Tetsuo Kochi

Effects of partial paralysis on the swallowing reflex in conscious humans

The ability to swallow may be affected by administration of a small dose of muscle relaxant. To test the hypothesis that a subparalyzing dose of a muscle relaxant can impair swallowing, effects of partial paralysis produced by pancuronium on the swallowing reflex were investigated in eight conscious subjects. The swallowing reflex was induced by a bolus injection or a continuous infusion of distilled water into the mesopharynx. The swallowing function was assessed by electromyogram of suprahyoid muscles (EMGSH), mesopharyngeal pressure (Pmeso), and hypopharyngeal pressure (Phypo). Peripheral muscle activity was simultaneously determined by train of four ratio (TOFR) of hypothenar muscles to electrical stimulation of ulnar nerve and by hand grip strength (HGS). Following control measurements, measurements during partial paralysis and after recovery from partial paralysis were performed after intravenous administration of pancuronium 0.02 mg/kg. Partial paralysis significantly depressed EMGSH (bolus injection 44.1 +/- 10.0%, continuous infusion 55.9 +/- 10.2% of control value, P less than 0.01). Pmeso also significantly decreased (bolus injection 64.9 +/- 6.7 to 47.8 +/- 5.8 mmHg, P less than 0.01; continuous infusion 63.4 +/- 7.7 to 52.5 +/- 5.8 mmHg, P less than 0.05). The TOFR of peripheral muscles decreased to 81.4 +/- 6.7% of control value (P less than 0.01), and HGS was reduced from 44.6 +/- 1.9 to 39.4 +/- 2.0 kg (P less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of Sevoflurane on Diaphragmatic Contractility in Dogs

The effect of sevoflurane on diaphragmatic contractility was investigated in 12 anesthetized, mechanically ventilated dogs with the thorax opened. Animals were divided into two groups of six each: the sevoflurane and time control groups. We assessed contractility by the transdiaphragmatic pressure (Pdi) during supramaximal stimulation of the phrenic nerve at frequencies of 0.5, 10, 20, 50, and 100 Hz under quasiisometric conditions. The integrated electrical activity (Edi) of the crural and costal parts of the diaphragm (Edi cru, Edi cost) was also measured. In the sevoflurane group, diaphragmatic contractility was determined during three levels of anesthesia, specifically 0, 1.0, and 1.5 minimum alveolar anesthetic concentration (MAC). Measurements were made at the start of the stimulation (initial) and at the end of the 2-s period (2-s). Increasing the depth of sevoflurane anesthesia did not cause any significant differences in Pdi and Edi at 0.5-, lo-, and 20-Hz stimulation. By contrast, at 50- and 100-Hz stimulation, initial Pdi during 1.0 and 1.5 MAC sevoflurane exposure decreased significantly compared with the 0 MAC value (P < 0.05). In addition, there was a statistical difference in 2-s Pdi between 1.0 and 1.5 MAC at 100-Hz stimulation (P < 0.05). The Edi cru showed similar changes in Pdi at both measurements, whereas there was no remarkable change in Edi cost. There was no significant change either in Pdi or in Edi with respect to time in the time control group. We conclude from these results that sevoflurane impairs diaphragmatic contractility through its inhibitory effect on neuromuscular transmission, predominantly of the crural part.

Differences in respiratory reflex responses from the larynx, trachea, and bronchi in anesthetized female subjects

