit scores and larger brain infarct volumes than the Isoflurane and Vehicle+Isoflurane groups (P < 0.01). CONCLUSION: The present study demonstrates that preconditioning with isoflurane reduces focal cerebral ischemic injury in rats, and the adenosine A1 receptor antagonist (DPCPX) attenuates the neuroprotection induced by isoflurane preconditioning.

Adenosine A1 Receptor Antagonists↗
PubMed1995

Coronary vasodilation by isoflurane. Abrupt versus gradual administration.

BACKGROUND: Under certain circumstances, isoflurane is associated with coronary artery vasodilation. The objective of the current study was to ascertain whether the rate of administration of isoflurane influences its vasodilating effect in the coronary circulation. METHODS: Seven open-chest dogs anesthetized with fentanyl and midazolam were studied. The left anterior descending coronary artery was perfused via either of two pressurized (80 mmHg) reservoirs; reservoir 1 (control) was supplied with arterial blood free of isoflurane, and reservoir 2 was supplied with blood from an extracorporeal oxygenator, which was provided with 95% O2/5% CO2 gas that passed through calibrated vaporizer. Coronary blood flow (CBF) was measured with Doppler flow transducer. In each dog, isoflurane was administered according to two protocols; abrupt (isoflurane-A) or gradual (isoflurane-G). In isoflurane-A, the left anterior descending coronary artery was switched from reservoir 1 to reservoir 2 after the latter was filled with blood previously equilibrated with 1.4% (1 MAC) isoflurane. In isoflurane-G, the left anterior descending coronary artery was switched to reservoir 2 with vaporizer set at 0% isoflurane; then the vaporizer was adjusted to 1.4% isoflurane, which produced a gradual increase in isoflurane concentration within reservoir 2 that reached a level equivalent to that in isoflurane-A (as evaluated by gas chromatography) by 30 min. CBF during maximally dilating, intracoronary infusion of adenosine served as a reference to assess effects of isoflurane. RESULTS: Isoflurane-A caused marked increases in CBF, which, at constant perfusion pressure, reflected pronounced reductions in vascular resistance. These increases in CBF were 80% of those with adenosine. Although isoflurane-G also caused increases in CBF, the increases were only 45% of those caused by isoflurane-A. CONCLUSIONS: The current findings demonstrate that the extent of coronary vasodilation by isoflurane was not dependent only on its blood concentration but also on the rate at which this blood concentration was achieved; a gradual increase in blood concentration blunted the vasodilator effect. Differences in the rate of administration of isoflurane likely contributed to its widely variable coronary vasodilating effects in previous studies.

Adenosine↗
PubMed2006

Isoflurane exerts neuroprotective actions at or near the time of severe traumatic brain injury.

Isoflurane improves outcome vs. fentanyl anesthesia, in experimental traumatic brain injury (TBI). We assessed the temporal profile of isoflurane neuroprotection and tested whether isoflurane confers benefit at the time of TBI. Adult, male rats were randomized to isoflurane (1%) or fentanyl (10 mcg/kg iv bolus then 50 mcg/kg/h) for 30 min pre-TBI. Anesthesia was discontinued, rats recovered to tail pinch, and TBI was delivered by controlled cortical impact. Immediately post-TBI, rats were randomized to 1 h of isoflurane, fentanyl, or no additional anesthesia, creating 6 anesthetic groups (isoflurane:isoflurane, isoflurane:fentanyl, isoflurane:none, fentanyl:isoflurane, fentanyl:fentanyl, fentanyl:none). Beam balance, beam walking, and Morris water maze (MWM) performances were assessed over post-trauma d1-20. Contusion volume and hippocampal survival were assessed on d21. Rats receiving isoflurane pre- and post-TBI exhibited better beam walking and MWM performances than rats treated with fentanyl pre- and any treatment post-TBI. All rats pretreated with isoflurane had better CA3 neuronal survival than rats receiving fentanyl pre- and post-TBI. In rats pretreated with fentanyl, post-traumatic isoflurane failed to affect function but improved CA3 neuronal survival vs. rats given fentanyl pre- and post-TBI. Post-traumatic isoflurane did not alter histopathological outcomes in rats pretreated with isoflurane. Rats receiving fentanyl pre- and post-TBI had the worst CA1 neuronal survival of all groups. Our data support isoflurane neuroprotection, even when used at the lowest feasible level before TBI (i.e., when discontinued with recovery to tail pinch immediately before injury). Investigators using isoflurane must consider its beneficial effects in the design and interpretation of experimental TBI research.

Anesthetics, Intravenous↗
PubMed2000

Isoflurane delays but does not prevent cerebral infarction in rats subjected to focal ischemia.

