Takuji Hirose

An ATP-driven Cl− pump regulates Cl− concentrations in rat hippocampal neurons

To investigate the role of Cl(-)-stimulated Mg(2+)-ATPase (Cl(-)-ATPase) in neurons, we examined the effects of ethacrynic acid (0.3 mM), which completely inhibits Cl(-)-ATPase on the intracellular Cl- concentrations of cultured rat hippocampal neurons, using Cl(-)-sensitive fluorescent probes. Ethacrynic acid and ATP consuming treatment increased the intracellular Cl- concentration, but elevation of the extracellular K+ concentration up to 10 mM, inhibition of Na+/K(+)-ATPase, or dissolution of H+ gradients had no effect. Furosemide (0.1 mM), an inhibitor of Na+/K+/Cl- co-transport, decreased the intracellular Cl- concentrations. These results indicate that an ethacrynic acid-sensitive and ATP-driven Cl- pump functions to reduce intraneural Cl- concentrations.

Breakage of Epidural Catheters: A Comparison of an Arrow Reinforced Catheter and Other Nonreinforced Catheters

IMPLICATIONSAlthough breakage of an epidural catheter is rare, our ex vivo study suggests that compared with three other epidural catheters, the Arrow catheter is more likely to stretch and break. The segment between the 7- and 8-cm marks may be an area especially vulnerable to breakage.

Failed tracheal intubation using a laryngoscope and intubating laryngeal mask

Purpose: To report unexpected failed tracheal intubation using a laryngoscope and an intubating laryngeal mask, and difficult ventilation via a facemask, laryngeal mask and intubating laryngeal mask, in a patient with an unrecognized lingual tonsillar hypertrophy.Clinical features: A 63-yr-old woman, who had undergone clipping of an aneurysm seven weeks previously, was scheduled for ventriculo-peritoneal shunt. At the previous surgery, there had been no difficulty in ventilation or in tracheal intubation. Her trachea remained intubated nasally for 11 days after surgery. Preoperatively, her consciousness was impaired. There were no restrictions in head and neck movements or mouth opening. The thyromental distance was 7 cm. After induction of anesthesia, manual ventilation via a facemask with a Guedel airway was suboptimal and the chest expanded insufficiently. At laryngoscopy using a Macintosh or McCoy device, only the tip of the epiglottis, but not the glottis, could be seen, and tracheal intubation failed. There was a partial obstruction during manual ventilation through either the intubating laryngeal mask or conventional laryngeal mask; intubation through each device failed. Digital examination of the pharynx, after removal of the laryngeal mask, indicated a mass occupying the vallecula. Lingual tonsillar hypertrophy (1×1×2 cm) was found to be the cause of the failure. Awake fibrescope-aided tracheal intubation was accomplished.Conclusions: Unexpected lingual tonsillar hypertrophy can cause both ventilation and tracheal intubation difficult, and neither the laryngeal mask nor intubating laryngeal mask may be helpful in the circumstances.RésuméObjectif: Signaler l’échec imprévisible d’une intubation avec laryngoscope et masque laryngé d’intubation, et la ventilation difficile avec masque, masque laryngé ou masque laryngé d’intubation, chez une patiente atteinte d’une hypertrophie non connue de l’amygdale linguale.Éléments clinques: Un shunt ventriculo-péritonéal a été planifié chez une femme de 63 ans qui avait subi une ligature d’anévrisme sept semaines auparavant,. Aucune difficulté d’intubation endotrachéale ou de ventilation n’avait eu lieu lors de cette opération. L’intubation nasale de la trachée a été maintenue pendant 11 jrs après l’intervention. Avant le shunt, on a noté des troubles de la conscience. Les mouvements de la tête et du cou ou l’ouverture de la bouche ne présentaient pas de limitations. La distance thyromentonnière était de 7 cm. Après l’induction de l’anesthésie, la ventilation manuelle au moyen d’un masque et d’une canule de Guedel était inadéquate et l’expansion thoracique insuffisante. Pendant la laryngoscopie à l’aide d’une lame Macintosh ou McCoy, seule la pointe de l’épiglotte, et non la glotte, a été visualisée et l’intubation a échoué. Il y a eu une obstruction partille pendant la ventilation manuelle au travers du masque laryngé d’intubation ou du masque laryngé traditionnel; l’intubation a échoué aussi avec chacun des masques. Le masque laryngé une fois retiré, l’examen du pharynx au doigt a indiqué une masse occupant la fossette glosso-épiglottique. L’hypertrophie de l’amygdale linguale (1×1×2 cm) a été reconnue comme cause de l’échec. L’intubation fibroscopique vigile a été réalisée.Conclusions: L’hypertrophie méconnue de l’amygdale linguale peut causer des difficultés de ventilation et d’intubation et, ni le masque laryngé ni le masque laryngé d’intubation ne peuvent être utiles dans ces circonstances.

The effect of ketamine isomers on both mice behavioral responses and c-Fos expression in the posterior cingulate and retrosplenial cortices.

