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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.

In order to test the hypothesis that the effects on ventilation of nasal inhalation of sevoflurane during induction of anaesthesia differ from those of oral inhalation, 20 patients underwent inhalation induction of anaesthesia with sevoflurane 5% either through the nasal route or the oral route. In 10 patients who breathed through the nose (N-group), there was an immediate decrease in tidal volume with no change in respiratory duration whereas no similar change was observed in the 10 patients who breathed through the mouth (O-group). The time from the start of sevoflurane inhalation to the onset of sleep was significantly shorter in the O-group compared with the N-group [86.2 +/- 4.4 (mean +/- SE) vs. 115.0 +/- 8.4 sec, P < 0.01].

Purpose: The purpose of this study was to determine the effect of increasing the concentrations of sevoflurane anaesthesia on the distribution of diaphragm blood flow (Qdi) in ten dogs during mechanical ventilation., Methods: Animals were divided into two groups, sevoflurane (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 sevoflurane after a 30 min period of steady-state conditions. Cardiac output (CO) and the mean arterial blood pressure (MBP) were also measured., Results: Sevoflurane 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 time control group., Conclusion: Sevoflurane anaesthesia changes the distribution of Qdi with a greater reduction occurring in Qcru than in Qcost.

Mechanical hyperventilation may produce hypocapnic apnoea below the carbon dioxide off-switch threshold whereas an increase in arterial PCO2 after post-hyperventilation apnoea causes reappearance of respiratory effort above the carbon dioxide on-switch threshold. To study the effects of surgical stimulation on these two thresholds, we have measured end-tidal PCO2 (PE'CO2) at the two thresholds, before and during surgical stimulation, in 14 patients undergoing mastectomy, anaesthetized with sevoflurane (1.2 MAC). Based on the reproducibility of the results, data from 11 patients were analysed and data from the three other patients were discarded. Before surgical stimulation, mean resting PE'CO2' off-switch threshold and on-switch threshold were 5.7 (SEM 0.2), 5.2 (0.2) and 6.1 (0.2) kPa, respectively. The off-switch threshold was significantly less than resting PE'CO2 (P < 0.01) but the on-switch threshold was significantly greater than resting PE'CO2 (P < 0.01). During surgical stimulation, resting PE'CO2' off-switch threshold and on-switch threshold were 4.8 (0.2), 4.1 (0.2) and 4.7 (0.2) kPa, respectively. Although the off-switch threshold was significantly less than resting PE'CO2 (P < 0.01), there were no significant differences between resting PE'CO2 and on-switch threshold. These results indicate that surgical stimulation does not affect equally the carbon dioxide on- and off-switch thresholds.

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-, 10-, 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 less than 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 less than 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.

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.

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 less than 0.05). From these results, we conclude that sevoflurane impairs diaphragmatic function in deep anaesthesia.

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