Background Animal studies show that airway receptors responsible for eliciting respiratory protective reflexes are not uniformly distributed in the airways. Based on this information, it is possible that the protective reflex responses to airway irritation in humans may vary, depending on the site of stimulation. The purpose of this study is to examine whether the protective reflex responses evoked from the larynx are different from those evoked from the lower airways and to see how change in depth of anesthesia modifies the protective reflex responses evoked from individual sites. Methods The airway mucosa of the larynx, tracheal carina, and bronchi were stimulated by injection of distilled water (0.5 ml) at two different depths of sevoflurane anesthesia (1.2 and 1.8 MAC) in 11 female subjects breathing spontaneously through the laryngeal mask airway. The respiratory responses were monitored by measuring ventilatory flow and airway pressure. Results At 1.2 MAC of sevoflurane anesthesia, both laryngeal and tracheal stimulation caused protective responses, such as forceful expiratory efforts, apnea, and spasmodic panting, whereas bronchial stimulation caused little or no such responses. There was no significant difference in the incidence of different types of reflex responses between the larynx and the trachea. At 1.8 MAC of sevoflurane, the nature of the elicited responses was very similar to that observed at 1.2 MAC of sevoflurane, showing little dose‐dependence of anesthetic effect. Conclusions The respiratory reflex responses evoked by injection of water vary, depending on the site of stimulation. The incidence of various reflex responses was not affected by the changing depth of anesthesia. The sensitivity to airway irritation seems to be greater at the larynx and trachea than at the more peripheral airways.

Epidural anesthesia for patients with amyotrophic lateral sclerosis.

Amyotrophic lateral sclerosis (ALS) is characterized by pathologic degeneration of the lower motor neurons, motor nuclei of the caudal brainstem, and the descending pathways of the upper motor neurons. Progressive muscular atrophy and bulbar palsy with fasciculations are its clinical manifestations. Atrophy and weakness of respiratory muscles eventually lead to respiratory failure and death. The impairment of respiratory function, together with the weakened upper airway muscles, may affect anesthetic management. The response to muscle relaxants, either depolarizing or nondepolarizing, is also altered in ALS. Patients with ALS require special care throughout the perioperative period. The following case reports illustrate the safety and usefulness of epidural anesthesia in patients with ALS.

Different effects of halothane and enflurane on diaphragmatic contractility in vivo.

We examined the effects of halothane and enflurane on diaphragmatic contractility in 12 anesthetized, mechanically ventilated dogs. The diaphragmatic force was assessed from transdiaphragmatic pressure (Pdi) developed at functional residual capacity against an occluded airway during cervical phrenic nerve stimulation. Animals were randomly assigned to two groups, a halothane group (n = 6) and an enflurane group (n = 6). The Pdi stimulus-frequency relationship was compared at anesthetic levels of 1, 1.5, and 2 MAC (minimum alveolar concentration) in each group. The sequence of changing anesthetic concentration was randomized. In addition, the Pdi- frequency relationship was also compared between 1 MAC of halothane and enflurane in 8 of 12 dogs. In animals anesthetized with enflurane, Pdi significantly decreased with 50− and 100-Hz stimulation in the presence of increasing MAC values, whereas Pdi at10-Hz stimulation was not affected by the depth of anesthesia. Pdi with 20-Hz stimulation during 2 MAC enflurane also decreased significantly below Pdi levels seen at 1 and 1.5 MAC. By contrast, with halothane there was no difference in Pdi at any of the stimulation frequencies during any of the three levels of anesthesia. There was no statistical difference, however, between Pdi-frequency relationships during 1 MAC of halothane and enflurane in eight animals. From these results, we conclude that halothane does not impair diaphragmatic contractility any more than enflurane does, but enflurane decreases force generation of the diaphragm at high stimulation frequencies in a dose-related fashion. This depressant effect of enflurane occurs mainly through the impairment of neuromuscular transmission and/or membrane excitability. Part of its effect is probably related, however, to the impairment of excitation-contraction coupling, as suggested by the depression of Pdi at 2 MAC in response to 20-Hz stimulation.

