Tohru Ide

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.

Minimum alveolar anesthetic concentrations for airway occlusion in cats : A new concept of minimum alveolar anesthetic concentration-airway occlusion response

Minimum alveolar anesthetic concentration (MAC) is defined as an end-tidal concentration of inhaled anesthetic required to prevent purposeful movement (positive motor response) in 50% of subjects to somatic noxious stimuli. Although MAC for visceral noxious stimuli has not been well investigated, airway occlusion can be a noxious respiratory stimulus that can induce a visceral sensation of choking. In this study, MAC for airway occlusion (MAC-AOR) was determined during halothane, isoflurane, and sevoflurane anesthesia and compared with the MAC values for somatic noxious stimuli such as toe pinch (MAC-pinch) or tetanic stimulus (MAC-tetanus) in cats. Thirty-four adult cats were used. In 24 cats, the motor responses to three different stimuli (toe pinch, tetanic stimulus, and airway occlusion for 6 min) were observed during inhaled anesthesia and rated as positive or negative. The concentration of an inhaled anesthetic was changed in steps of 0.1%-0.2 vol% until the bracketing procedure (i.e., the highest concentration of inhaled anesthetic permitting a positive motor response and the lowest concentration preventing the response were determined) was completed. In 10 cats, the effect of anesthetic duration on MAC-AOR was also investigated. Each mean MAC (MAC-pinch, MAC-AOR, and MAC-tetanus, respectively) was as follows: halothane 0.99, 1.13, and 1.46; isoflurane 1.50, 1.65, and 2.22; and sevoflurane 3.07, 3.38, and 3.95. The first and last MAC-AOR values determined during 6-h halothane anesthesia were 1.10 and 1.11, respectively. In conclusion, airway occlusion can be a noxious stimulus and can induce an all-or-none type of motor response, depending on the depth of inhalational anesthesia in cats. This phenomenon can permit the introduction a new concept of MAC-AOR. Implications: Airway occlusion can be a noxious visceral stimulus and induce all-or-none type of motor response in cats, depending on the depth of inhalational anesthesia. This permits the introduction of a new concept of minimum alveolar anesthetic concentration airway occlusion response.

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.

Contribution of peripheral chemoreception to the depression of the hypoxic ventilatory response during halothane anesthesia in cats

BACKGROUND The effects of inhalational anesthetics on the hypoxic ventilatory response are complex. This study was designed to determine the contribution of peripheral chemoreception to the depression of hypoxic ventilatory response seen with halothane anesthesia. METHODS Cats were anesthetized with pentobarbital sodium and alpha-chloralose and artificially ventilated. Respiratory output was evaluated by phasic inspiratory activity of the phrenic nerve. In 12 cats, this activity was measured during inhalation of an hypoxic gas mixture with halothane, 0, 0.1, and 0.8%, with intact or denervated carotid bodies. In 10 cats, a carotid body was isolated from the systemic circulation and perfused with hypoxic Krebs-Ringer solution equilibrated with halothane, 0, 0.1, and 0.8%. RESULTS The hypoxic ventilatory response was depressed in a dose-dependent manner during halothane anesthesia. In carotid body perfusion studies, the response was significantly depressed only with halothane, 0.80%. CONCLUSION The hypoxic ventilatory response is depressed by a high dose of halothane through a peripheral effect at the carotid body.

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

Inhaled Furosemide Inhibits Behavioral Response to Airway Occlusion in Anesthetized Cats

Background A recent study showed that inhaled furosemide greatly improves experimentally induced dyspnea in humans. The objective of the current study is to test the hypothesis that inhaled furosemide suppresses the behavioral response to airway occlusion without changing the behavioral response to a somatic noxious stimulus in anesthetized animals. Methods In 10 spontaneously breathing cats anesthetized with isoflurane, anesthetic ED50 was determined by measuring an end-tidal anesthetic concentration while observing escape behavior. The monitored behavior consisted of purposeful movement of the head and forearm after endotracheal tube occlusion. The duration from the start of airway occlusion to the onset of the positive response (DOCCL) was measured at the highest concentration of isoflurane permitting the positive motor response to airway occlusion before pretreatment. ED50 values (minimum alveolar concentration) for the suppression of a somatic motor response to a noxious stimulus induced by toe pinch (toe-pinch ED50) were also determined. Then, the effects of inhaled furosemide or vehicle on the ED50 for the suppression of the behavioral response to airway occlusion, DOCCL, and toe-pinch ED50 were evaluated in a randomized, cross-over design. Results The ED50 for the suppression of the behavioral response to airway occlusion significantly decreased (P < 0.01) and DOCCL was significantly prolonged (P < 0.01) after furosemide inhalation, whereas vehicle inhalation did not change these measurements. The decrease in ED50 for the suppression of the behavioral response to airway occlusion after furosemide inhalation lasted 3 h. Furosemide inhalation did not affect the toe-pinch ED50. Conclusion Inhaled furosemide suppressed the behavioral response to airway occlusion in anesthetized animals without affecting the response to somatic noxious stimulus. The authors’ animal model of respiratory distress may be applicable to the study of dyspnea in regard to its mechanism and treatment.

