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Comparison of maintenance and recovery characteristics of sevoflurane-nitrous oxide and enflurane-nitrous oxide anaesthesia.

We compared maintenance of anaesthesia and recovery using either sevoflurane or enflurane anaesthesia in ASA I-III patients undergoing surgery with an anticipated minimum duration of 3 h. Serum fluoride concentrations were also measured to assess the potential for renal toxicity. After induction of anaesthesia with thiopentone, patients received, for maintenance, either 1.5% end-tidal sevoflurane (0.73 MAC) with N2O 58% (0.58 MAC) (n = 40) or 1.2% end-tidal enflurane (0.7 MAC) with N2O 57% (0.57 MAC) (n = 40). Other drugs administered during anaesthesia were similar in all groups. Haemodynamic measurements, recovery times, as well as post-operative nausea and vomiting were comparable in both groups. The mean peak plasma inorganic fluoride ion concentrations were reached 4 h after operation in both groups (27.7 microM L-1 for sevoflurane and 16.75 microM L-1 for enflurane, P < 0.05) declining 50% within 24 h in both groups. A positive correlation (P < 0.05) was found between anaesthetic exposure (MAC h) and fluoride concentrations in the two groups. Sevoflurane anaesthesia resulted in similar haemodynamic stability, recovery times and post-operative side effects as enflurane anaesthesia, but produced significantly greater serum fluoride levels.

Analgesics, Opioid↗

A comparison of the maintenance and recovery charcateristic of sevoflurane-nitrous oxide against isoflurane-nitrous oxide anaesthesia.

BACKGROUND: To compare the maintenance and recovery characteristics of sevoflurane and isoflurane anaesthesia in Malaysian patients. METHOD: This is a prospective, open labelled, randomized, controlled study. Sixty unpremedicated ASA I or II patients (aged 18-50 years), scheduled for elective breast lump excision were randomly allocated to receive either isoflurane or sevoflurane for the maintenance of anaesthesia following fentanyl and propofol intravenous induction. The systolic, diastolic, mean arterial blood pressure and heart rate were measured. The speed of recovery was measured by time to eye opening, time to following simple command, and time to correctly giving own names and address. The incidence of postoperative complication was also recorded. RESULTS: The trend of systolic blood pressure was significantly higher in the isoflurane group as compared to the sevoflurane group for the duration of anaesthesia (p < 0.001, by ANOVA for repeated measurement) but the trend of heart rate was similar for both groups. The recovery time was faster in the isoflurane group. [mean time of eye opening (SD) = 6.8 (2.2) vs 10.7 (4.4) min, p < 0.001; mean time of sticking tongue out (SD) = 7.9 (2.9) vs 11.5 (4.7) min, p < 0.01; mean time of giving own name (SD) = 7.8 (2.7) vs 11.8 (4.8) min, p < 0.001, mean time of giving own address (SD) = 8.4 (2.9) vs 12.0 (4.7) min, p < 0.01]. No major adverse effects were encountered postoperatively and the incidences of minor adverse effects were low in both groups. CONCLUSION: We concluded that sevoflurane is a safe alternative to isoflurane but in these short procedures, awakening time was surprisingly slower than after isoflurane.

Adolescent↗

Ischemic depolarization during halothane-nitrous oxide and isoflurane-nitrous oxide anesthesia. An examination of cerebral blood flow threshold and times to depolarization.