Diaphragmatic function during sevoflurane anaesthesia in dogs

The effect of increasing the concentration of sevoflurane anaesthesia on diaphragmatic function was investigated in six mechanically ventilated dogs. Diaphragmatic function was assessed by measuring the transdiaphragmatic pressure (Pdi) generated during bilateral supramaximal stimulation of the cervical phrenic nerves at frequencies of 0.5, 10, 20, 50, and 100 Hz under quasi-isometric conditions. Measurements were performed at 1, 1.5 and 2 MAC concentrations after maintaining stable conditions for one hour. The Pdi-stimulus frequency relationship was compared at each anaesthetic concentration. The sequence of changing anaesthetic depth was altered in random fashion among animals. The Pdi amplitude generated by single twitch (0.5 Hz) was unchanged at the three concentrations. In addition, no change in Pdi during 10, 20, 50 Hz stimulation was noted at any of the three levels of anaesthesia. By contrast, Pdi with 100 Hz stimulation during 2 MAC sevoflurane exposure (28.1 ±5.0 cmH2O) decreased below Pdi levels seen at 1 and 1.5 MAC (35.3 ±4.3 cmH2O and 31.5 ±4.3 cmH2O, respectively) (P < 0.05). From these results, we conclude that sevoflurane impairs diaphragmatic function in deep anaesthesia.RésuméL’effect d’une augmentation de la concentration de sevoflurane sur la fonction diaphragmatique a été investigué chez six chiens ventillés mécaniquement. La fonction diaphragmatique a été évaluée en mesurant la pression trans-diaphragmatique (Pdi) développée durant la stimulation supramaximale bilatérale des nerfs phréniques cervicaux à des fréquences de 0,5, 10, 20, 50, et 100 Hz durant les conditions quasi-isométriques. Les mesures ont été faites à 1, 1,5 et 2 MAC après le maintien d’une condition stable pour une heure. La relation entre la Pdi et la fréquence de la stimulation a été comparée avec chaque concentration de l’anesthésique. La fréquence du changement de la profondeur de l’anesthésie a été altérée d’une façon randomisée parmi les animaux. L’amplitude de la Pdi générée par une stimulation de 0,5 Hz a été inchangée aux trois différentes concentrations. En plus, aucun changement dans la Pdi durant la stimulation à 10, 20 et 50 Hz n’a été noté avec les trois niveaux de l’anesthésie. Par contre, la Pdi avec une stimulation de 100 Hz durant l’exposition à 2 MAC de sevoflurane (28,1 ±5,0 cm H2O) a diminué en bas des niveaux de Pdi observés à 1 et 1,5 MAC(35,3 ±4,3 cm H2O et 31,5 ±4,3 cm H2O, respectivement) (P < 0,05). A partir de ces résultats, on conclut que le sevoflurane altère la fonction diaphragmatique lors d’une anesthésie profonde.

Breathing pattern and occlusion pressure waveform in humans anesthetized with halothane or sevoflurane.

To examine the ventilatory effects of sevoflurane, breathing pattern, airway occlusion pressure waveform, and the mechanical variables of the respiratory system were determined in seven subjects anesthetized with sevoflurane and in an additional seven subjects anesthetized with halothane. All patients breathed 1 MAC of anesthetic using oxygen as the carrier gas, and the measurements were performed in the absence of surgical stimulation. The durations of inspiration and expiration were significantly longer during sevoflurane than during halothane administration. Tidal volumes were larger in the sevoflurane group than in the halothane group. Occlusion pressure waveforms were also markedly different between the two groups. Occlusion pressure during the initial 300–400 ms tended to be less in the sevoflurane-anesthetized than in the halothane-anesthetized subjects. There was no evidence of an active Hering-Breuer reflex with either anesthetic. Mechanical variables of the respiratory system were essentially identical between the two anesthetics. We conclude that (a) the ventilatory effects of halothane and sevoflurane are different, (b) the difference in the respiratory timing and depth of breathing originates from the action of the anesthetics on the central respiratory neural network, and (c) the different shape of the tracheal occlusion pressure may be largely due to the different effects of halothane and sevoflurane on the muscles of the rib cage.