BACKGROUND: Several investigations have shown that volatile anesthetics can reduce ischemic cerebral injury. In these studies, however, neurologic injury was evaluated only after a short recovery period. Recent data suggest that injury caused by ischemia is a dynamic process characterized by continual neuronal loss for a prolonged period. Whether isoflurane-mediated neuroprotection is sustained after a longer recovery period is not known. The current study was conducted to compare the effect of isoflurane on brain injury after short (2-day) and long (14-day) recovery periods in rats subjected to focal ischemia. METHODS: Fasted Wistar-Kyoto rats were anesthetized with isoflurane and randomly allocated to an awake (n = 36) or an isoflurane (n = 34) group. Animals in both groups were subjected to focal ischemia by filament occlusion of the middle cerebral artery. Pericranial temperature was servocontrolled at 37 degrees C throughout the experiment. In the awake group, isoflurane was discontinued and the animals were allowed to awaken. In the isoflurane group, isoflurane anesthesia was maintained at 1.5 times the minimum alveolar concentration. After 70 min of focal ischemia, the filament was removed. Animals were killed 2 days (awake, n = 18; isoflurane, n = 17) and 14 days (awake, n = 18; isoflurane, n = 17) after ischemia. The volumes of cerebral infarction and selective neuronal necrosis in the animals were determined by image analysis of hematoxylin and eosin-stained coronal brain sections. RESULTS: Cortical and subcortical volumes of infarction were significantly less in the isoflurane 2-day group (26 +/- 23 mm3 and 17 +/- 6 mm3, respectively) than in the awake 2-day group (58 +/- 35 mm3, P < 0. 01; and 28 +/- 12 mm3, P < 0.01, respectively). By contrast, cortical and subcortical volumes of infarction in the awake (41 +/- 31 mm3 and 28 +/- 16 mm3, respectively) and isoflurane (41 +/- 35 mm3 and 19 +/- 8 mm3, respectively) 14-day groups were not different (cortex, P = 0.99; subcortex, P = 0.08). The volume of cortical tissue in which selective neuronal necrosis was observed, however, was significantly less in the isoflurane 14-day group (5 +/- 4 mm3) than in the awake 14-day group (17 +/- 9 mm3, P < 0.01). The total number of necrotic neurons in the region of selective neuronal necrosis was significantly smaller in the isoflurane 14-day group than in the awake 14-day group (P < 0.01). CONCLUSION: Compared with the awake state, isoflurane reduced the extent of infarction assessed 2 days after focal ischemia in rats. At 14 days, however, only selective neuronal necrosis, but not infarction, was reduced by isoflurane. These results suggest that isoflurane delays but does not prevent cerebral infarction caused by focal ischemia. Isoflurane may attenuate the delayed development of selective neuronal necrosis in periinfarct areas in this animal model.

Anesthetics, Inhalation↗
PubMed2004

Effect of isoflurane on neuronal apoptosis in rats subjected to focal cerebral ischemia.

UNLABELLED: Although isoflurane can reduce ischemic neuronal injury after short postischemic recovery intervals, this neuroprotective efficacy is not sustained. Neuronal apoptosis can contribute to the gradual increase in infarct size after ischemia. This suggests that isoflurane, although capable of reducing early neuronal death, may not inhibit ischemia-induced apoptosis. We investigated the effects of isoflurane on markers of apoptosis in rats subjected to focal ischemia. Fasted Wistar-Kyoto rats were anesthetized with isoflurane and randomly allocated to awake (n = 40) or isoflurane (n = 40) groups. Animals in both groups were subjected to focal ischemia by filament occlusion of the middle cerebral artery for 70 min. Pericranial temperature was servo-controlled at 37 degrees C +/- 0.2 degrees C throughout the experiment. In the awake group, isoflurane was discontinued and the animals were allowed to awaken. In the isoflurane group, isoflurane anesthesia was maintained at 1.5 MAC (minimum alveolar anesthetic concentration). Animals were killed 7 h, 1 day, 4 days, or 7 days after reperfusion (n = 10/group/time point). The area of cerebral infarction was measured by image analysis in a hematoxylin and eosin stained section. In three adjacent sections, apoptotic neurons were identified by TUNEL staining and immunostaining for active caspase-9 and caspase-3. Infarct size was smaller in the isoflurane group than the awake group 7 h, 1 day, and 4 days after reperfusion (P < 0.05). However, this difference was absent 7 days after reperfusion. The number of apoptotic (TUNEL, caspase-3, and caspase-9 positive) cells 1 day after ischemia was significantly more in the awake versus isoflurane group. After a recovery period of 4 or 7 days, the number of apoptotic cells in the isoflurane group was more than in the awake group. After 7 days, the number of caspase-3 and -9 positive neurons was more in the isoflurane group (P < 0.05). The data indicate that isoflurane delays but does not prevent the development of cerebral infarction caused by ischemia. Isoflurane reduced the development of apoptosis early after ischemia but did not prevent it at later stages of postischemic recovery. IMPLICATIONS: The effect of isoflurane on neuronal apoptosis was investigated in rats subjected to focal cerebral ischemia. In isoflurane-anesthetized animals, ischemia-induced apoptosis occurred during the later stages of postischemic recovery. Isoflurane did not inhibit postischemic neuronal apoptosis.