Ketamine, a non-competitive NMDA receptor antagonist, is a racemic mixture. S(+) ketamine is presumed to be more potent as an anesthetic than R(-) ketamine, and causes less postanesthetic stimulation of locomotor activity than R(-) ketamine in animals at equihypnotic doses. In the present study, we investigated the effect of S(+), R(-), and racemic ketamines on mice behavioral responses and c-Fos expression in the posterior cingulate and retrosplenial cortices (PC/RS), which are suggested to be the brain regions responsible for NMDA-receptor-antagonist-induced psychotomimetic activity. Ataxia and head weaving and c-Fos expression in the PC/RS were significantly more induced by both S(+) and racemic ketamines than by R(-) ketamine at the same dose. S(+) ketamine induced significantly more potent ataxia than racemic ketamine at the same dose. Ketamine-induced c-Fos expression in the PC/RS correlated well with the intensity of behavioral responses. These results imply that R(-) ketamine is weaker than both S(+) and racemic ketamines in a psychotomimetic effect. Also, S(+) ketamine is more potent than racemic ketamine in a psychotomimetic effect and possibly in an anesthetic effect. They also indicate that PC/RS is at least one of the specific brain regions responsible for ketamine-induced behavioral responses in animals and a psychotomimetic activity in humans.

Enflurane-induced Release of an Excitatory Amino Acid, Glutamate, from Mouse Brain Synaptosomes

To clarify the mechanisms of enflurane-induced convulsions, we examined the effects of enflurane, halothane, and diethyl ether on the release of an excitatory neurotransmitter, glutamate, from isolated pinched-off nerve terminals (synaptosomes) of the mouse cerebral cortex. At concentrations corresponding to those used clinically (0.75 and 1.25 mM), enflurane released more glutamate than did halothane. Diethyl ether (10 and 58 mM) had no effect on glutamate release. Enflurane (0.75-15 mM) increased glutamate and aspartate release in a dose-dependent manner but had little effect on the release of the inhibitory neurotransmitters glycine and gamma-aminobutyric acid or on the release of glutamine. A glutamate uptake inhibitor, kainic acid (1 mM), did not affect enflurane-induced glutamate release. Replacement of the mediums Ca2+ by Co2+, or exposure to cold (about 2 degrees C), suppressed the enflurane-induced glutamate release. Depolarization caused by 40 mM K+ increased the basal level of glutamate released, and enflurane-induced glutamate release was lower after depolarization. Enflurane had no effect in synaptosomes prepared from the cerebellum, diencephalon and pons, or medulla oblongata. Thus, enflurane increased Ca(2+)- and temperature-dependent glutamate release, especially from synaptosomes of the cerebral cortex. These data provide a pathophysiologic explanation for enflurane-induced convulsions.

Electroencephalographic arousal response during tracheal intubation and laryngeal mask airway insertion after induction of anaesthesia with propofol

Laryngoscopy and tracheal intubation, or insertion of a laryngeal mask airway may lead to an arousal response on the electroencephalogram. We studied whether more intense stimulation (laryngoscopy and tracheal intubation) causes a greater arousal response than less intense stimulation (laryngeal mask airway insertion). Thirty‐four patients (ASA I–II) were anaesthetised with propofol 3 mg.kg−1, followed by vecuronium 0.15 mg.kg−1 and a propofol infusion of 10 mg.kg−1.h−1. Three minutes after induction of anaesthesia, either laryngoscopy and tracheal intubation (n = 18), or laryngeal mask airway insertion (n = 16) was performed. Laryngoscopy and tracheal intubation caused a significantly greater increase in blood pressure (but not heart rate) than laryngeal mask airway insertion (p < 0.05). Electroencephalogram responses were not different. More intense stimulation does not cause a greater arousal response during propofol anaesthesia.

Ethacrynic acid-induced glutamate release from mouse brain synaptosomes

A loop diuretic, ethacrynic acid (0.3 mM), released glutamate from mouse brain synaptosomes as potently as 40 mM K+, and was more potent than furosemide and bumetanide. Ethacrynic acid-induced glutamate release was suppressed by depletion of Ca2+ or Cl- from the incubation medium. The findings suggest that ethacrynic acid enhances glutamate release through Cl(-)-related depolarization of nerve endings.

Ethacrynic acid-induced convulsions and brain noradrenaline in mice

The intracerebroventricular injection of ethacrynic acid (a 50% convulsive dose; 50 micrograms/mouse) accelerated brain noradrenaline turnover and decreased noradrenaline contents. The decrease in noradrenaline contents was antagonized by 2-amino-5-phosphonovalerate but not by diazepam. Both 2-amino-5-phosphonovalerate and diazepam suppressed the incidence of ethacrynic acid-induced convulsions while reserpine, alpha-methyl-para-tyrosine or FLA-63 augmented it. The results suggest that stimulation by ethacrynic acid of excitatory amino acid neurons enhances-noradrenergic neuronal anticonvulsive activity.