BACKGROUND: Isoflurane-N2O anesthesia (as compared with halothane-N2O) reduces the cerebral blood flow (CBF) at which electroencephalographic changes occur in humans subjected to carotid occlusion. In contrast, no differences were seen in rats when cortical depolarization (instead of the electroencephalogram) was used as the ischemic marker during equi-MAC isoflurane-N2O and halothane-N2O anesthesia. To extend these findings, we used laser-Doppler flowmetry to continuously examine CBF (CBFLDF) and attempted to better define the relation between CBF and the time to depolarization (as a measure of the rate of energy depletion after ischemia). METHODS: Cortical CBFLDF was measured in normothermic, normocarbic rats, and the cortical direct-current potential was recorded using glass microelectrodes. Animals were anesthetized with 0.75 MAC halothane or 0.75 MAC isoflurane, both in 60% N2O. After baseline recordings, both carotid arteries were occluded. Five minutes later mean arterial pressure was rapidly reduced to and held at target values of 50, 45, 40, 30 or 0 mmHg. This mean arterial pressure was maintained (and CBFLDF was continually monitored) until depolarization occurred, or for a maximum of 20 min. RESULTS: CBFLDF values before and after carotid occlusion (but before hypotension) were similar in the two groups. As intended, CBFLDF decreased as postocclusion mean arterial pressure was reduced and the incidence of cortical depolarization increased. The delay until depolarization, defined as the interval between the moment CBFLDF reached 25% of the preocclusion baseline until depolarization occurred, decreased as CBFLDF was reduced. However, there were no intergroup differences except after a circulatory arrest (CBF = 0), where cortical depolarization was seen approximately 30 s later in isoflurane-N2O-anesthetized rats. CONCLUSIONS: The CBF threshold for cortical depolarization as measured by laser-Doppler flowmetry did not differ significantly between halothane-N2O- and isoflurane-N2O-anesthetized rats. There were also no important differences in the times until depolarization, other than a small difference when flow = 0. If the time to depolarization is reflects the potential ischemic injury, the it is unlikely that isoflurane-N2O conveys any protective advantage relative to halothane-N2O.

Anesthesia, Inhalation↗

Correlation of inbred mouse sensitivity to nitrous oxide antinociception with brain nitric oxide synthase activity following exposure to nitrous oxide.

Inhibition of nitric oxide synthase (NOS) antagonizes nitrous oxide (N2O)-induced antinociception in mice. This study was conducted to compare brain NOS activity in high responding C57BL/6 mice, low responding DBA/2 mice and S5 mice selectively bred for low responsiveness to N2O. Exposure to 70% N2O suppressed acetic acid-induced abdominal constrictions in C57BL/6 mice but not DBA/2 or S5 mice. N2O exposure also elevated NOS activity in brains of C57BL/6 mice but not DBA/2 or S5 mice. The absence of these effects in DBA/2 or S5 mice is further support for the hypothesis that nitric oxide (NO) may play a critical role in N2O-induced antinociception in mice.

Analgesics, Non-Narcotic↗

Nitrous oxide anaesthesia and vomiting. The effect of nitrous oxide anaesthesia on the incidence of vomiting following gynaecological laparoscopy.

Eighty-seven patients undergoing routine laparoscopy were divided randomly into two groups to study the effect of nitrous oxide anaesthesia on the incidence of postoperative vomiting. Patients in group A received nitrous oxide as part of their anaesthetic, while in group B nitrous oxide was omitted. Significantly fewer patients in group B vomited when compared with group A (17 percent and 49 percent respectively; p less than 0.005). We suggest that an anaesthetic technique which avoids nitrous oxide may be especially indicated in patients undergoing laparoscopy.

Adult↗

Propofol-nitrous oxide versus thiopentone-isoflurane-nitrous oxide anaesthesia for uvulopalatopharyngoplasty in patients with sleep apnea.

A randomized prospective study was performed to compare the recovery in 41 patients undergoing uvulopalatopharyngoplasty (UPPP) with either propofol-nitrous oxide-fentanyl or thiopentone-isoflurane-nitrous oxide-fentanyl anaesthesia. The patients were referred to UPPP after examination including polysomnography and otorhinolaryngological examination. The propofol group received propofol 2 mg.kg-1 for induction followed by an infusion of 10 mg.kg-1.h-1 after intubation. The thiopentone-isoflurane group received 5 mg.kg-1 of thiopentone for induction followed by isoflurane (0.5-2%) after intubation. Other medication was similar in both groups. In the propofol group the patients had a significantly better oxygen saturation during the first postoperative hour (P < 0.05), and a higher rate of breathing (P < 0.05), indicating a more rapid recovery of the physiologic control of breathing. Pain as measured by visual analogue score was lower (P < 0.05) during the second postoperative hour compared with the isoflurane group. Apneic episodes occurred with similar frequency in both groups, and they were related to the severity of obstructive sleep apnea (OSA). We conclude that propofol is preferable to thiopentone-isoflurane in UPPP operations, because physiologic respiratory control recovers faster and postoperative pain is less intense.