The inhibitory influence of pulmonary vagal afferents on respiratory distress induced by airway occlusion in halothane-anesthetized cats

Although the sensation of dyspnea is common, the mechanisms underlying the sensation have not been fully elucidated.Dyspnea, which is a subjective sensation induced by various respiratory and nonrespiratory stimuli, ranges in intensity from an awareness of difficulty in breathing to an incapacitating state of respiratory distress. It need not be an all or none concept when tolerable; however, intolerable dyspnea is often accompanied by some kind of escape response. In a previous study, we developed a new concept of minimum alveolar anesthetic concentration for airway occlusion (MAC-AOR). Using this model, we assessed the influence of pulmonary vagal afferents on respiratory distress induced by airway occlusion. Adult cats (n = 13) of both sexes weighing 2.7-5.6 kg (3.9 +/- 0.3 kg, mean +/- SE) were anesthetized with halothane and tracheally intubated. After determination of MAC-AOR, anesthesia was maintained with the highest concentration of halothane permitting the positive motor response identified by visual inspection or electromyogram (EMG) of the forearm, usually of the head or extremities. Twisting or jerking of the head was considered a positive response, but twitching or grimacing was not. A slight movement of the shoulder and/or the extremities was not considered positive, nor were coughing, swallowing and chewing, or rigidity recognized as the increase of tonic activity on the forearm EMG. The duration from the start of airway occlusion to the onset of the positive response (DOCCL) was considered as behavioral measures of the tolerable limit of respiratory distress. DOCCL was measured before (Control 1), during, and after (Control 2) lung expansion induced by the injection of the inhaled gas of 5 mL/kg or 10 mL/kg (LE5 or LE10) at functional residual capacity level. Subsequently, 6 of 13 cats received bilateral vagotomies, and the same procedure was repeated at the same concentration as stated above. Then, MAC-AOR after vagotomy was determined again. Before vagotomy, the values of DOCCL during lung expansion (238 +/- 30 s during LE5 and 288 +/- 24 s during LE10) were significantly longer than Control 1 (169 +/- 29 s) and Control 2 (154 +/- 29 s) values (P < 0.01). After vagotomy, the effect of lung expansion on DOCCL was totally abolished. MAC-AOR after vagotomy (1.4% +/- 0.1%) was significantly higher than that before vagotomy (1.1% +/- 0.1%) (P < 0.01). We have demonstrated that vagotomy abolishes the prolongation effect of the lung expansion on DOCCL and increases the value of MAC-AOR in this animal model. These results suggest that pulmonary vagal afferents play an important role in relief of respiratory distress developed during airway occlusion. Implications: In anesthetized cats, we found that lung expansion reduces the tolerable limit to airway occlusion and vagotomy decreased minimum alveolar anesthetic concentration for airway occlusion, which suggests that pulmonary vagal afferents play an important role in relief of respiratory distress. (Anesth Analg 1998;86:398-402)

The effect of epidural anesthesia on respiratory distress induced by airway occlusion in isoflurane-anesthetized cats