Diaphragmatic activity during isoflurane anaesthesia in dogs

The effect of isoflurane administration on diaphragmatic activity was investigated in six anaesthetized mechanically ventilated dogs. Diaphragmatic strength was assessed by measuring the transdiaphragmatic pressure (Pdi) generated during supramaximal stimulation of both cervical phrenic nerves at frequencies of 0.5, 10, 20, 50 and 100 Hz under partially isometric conditions at 1, 1.5 and 2 minimum alveolar anaesthetic concentrations (MAC), after maintaining 1 h of stable conditions. Pdi measurements were made at the start of the stimulation (initial) and at the end of a 2‐s period (2‐s). The force‐frequency relationship was compared at each anaesthetic level. For single twitch (0.5 Hz) stimulation, the time constant of diaphragmatic relaxation was also assessed. The sequence of changing anaesthetic depth was altered in random fashion between animals. Pdi amplitude at single twitch stimulation was unchanged at the three anaesthetic concentrations. There was no significant difference in initial Pdi at various stimulus frequencies with increasing depth of isoflurane anaesthesia. In addition, no change in 2‐s Pdi during low frequency stimulation (10 and 20 Hz) was noted during any of the three levels of anaesthesia. By contrast, 2‐s Pdi with 50 Hz stimulation during 2 MAC isoflurane exposure decreased significantly below Pdi levels seen at 1 and 1.5 MAC (P

Ventilatory Responses to Inspiratory Resistive Loading Before and After Gastrectomy During Isoflurane Anesthesia

We tested the hypothesis that steady-state responses to inspiratory-flow-resistive loading would be preserved immediately after upper abdominal surgery in anesthetized patients. Twenty patients were studied immediately before and after gastrectomy under 1 minimum alveolar anesthetic concentration (MAC) of isoflurane anesthesia. Ventilation, airway occlusion pressure, and PaCO2 were measured before and during inspiratory-flow-resistive breathing lasting from 6 to 7 min. Ten of 20 subjects were tested with resistance of 51.8 cm H2 O centered dot L-1 centered dot s-1 (Load 1) and the remaining 10 subjects were tested with resistance of 83.3 cm H2 O centered dot L-1 centered dot s-1 (Load 2). Ventilatory variables obtained immediately before and after surgery were compared in each group. Baseline ventilation increased postoperatively with greater frequency of breathing and comparable tidal volume (V (T)). Immediately after the application of resistive load, minute ventilation (V (I)) significantly decreased both pre- and postoperatively, due primarily to the decrease of VT. During sustained loading, VI gradually increased and reached steady state in 2-3 min. After 5 min of loading, PaCO2 returned to the control level with Load 1 whereas with Load 2, it was higher than the control value. The magnitude and time course of reduced ventilation in response to resistive load were identical between pre- and postoperative conditions. We conclude that the ability of maintaining ventilation to imposed inspiratory-flow-resistive loading is well preserved during 1 MAC of isoflurane anesthesia before and after gastrectomy. (Anesth Analg 1995;80:1199-1205)

Thoracic epidural anesthesia causes rib cage distortion in anesthetized, spontaneously breathing dogs.

The effects of thoracic epidural anesthesia on the performance of the parasternal intercostal muscles were investigated by measuring electromyographic activity and length changes of the parasternals (EMG activities and length, respectively, of the parasternals) in seven pentobarbital anesthetized, spontaneously breathing dogs. Epidural injection of 0.1 mL/kg of 2% lidocaine decreased tidal volume and minute ventilation during unstimulated breathing. These changes were accompanied by complete abolishment of EMG activities of the parasternals and passive elongation of the parasternals during inspiration. At equivalent end-tidal PCO2 values (70 and 80 mm Hg) during CO2 rebreathing, tidal volume and minute ventilation were lower after epidural block compared to the corresponding values before the block. Thoracic epidural anesthesia impaired contraction of the parasternals and conceivably other respiratory muscles in the rib cage as well and could induce a distortion of the rib cage. The authors conclude that respiratory muscles in the rib cage contribute considerably to the maintenance of ventilation in anesthetized dogs.