Adult↗

Hydroxylamine oxidation and subsequent nitrous oxide production by the heterotrophic ammonia oxidizer Alcaligenes faecalis.

Nitrous oxide (N2O), a greenhouse gas, is emitted during autotrophic and heterotrophic ammonia oxidation. This emission may result from either coupling to aerobic denitrification, or it may be formed in the oxidation of hydroxylamine (NH2OH) to nitrite (NO2(-). Therefore, the N2O production during NH2OH oxidation was studied with Alcaligenes faecalis strain TUD. Continuous cultures of A. faecalis showed increased N2O production when supplemented with increasing NH2OH concentrations. 15N-labeling experiments showed that this N2O production was not due to aerobic denitrification of NO2(-). Addition of 15N-labeled NH2OH indicated that N2O was a direct by-product of NH2OH oxidation, which was subsequently reduced to N2. These observations are sustained by the fact that NO2(-) production was low (0.23 mM maximum) and did not increase significantly with increasing NH2OH concentration in the feed. The NH2OH-oxidizing capacity increased with increasing NH2OH concentrations. The apparent Vmax and K(m) were 31 nmol min-1 mg dry weight-1 and 1.5 mM respectively. The culture did not increase its growth yield and was not able to use NH2OH as the sole N source. A non-haem hydroxylamine oxidoreductase was partially purified from A. faecalis strain TUD. The enzyme could only use K3Fe(CN)6 as an electron acceptor and reacted with antibodies raised against the hydroxylamine oxidoreductase of Thiosphaera pantotropha.

Alcaligenes↗

The scavenger device for nitrous oxide administration.

Nitrous oxide levels of 300 to 500 ppm occur when nitrous oxide is administered in the emergency department using the Nitronox machine without use of the scavenger device, which traps expired nitrous oxide gases and vents them to the outside environment. A scavenger device that can limit nitrous oxide gas to zero ppm in the emergency department setting has been developed. We think that development of the scavenger device is a significant advance for the safe administration of nitrous oxide in the emergency department.

Air Pollutants, Occupational↗

Nitrous oxide does not alter bispectral index: study with nitrous oxide as sole agent and as an adjunct to i.v. anaesthesia.

We have studied the effect of nitrous oxide on bispectral index (BIS), calculated from a bipolar encephalogram. Inhalation of 70% nitrous oxide resulted in loss of consciousness in all healthy volunteers (n = 10) but no change in BIS. Brief inhalation up to 1.2% sevoflurane also resulted in loss of consciousness in volunteers (n = 5), but with sevoflurane, BIS decreased. BIS and the haemodynamic effects of adding nitrous oxide were also measured during coronary artery bypass surgery in patients (n = 10) receiving midazolam and fentanyl infusions. Measurements were made after 0%, 33%, 66% and 0% nitrous oxide, just before skin incision and after sternotomy. Nitrous oxide caused no change in BIS. BIS may indicate a sufficient hypnotic depth to prevent awareness during surgery, but our study demonstrated that pharmacological unconsciousness-hypnosis can also be reached by mechanisms to which BIS is not sensitive. Thus BIS is a sufficient but not a necessary criterion for adequate depth of anaesthesia or prevention of awareness.

Adult↗

Nitrous-oxide analgesia during ambulance transportation. Airborne levels of nitrous oxide.

