Anesthesia and analgesia
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Anesthesia and analgesia · Jan 1999
The effects of ketamine and propofol on neuronal nicotinic acetylcholine receptors and P2x purinoceptors in PC12 cells.
We studied the effects of ketamine and propofol on two ligand-gated ion channels mediating fast synaptic transmission through sympathetic ganglia, neuronal nicotinic acetylcholine receptors (nAchRs), and P2X purinoceptors in a rat pheochromocytoma cell line PC12 using whole cell voltage clamp recording. Ketamine and propofol similarly inhibited the nicotine-induced inward current reversibly and dose-dependently at the membrane potential of -60 mV but had no effects on the adenosine triphosphate-induced current. Both anesthetics accelerated the current decay during agonist application, resulting in greater inhibition on the steady current than the peak current. The 50% inhibition concentration values for the steady current were lower than the clinically relevant concentrations for ketamine (2.8+/-0.6 microM) and higher than those for propofol (5.4+/-0.6 microM). Both anesthetics induced an addition of the fast component to the decay phase and an acceleration of the slow component, which suggests an open channel blockade or an enhancement of desensitization as a mechanism. The effects on closed channels seemed to be small because preincubation with the anesthetics did not significantly augment the block. Inhibition was voltage-independent at membrane potentials between -20 and -70 mV and was consistent with a noncompetitive block. Inhibition of the neuronal nAchR-mediated current may lead to the suppression of synaptic transmission in sympathetic ganglia by ketamine, but not by propofol, at the clinically relevant concentrations. However, these results are not consistent with changes in sympathetic nerve activities reported for animals or humans anesthetized with ketamine or propofol, which suggests effects from other systems, such as the central nervous system in vivo. ⋯ Ketamine (at smaller than clinically relevant concentrations) and propofol (at larger than clinically relevant concentrations) inhibited neuronal nicotinic acetylcholine receptor-mediated current in PC12 cells, which possess the receptors that resemble those in postganglionic sympathetic neurons. These findings are not consistent with in vivo experiments, which suggests that effects from other systems, such as the central nervous system, are of importance.
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Anesthesia and analgesia · Jan 1999
Randomized Controlled Trial Clinical TrialPeripheral antihyperalgesic effect of morphine to heat, but not mechanical, stimulation in healthy volunteers after ultraviolet-B irradiation.
The objective of this study was to evaluate direct peripheral analgesic effects of morphine using a peripheral model of hyperalgesia and the technique of IV regional anesthesia (IVRA), thus allowing the differentiation between central and peripheral mechanisms of action. Two spots on the ventral sides of both forearms in 12 volunteers were irradiated with ultraviolet (UV)-B to induce thermal and mechanical hyperalgesia. One day after the induction of the inflammatory reaction, 40 mL of morphine hydrochloride 0.01% was administered via IVRA. Calibrated heat and phasic mechanical stimuli were applied to differentially determine impairments of tactile and nociceptive perception. Touch and phasic mechanical stimuli of noxious intensity to normal skin did not reveal altered responsiveness caused by morphine. In contrast, the administration of morphine significantly increased heat pain thresholds in the UV-B-pretreated skin areas. The peripheral antihyperalgesic effects of morphine were demonstrated only in inflamed skin areas. Direct central analgesic effects were ruled out by the lack of measurable plasma concentrations of morphine and its metabolites. Morphine 0.01% significantly diminished thermal, but not mechanical, hyperalgesia by a peripheral mode of action, which suggests inhibition of effector pathways leading to heat, but not mechanical, sensitization. ⋯ The peripheral analgesic effects of morphine were studied using modified IV regional anesthesia. When administered 1 day after the induction of dermal inflammation, morphine 0.01% diminished heat, but not primary mechanical, hyperalgesia. Therefore, suppression of mechanical hyperalgesia seen in previous studies could be predominantly due to inhibition of secondary (central) mechanical hyperalgesia.
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Anesthesia and analgesia · Jan 1999
Randomized Controlled Trial Clinical TrialRecovery characteristics of sevoflurane and halothane in preschool-aged children undergoing bilateral myringotomy and pressure equalization tube insertion.
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. ⋯ 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.
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Anesthesia and analgesia · Jan 1999
Randomized Controlled Trial Comparative Study Clinical TrialFiberoptic-guided airway exchange of the esophageal-tracheal Combitube in spontaneously breathing versus mechanically ventilated patients.
The aim of this study was to compare fiberoptic-guided airway exchange of the esophageal-tracheal Combitube (ETC, Kendall-Sheridan Catheter Corp., Argyle, NY) with an endotracheal tube in spontaneously breathing versus mechanically ventilated patients. Forty patients with Mallampati score III and IV scheduled for elective surgery were randomly allocated into two groups (n = 20 each): nonparalyzed, spontaneously breathing or paralyzed, mechanically ventilated patients. After anesthetic induction and insertion of the ETC, a fiberoptic bronchoscope threaded into an armored endotracheal tube was passed transnasally into the larynx. Endotracheal intubation was successful in 18 spontaneously breathing patients and in 15 patients during controlled ventilation. Successful airway exchange was completed in significantly less time (P < 0.05) in spontaneously breathing patients (9+/-3 min; mean +/- SD) than in mechanically ventilated patients (13+/-4 min). Both methods allowed for continuous airway control and maintenance of ventilation and oxygenation. The described method is a means of replacing the ETC with an endotracheal tube without interruption of airway control or ventilation. Replacing the ETC with an endotracheal tube using this method is more readily accomplished during spontaneous ventilation than during controlled ventilation. ⋯ We describe the replacement of the Combitube by an endotracheal tube by the aid of fiberoptic bronchoscopy and without interruption of airway control or ventilation. The performance of this technique was facilitated by spontaneous ventilation compared with mechanical ventilation.