UNLABELLED The role of afferent information from the chest wall in the genesis of dyspnea is not fully elucidated. We have developed an animal model for the study of airway occlusion (AO) and proposed new concepts of minimum alveolar anesthetic concentration for AO (MACAOR) and the duration from the start of AO to the onset of the positive motor response (DOCCL) to evaluate respiratory distress quantitatively. We examined the effects of thoracic epidural anesthesia on respiratory distress by using our animal model. Adult cats (n = 24) were anesthetized with isoflurane, and an epidural catheter was placed after T9 laminectomy. After determination of MACAOR, DOCCL was measured. Animals were then randomly assigned into three groups: the EPD Group (n = 12) received epidural 1% lidocaine (0.4 mL/kg), IM saline (0.4 mL/kg), and saline infusion. The IM Group (n = 6) received epidural saline (0.4 mL/kg), IM 1% lidocaine (1 mL/kg), and saline infusion. The PHE Group (n = 6) received epidural 1% lidocaine (0.4 mL/kg) and IV phenylephrine (0.5-1 microg. kg(-1). min(-1)) to maintain a stable arterial blood pressure. DOCCL and MACAOR were measured in each animal at 15 min after the administration of drugs. Plasma lidocaine concentrations were measured before and after epidural or IM injection. DOCCL was significantly longer after epidural injection in all groups than before the injection. Although there was no significant difference in the values of MACAOR between before and after the epidural injection in the EPD Group, the IM administration of lidocaine in the IM Group significantly reduced MACAOR. Plasma concentrations of lidocaine were similar in all groups at all measurement points. Our data indicate that thoracic epidural anesthesia using 1% lidocaine significantly reduced respiratory distress induced by AO. This effect is most likely caused by a systemic effect of lidocaine rather than by reduced afferent information from the chest wall. IMPLICATIONS Thoracic epidural anesthesia reduced respiratory distress induced by airway occlusion. This effect is most likely caused by the systemic effect of lidocaine, rather than by the reduced afferent information from the chest wall.

Distribution of diaphragm blood flow during sevoflurane anaesthesia in dogs

PurposeThe purpose of this study was to determine the effect of increasing the concentrations of sévoflurane anaesthesia on the distribution of diaphragm blood flow (Qdi) in ten dogs during mechanical ventilation.MethodsAnimals were divided into two groups, sévoflurane (n = 6) and time control (n = 4) groups. Blood flow to the crural and the costal diaphragm (Qcru, Qcost) was determined by the hydrogen clearance technique at 0, 0.5, 1.0 and 1.5 minimum alveolar concentration (MAC) of sévoflurane after a 30 min period of steady-state conditions. Cardiac output (CO) and the mean arterial blood pressure (MBP) were also measured.ResultsSevoflurane anaesthesia caused a reduction in CO (L · min−1) from a control value of 1.51 ± 0.21 to 1.38 ±0.1 (0.5 MAC), 1.09 ± 0.15 (1.0 MAC) and 0.98 ± 0.12 (1.5 MAC) (Mean ± SD). Mean blood pressure, Qcru and Qcost also decreased with increasing depth of anaesthesia. In addition, the decrease of Qcru was greater than that of Qcost at all levels of MBP and CO. No change occurred in these variables in the lime control group.ConclusionSevoflurane anaesthesia changes the distribution of Qdi with a greater reduction occurring in Qcru than in Qcost.RésuméObjectifDéterminer les effets de l’augmentation de la concentration du sévoflurane sur la distribution du débit sanguin diaphragmatique (Qdi) sur dix chiens pendant la ventilation automatique.MéthodesLes animaux ont été répartis en deux groupes, sévoflurane (n = 6) et contrôle (n = 4). Le débit sanguin au diaphragme crural et costal (Qcru, Qcost) a été déterminé avec la technique de clairance de l’hydrogène aux concentrations alvéolaires minimales (MAC) de 0, 05, 1,0 et 1,5 de sévoflurane après 30 min de. stabilisation. Le débit cardiaque (DC) et la pression artérielle moyenne (PĀM) ont aussi été mesurés.RésultatsL’anesthésie au sévoflurane a provoqué une baisse du DC (L · min−1) comparativement à la valeur de contrôle de 1,51 ± 0,21 à 1,38 ±0,1 (à 0,5 MAC), à 1,09 ± 0,15 (à 1,0 MAC) et à 0,98 ± 0,12 (à 1,5 MAC) (moyenne ± ET). La pression artérielle moyenne, le Qcr et le Qcost ont aussi diminué avec l’approfondissement de l’anesthésie. En outre, la diminution du Qcru a été plus importante que celle du Qcost à tous les niveaux de PĀM et de DC. On n ’a noté aucun de ces changements dans le group contrôle.ConclusionL’anesthésie au sévoflurane modifie la distribution3 du Qdi mais le Qcru diminue plus que le Qcost.