A model experiment was performed for studying nitrous-oxide levels in the breathing zones of the different members of an ambulance team, viz. the anesthetist, the accompanying person in the ambulance coupé, and the ambulance driver. Without a functioning local exhaust coupled to the exhalation valve, the integrated average level of nitrous oxide in the breathing zone of the anesthetist was 650-1,700 ppm, with top concentrations up to 7,500 ppm. Under the same conditions, the accompanying person in the ambulance coupé was exposed to average concentrations of 58-280 ppm, with top concentrations up to 660 ppm. The mean exposure of the driver was 9-45 ppm (max. 81 ppm). However, the exposure to nitrous oxide was considerably decreased in all parts of the ambulance by an effective local exhaust system. A prerequisite for nitrous-oxide analgesia in ambulances is an effective local exhaust coupled to the exhalation valve or face mask. The ambulance coupé ought to be equipped with a motor-driven exhaust fan in the roof, the ordinary inlet fan of the ambulance should be switched on at maximum speed, and any additional heater or fan in the ambulance coupé should be placed inside the coupé and not behind the driver's seat.

Air Pollutants↗

Purification and characterization of a nitrous oxide reductase from Thiosphaera pantotropha. Implications for the mechanism of aerobic nitrous oxide reduction.

The aerobic denitrifer Thiosphaera pantotropha is able to reduce simultaneously nitrous oxide and oxygen even after anaerobic growth [Bell, L. C. & Ferguson, S. J. (1991) Biochem J. 273, 423-427]. A nitrous oxide reductase was purified from anaerobically grown T. pantotropha cells. It is argued, on the basis of inhibitor sensitivities and from immunological evidence, that the same nitrous oxide reductase is involved in nitrous oxide reduction in aerobically grown cells. The purified nitrous oxide reductase was shown to have molecular properties very similar to nitrous oxide reductases previously isolated from anaerobically denitrifying bacteria. The visible absorption spectra of the T. pantotropha enzyme resemble those of the oxygen-affected form of nitrous oxide reductases from other organisms. It is thus concluded that the T. pantotropha nitrous oxide reductase is not peculiarly resistant to the structural changes caused by oxygen. The activity of the purified T. pantotropha nitrous oxide reductase was reconstituted in vitro using horse heart cytochrome c, T. pantotropha cytochrome c551 and T. pantotropha pseudoazurin as electron donors. It is suggested on this basis that either of the T. pantotropha electron-carrier proteins are possible physiological electron donors to T. pantotropha nitrous oxide reductase. Oxygen was shown not to inhibit the in-vitro reduction of nitrous oxide with horse heart ferrocytochrome c as electron donor to the reductase.

Aerobiosis↗

Accidental death by nitrous oxide inhalation.

Nitrous oxide is a popular inhalation anesthetic-analgesic agent. Its euphoric action and its availability have led to its abuse. We report a case of fatal accidental asphyxia due to nitrous oxide abuse. The deceased was a hospital worker who had access to the hospital supply of nitrous oxide. His death was due to hypoxemia and asphyxiation, secondary to nitrous oxide inhalation.

Adult↗

Nitrogen oxides and hydroxyguanidines: formation of donors of nitric and nitrous oxides and possible relevance to nitrous oxide formation by nitric oxide synthase.

The involvement of nitric oxide in numerous biological functions has led to the intense study of nitric oxide (NO) generation by the nitric oxide synthases (NOS) responsible. In addition to NO, nitric oxide synthases produce N(G)-hydroxy-L-arginine, superoxide anion and, indirectly, NOx species such as peroxynitrite and, possibly, nitrous oxide (N2O). Consequently, the interactions of N(G)-hydroxy-L-arginine with NO and other oxides of nitrogen (NOx) are of considerable interest. N(G)-Hydroxy-L-arginine and other monosubstituted hydroxyguanidines react with aqueous aerobic NO, peroxynitrite, and various NOx and nitrosating agents to form compounds that subsequently release NO and N2O. Spectrometric data indicate that the nitrosation product of N(G)-hydroxy-L-arginine is of the same N-nitroso-N-hydroxy/diazeniumdiolate (formerly "NONOate") structure as previously found for the nitrosation products of other model hydroxyguanidines. These decompose in aqueous solution in a pH-dependent manner to yield mainly NO and ureas at low pH, N2O and cyanamides at basic pH, and what appear to be primary nitrosamines/ nitrosoimines. Studies on purified iNOS using a mass spectrometer with a gas-permeable membrane inlet identified both NO and N2O (or 15NO and 15N15NO with 15N-labeled L-arginine as substrate) as products of NOS activity. These experiments suggest that much more NO than N2O is produced under the conditions studied and that N2O formation can be rationalized via the reaction of NOx species with N(G)-hydroxy-L-arginine.