Anesthetics, Inhalation↗
PubMed2006

[Effects of isoflurane on lung surfactant protein A in rats].

OBJECTIVE: To examine the effects of different concentrations of Isoflurane on the level of surfactant protein A(SP-A) and the expression of SP-A mRNA in the lung of rats. METHODS: Thirty-two male Wistar rats were randomly divided into 4 groups: control group received 40% (volume fraction) O2 inhalation (40% O2, n=8); 0.7% isoflurane group (n=8), 1.5% isoflurane group (n=8), and 2.0% isoflurane group (n=8). They were treated with 40% O2 with 0.7%, 1.5% and 2.0% isoflurane respectively. In each group, the rats inhaled experimental gas for 8 hours, and then were put to death immediately. Morphological changes of type II pneumocytes were observed by transmission electron microscopy. Surfactant protein content in broncho-alveolar lavage fluid (BALF) was measured with Western Blotting. The level of intracellular SP-A was examined with immunohistochemistry (IHC). To assess the relative levels of SP-A mRNA in lung tissue, reverse transcriptase-polymerase chain reaction (RT-PCR) was used with the co-amplification of the "housekeeping" gene GAPDH as internal control. RESULTS: Morphological changes of type II pneumocytes were distinct in 1.5% isoflurane and 2.0% isoflurane groups. Isoflurane, after three doses, significantly reduced the SP-A content in BALF. Control group, 437,112+/-25,654; 0.7% isoflurane group, 355,789+/-28,116; 1.5% isoflurane group, 238,554+/-31,531; 2.0% isoflurane group, 223,632+/-25,710 (P<0.01); Intracellular SP-A content of 1.5% and 2.0% isoflurane groups was less than that of the control, whereas 0.7% isoflurane groups did not show any significant difference from the control. RT-PCR indicated a reduced expression of SP-A mRNA in the lung after 1.5% and 2.0% isoflurane exposure. Control group, 1.47+/-0.18; 1.5% isoflurane group, 1.19+/-0.13; 2.0% isoflurane group, 1.13+/-0.12 (P<0.01). CONCLUSION: These findings indicate that 1.5% or more than 1.5% isoflurane exposure for eight hours could decrease the expression of the SP-A mRNA and synthesis of SP-A in rats, and maybe it could also affect the secretion and reuse.

Anesthetics, Inhalation↗
PubMed1997

Isoflurane mimics ischemic preconditioning via activation of K(ATP) channels: reduction of myocardial infarct size with an acute memory phase.

BACKGROUND: The authors tested the hypothesis that isoflurane directly preconditions myocardium against infarction via activation of K(ATP) channels and that the protection afforded by isoflurane is associated with an acute memory phase similar to that of ischemic preconditioning. METHODS: Barbiturate-anesthetized dogs (n = 71) were instrumented for measurement of systemic hemodynamics. Myocardial infarct size was assessed by triphenyltetrazolium chloride staining. All dogs were subjected to a single prolonged (60 min) left anterior descending coronary artery (LAD) occlusion followed by 3 h of reperfusion. Ischemic preconditioning was produced by four 5-min LAD occlusions interspersed with 5-min periods of reperfusion before the prolonged LAD occlusion and reperfusion. The actions of isoflurane to decrease infarct size were examined in dogs receiving 1 minimum alveolar concentration (MAC) isoflurane that was discontinued 5 min before prolonged LAD occlusion. The interaction between isoflurane and ischemic preconditioning on infarct size was evaluated in dogs receiving isoflurane before and during preconditioning LAD occlusions and reperfusions. To test whether the cardioprotection produced by isoflurane can mimic the acute memory of ischemic preconditioning, isoflurane was discontinued 30 min before prolonged LAD occlusion and reperfusion. The mechanism of isoflurane-induced cardioprotection was evaluated in two final groups of dogs pretreated with glyburide in the presence or absence of isoflurane. RESULTS: Myocardial infarct size was 25.3 +/- 2.9% of the area at risk during control conditions. Isoflurane and ischemic preconditioning produced significant (P < 0.05) and equivalent reductions in infarct size (ischemic preconditioning alone, 9.6 +/- 2.0; isoflurane alone, 11.8 +/- 2.7; isoflurane and ischemic preconditioning, 5.1 +/- 1.9%). Isoflurane-induced reduction of infarct size also persisted 30 min after discontinuation of the anesthetic (13.9 +/- 1.5%), independent of hemodynamic effects during LAD occlusion. Glyburide alone had no effect on infarct size (28.3 +/- 3.9%), but it abolished the protective effects of isoflurane (27.1 +/- 4.6%). CONCLUSIONS: Isoflurane directly preconditions myocardium against infarction via activation of K(ATP) channels in the absence of hemodynamic effects and exhibits acute memory of preconditioning in vivo.

Anesthetics, Inhalation↗