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Effects of lumbar epidural block on maximum expiratory strength were studied in 12 healthy volunteers. Subjects performed maximum expiratory effort against occluded airway at functional residual capacity (FRC) and total lung capacity (TLC) while measuring airway pressure and electromyogram of the abdominal muscles (EMGab). Cough strength was assessed by maximum expiratory pressure (PEmax) and peak EMGab (peak-EMGab). Following injection of 2% lidocaine 17.8±1.1 ml into the lumbar epidural space (L2.3±0.4), upper levels of analgesia ranged from T11 to T4 (T7.8±1.3). Peak-EMGab and PEmax were significantly reduced by lumbar epidural block at both lung volumes. Compared with severe reduction in peak-EMGab, PEmax was well maintained at TLC, but changes in PEmax were identical to those in peak-EMGab at FRC. When analgesia spread to higher than T6, PEmax at TLC decreased considerably. We conclude that lumbar epidural block producing analgesia above T6 paralyzes the abdominal muscles and severely impairs the ability of effective cough in healthy young men.

Mechanical influences independent of chemoreceptor function on ventilatory control were studied in halothane-anesthetized, artificially ventilated patients using the technique reported by Altose et al. (Respir Physiol 66: 171-180, 1986). Contribution of mechanical factor was indirectly assessed by comparing the values of arterial carbon dioxide tension at which the subjects started breathing efforts during CO(2) loading induced by the following two methods. 1) Partial rebreathing of expired gas and 2) Mechanical hypoventilation (successive decrease in inflation volume). These two maneuvers resulted in a similar rate of increase in end-expiratory carbon dioxide tension. However, contrary to the observation made by Altose et al. in awake volunteers, we found comparable values of ventilatory recruitment threshold for Pa(CO)(2). Thus, we speculate that halothane anesthesia and/or loss of consciousness impair transmission of afferent information from the lung and/or chest wall musculature. Such effects may be responsible for the depression of load compensatory mechanism during anesthesia.

We examined the effects of enflurane on the diaphragmatic function in 15 pentobarbital-anesthetized, mechanically ventilated dogs. They were divided into three groups of five animals each, according to the administered concentration of enflurane. The diaphragmatic function was assessed from transdiaphragmatic pressure (Pdi) and integrated diaphragmatic electromyography (Edi) developed at functional residual capacity against an occluded airway during bilateral supramaximal phrenic nerve stimulation at 0.5, 10, 20, 50 and 100 Hz under quasiisometric condition. After a control measurement, enflurane was administered at a constant end-expired concentration (0, 0.5 and 1 MAC) and the measurement was repeated after 1 hour of exposure. The Pdi amplitude generated by single twitch (0.5 Hz) and during 10, 20 and 50 Hz stimulation was unchanged between the groups. No change in Pdi during 100 Hz stimulation was noted during 0 and 0.5 MAC exposure, while it was reduced by 1 MAC of enflurane. When the values of Pdi were expressed as % of maximum Pdi (%Pdi,max) that developed during control measurement and analyzed in terms of %Pdi,max-stimulus frequency relationship, a significant decrease in %Pdi,max was noted for 100 Hz stimulation in 0.5 and 1 MAC groups compared to the control. Similarly, Edi during 100 Hz stimulation obtained in 0.5 and 1 MAC groups was markedly depressed compared to the control. Edi during 50 Hz stimulation was also decreased at 1 MAC. Relative changes in Edi following enflurane administration were greater than the corresponding changes of Pdi. These results demonstrate that enflurane impairs diaphragmatic function through its inhibitory effects on neuromuscular transmission.

In order to determine the respiratory effects of sevoflurane in humans, breathing pattern and mechanical behavior of respiratory system were investigated in ten subjects at anesthetic depth of 1 MAC (minimum alveolar concentration). Average tidal volume and breathing frequency amounted to 275 ml and 20.9 breaths per minute. Arterial carbon dioxide tension amounted to 45.6 mmHg. Duration of inspiration was 1.06s and that of expiration was 1.92s. Mean inspiratory flow rate amounted to 259 ml.s(-1). Average value of passive respiratory elastance determined by the method of Zin et al. amounted to 21.8 cmH(2)O. l(-1), while those of active respiratory elastance and resistance obtained by the method of Behrakis et al. were 28.0 cmH(2)O. l(-1) and 3.15 cmH(2)O. l(-1).s(-1), respectively. Values of these variables were compared to those reported in halothane and enflurane anesthesia and possible explanations of the differences between the anesthetics are discussed.

We examined the effect of enflurane on diaphragmatic contractility in six 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. Pdi-stimulus frequency relationship was compared at three levels of anesthesia, namely 1, 1.5, and 2 MAC (minimum alveolar concentration) of enflurane. The sequence of changing anesthetic concentration was randomized between animals. Pdi at 50 and 100 Hz stimulation was significantly decreased with increasing MAC while Pdi at 10 Hz stimulation was not affected by the depth of anesthesia. Pdi of 20 Hz stimulation was significantly decreased at 2 MAC as compared to those at 1 and 1.5 MAC. We conclude that enflurane decreases contractility of the diaphragm mainly through impairment of the neuromuscular transmission and/or membrane excitability. Part of its effects is, however, probably related to the impairment of excitation-contraction coupling, as suggested by the depression of Pdi at 2 MAC in response to 20 Hz stimulation.