Anesthesia and analgesia
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Anesthesia and analgesia · Jul 2000
Evidence for GABA(A) receptor agonistic properties of ketamine: convulsive and anesthetic behavioral models in mice.
We examined the potentiation by ketamine of the gamma-aminobutyric acid(A) (GABA(A)) receptor function using convulsive and anesthetic behavioral models in adult male ddY mice. General anesthetic potencies were evaluated by a rating scale, which provided the data for anesthetic scores, loss of righting reflex, duration, and recovery time. All drugs were administered intraperitoneally. Small subanesthetic doses of ketamine did inhibit tonic seizures induced by a large dose of the GABA(A) receptor antagonist bicuculline (8 mg/kg). The 50% effective dose value was 15 (95% confidence limits 10-22) mg/kg. Even large anesthetic doses (100-150 mg/kg) did not suppress clonic seizures in 50% of the animals. The GABA(A) receptor agonist, muscimol (0.32-1.12 mg/kg), potentiated ketamine-induced anesthesia in a dose-dependent fashion (P < 0.05). Similarly, the benzodiazepine receptor agonist, diazepam (1-3 mg/kg), augmented ketamine anesthesia in a dose-dependent manner (P < 0.05). Bicuculline (2-5 mg/kg) dose-dependently antagonized ketamine-induced anesthesia (P < 0.05). Neither the benzodiazepine receptor antagonist, flumazenil (2-20 mg/kg), nor the GABA synthesis inhibitor, L-allylglycine (200 mg/kg), affected the anesthetic action of ketamine. These results suggest that ketamine has GABA(A) receptor agonistic properties and that ketamine-induced anesthesia is mediated, at least in part, by GABA(A) receptors. ⋯ We examined the potentiation by ketamine of the gamma-aminobutyric acid(A) receptor function using convulsive and anesthetic behavioral models in mice. Subanesthetic doses of ketamine-inhibited tonic convulsions induced by the gamma-aminobutyric acid(A) receptor antagonist bicuculline. The gamma-aminobutyric acid(A) receptor agonist, muscimol, potentiated ketamine-induced anesthesia. Bicuculline antagonized ketamine anesthesia, but the benzodiazepine receptor antagonist, flumazenil, and the gamma-aminobutyric acid synthesis inhibitor, L-allyglycine, did not. The effects of ketamine on the gamma-aminobutyric acid(A) receptors appear to correlate with its anesthetic actions.
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Anesthesia and analgesia · Jul 2000
Randomized Controlled Trial Comparative Study Clinical TrialCerebral hemodynamic response to the introduction of desflurane: A comparison with sevoflurane.
Rapid increases in the inspired concentration of desflurane cause transient increases in heart rate and blood pressure. Desflurane also impairs cerebral autoregulation at clinical concentrations. Sevoflurane does not share these hemodynamic side effects. We compared the cerebral and systemic hemodynamic responses to the introduction of desflurane or sevoflurane after the induction of anesthesia with propofol. Twenty healthy adult patients scheduled for nonneurological surgery were recruited. After the induction of anesthesia with propofol, either desflurane or sevoflurane (n = 10 per group) was introduced at 7.2% or 2.2%, respectively, and increased to 10.8% or 3.3%, respectively, 2 min later. Middle cerebral artery blood flow velocity was measured continuously by using a 2-MHz transcranial Doppler ultrasound probe. Heart rate and blood pressure were recorded at 1-min intervals during the 12-min study period. Those patients receiving desflurane had significantly greater middle cerebral artery blood flow velocities, heart rates, and blood pressures than those receiving sevoflurane (P < 0.01). ⋯ The introduction of desflurane after the induction of anesthesia leads to significant disturbances in cerebral and systemic hemodynamics suggesting loss of cerebral autoregulation and cerebral hyperemia. This may have implications for patients undergoing anesthesia for intracranial surgery.
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Anesthesia and analgesia · Jul 2000
Randomized Controlled Trial Clinical TrialNitrous oxide prevents movement during orotracheal intubation without affecting BIS value.
We sought to determine whether the addition of nitrous oxide (N(2)O) to an anesthetic with propofol and remifentanil modifies the bispectral index (BIS) during the induction of anesthesia and orotracheal intubation. Thirty ASA physical status I or II patients were randomly allocated to receive either 50% air in oxygen (control group) or 60%-70% N(2)O in oxygen (N(2)O group) that was commenced via a mask simultaneously with the induction of anesthesia. Anesthesia was performed in all the patients with IV propofol at the target effect compartment site concentration of 4 microg/mL throughout the study. A target-controlled infusion (TCI) of remifentanil was initiated 3 min after the TCI of propofol and maintained at the effect-site concentration of 4 ng/mL until the end of the study. After loss of consciousness, and before the administration of vecuronium 0.1 mg/kg, a tourniquet was applied to one arm and inflated to a value more than the systolic blood pressure. An examiner, blinded to the presence of N(2)O, sought to detect any gross movement within the first minute after tracheal intubation, which was performed 10 min after remifentanil TCI began. Inspired and expired oxygen, N(2)O, and carbon dioxide were continuously monitored. A BIS value was generated every 10 s. Arterial blood pressure and heart rate (HR) were measured noninvasively every minute. Measures of mean arterial pressure (MAP), HR, and BIS were obtained before the induction, before the start of the remifentanil TCI, before laryngoscopy, and 5 min after intubation. No significant intergroup differences were seen in BIS, HR, and MAP throughout the study. Maximum changes in BIS, HR, and MAP with intubation were significant (P < 0.01) for both groups but comparable. Six patients in the control group and none in the N(2)O group moved after intubation (P < 0.05). ⋯ We demonstrated that 0.6 minimal alveolar concentration of nitrous oxide combined with a potent anesthetic and an opioid prevents movement after orotracheal intubation without affecting the bispectral index. This demonstrates that the bispectral index is not a useful neurophysiologic variable to monitor the level of anesthesia when nitrous oxide is added to a general anesthetic regimen using propofol and remifentanil.
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Anesthesia and analgesia · Jul 2000
Case ReportsRapacuronium administration to two children with Duchenne's muscular dystrophy.
Children with Duchenne's muscular dystrophy should not be exposed to succinylcholine because of the risk of hyperkalemic cardiac arrest and rhabdomyolysis. This report describes the response to rapacuronium bromide in two patients with Duchenne's muscular dystrophy. Both patients had a recovery index 2 times longer than that reported in children with normal neuromuscular function.