Arginine↗

Nitrous oxide reduction by members of the family Rhodospirillaceae and the nitrous oxide reductase of Rhodopseudomonas capsulata.

After growth in the absence of nitrogenous oxides under anaerobic phototrophic conditions, several strains of Rhodopseudomonas capsulata were shown to possess a nitrous oxide reductase activity. The enzyme responsible for this activity had a periplasmic location and resembled a nitrous oxide reductase purified from Pseudomonas perfectomarinus. Electron flow to nitrous oxide reductase was coupled to generation of a membrane potential and inhibited by rotenone but not antimycin. It is suggested that electron flow to nitrous oxide reductase branches at the level of ubiquinone from the previously characterized electron transfer components of R. capsulata. This pathway of electron transport could include cytochrome c', a component hitherto without a recognized function. R. capsulata grew under dark anaerobic conditions in the presence of malate as carbon source and nitrous oxide as electron acceptor. This confirms that nitrous oxide respiration is linked to ATP synthesis. Phototrophically and anaerobically grown cultures of nondenitrifying strains of Rhodopseudomonas sphaeroides, Rhodopseudomonas palustris, and Rhodospirillum rubrum also possessed nitrous oxide reductase activity.

Acetylene↗

Fifty percent nitrous oxide depresses recovery from anoxic heart failure induced by 100% nitrous oxide.

In experiments on an isolated rate heart lung preparation, the effects of 100% oxygen, 50% nitrous oxide or air on myocardial metabolism during recovery from anoxic heart failure were evaluated with intramyocardial high energy phosphates, lactate and glycogen. A hundred percent nitrous oxide was administered until the cardiac output decreased from 30 to 20 ml/min, and then 50% nitrous oxide, air or 100% oxygen was administered. Fifty percent nitrous oxide reduced the cardiac output and caused heart failure again. The ATP level and energy charge in hearts with 50% nitrous oxide were significantly lower than those in the others. These data indicate that 50% nitrous oxide during recovery from anoxic heart failure had deleterious effects on myocardial function and metabolism.

Journal Article↗

Propofol-nitrous oxide versus thiopental sodium-isoflurane-nitrous oxide for strabismus surgery in children.

STUDY OBJECTIVES: To assess the quality of anesthesia and recovery and the frequency of postanesthetic retching and vomiting with propofol anesthesia for pediatric strabismus surgery. DESIGN: Randomized, open, prospective study. SETTING: University hospital. PATIENTS: Forty children scheduled for strabismus surgery. INTERVENTIONS: The 40 patients were all premedicated with oral midazolam and received intraoperative opioids. They were divided into two groups: Twenty children received propofol at induction, followed by maintenance of anesthesia with propofol infusion and an oxygen-nitrous oxide (O2-N2O) mixture. The other 20 children received thiopental sodium at induction, followed by isoflurane in an O2-N2O mixture. MEASUREMENTS AND MAIN RESULTS: At induction, pain and spontaneous movements were seen significantly more with propofol (11 of 20 vs. 0 of 20 for pain and 13 of 20 vs. 0 of 20 for spontaneous movements; p < 0.001), whereas thoracic rigidity was observed only with thiopental sodium (4 of 20). During maintenance of anesthesia, significantly more oculocardiac reflexes were seen with propofol (10 of 20 vs. 3 of 20; p < 0.02). The interval between termination of anesthesia and extubation was significantly shorter with propofol (13 minutes vs. 16 minutes; p < 0.02). For the first 24 hours after surgery, significantly less retching and vomiting were observed in the propofol group (4 of 20 vs. 11 of 20; p = 0.02). CONCLUSIONS: Propofol induction and maintenance of anesthesia for strabismus surgery in children significantly lowers the frequency of postanesthetic retching and vomiting, but propofol is associated with pain and spontaneous movements at induction and a high frequency of oculocardiac reflexes during maintenance infusion.

Anesthesia Recovery Period↗