Maintaining the patency of the upper airway during breathing is of vital importance. The activity of various muscles is related to the patency of the upper airway. In the present study, we examined the respiratory motor activity in the efferent nerves innervating the upper airway muscles to determine the movements of the upper airway during respiration under normocapnic conditions (pH = 7.4) and in hypercapnic acidosis (pH = 7.2). Experiments were performed on arterially perfused decerebrate rats aged between postnatal days 21–35. We recorded the efferent nerve activity in a branch of the cervical spinal nerve innervating the infrahyoid muscles (CN), the hypoglossal nerve (HGN), the external branch of the superior laryngeal nerve (SLN), and the recurrent laryngeal nerve (RLN) with the phrenic nerve (PN). Inspiratory nerve discharges were observed in all these nerves under normocapnic conditions. The onset of inspiratory discharges in the CN and HGN was slightly prior to those in the SLN and RLN. When the CO2 concentration in the perfusate was increased from 5% to 8% to prepare for hypercapnic acidosis, the peak amplitudes of the inspiratory discharges in all the recorded nerves were increased. Moreover, hypercapnic acidosis induced pre-inspiratory discharges in the CN, HGN, SLN, and RLN. The onset of pre-inspiratory discharges in the CN, HGN, and SLN was prior to that of discharges in the RLN. These results suggest that the securing of the airway that occurs a certain time before dilation of the glottis may facilitate ventilation and improve hypercapnic acidosis.

The tongue can move freely and is important in oral motor functions. Tongue movement must be coordinated with movement of the hyoid, mandible, and pharyngeal wall, to which it is attached. Our previous study using isolated brainstem-spinal cord preparations showed that application of N-methyl-D-aspartate induces rhythmic activity in the hypoglossal nerve that is coincident with rhythmic activity in the ipsilateral trigeminal motor nerve. Partial or complete midline transection of the preparation only abolishes activity in the trigeminal motor nerve; therefore, the neuronal network contributing to coordinated activity of the jaw/tongue muscles is located on both sides of the preparation and sends motor commands to contralateral trigeminal motoneurons. Arterially perfused decerebrate rat preparations exhibit stable inspiratory activity in the phrenic nerve, with efferent nerves innervating the upper airway muscles (the hypoglossal nerve, a branch of the cervical spinal nerve, the external branch of the superior laryngeal nerve, and the recurrent laryngeal nerve) under normocapnic conditions (5% CO). During hypercapnia (8% CO), pre-inspiratory discharges appear in all nerves innervating upper airway muscles. Such coordinated activity in the pre-inspiratory phase contributes to dilation of the upper airway and improves hypercapnia.

An estimation of the appropriate tubing depth for fixation is helpful to prevent inadvertent endobronchial intubation and prolapse of cuff from the vocal cord. A feasible estimation formula should be established. We measured the anatomical length of the upper-airway tract through the oral and nasal pathways on cephalometric radiographs and tried to establish the estimation formula from the height of the patient. The oral upper-airway tract was measured from the tip of the incisor to the vocal cord. The nasal upper-airway tract was measured from the tip of the nostril to the vocal cord. The tracts were smoothly traced by using software. The length of the oral upper-airway tract was 13.2 ± 0.8 cm, and the nasal upper-airway tract was 16.1 ± 0.9 cm. We found no gender difference (p > .05). The correlations between the patients' height and the length of the oral and nasal upper-airway tracts were 0.692 and 0.760, respectively. We found that the formulas (height/10) − 3 (in cm) for oral upper-airway and (height/10) + 1 (in cm) for nasal upper-airway tract are the simple fit estimation formulas. The average error and standard deviation of the estimated values from the measured values were 0.50 ± 0.66 cm for the oral tract and 0.39 ± 0.63 cm for the nasal tract. Thus, considering the length of the intubation marker of each product (DM), we would like to propose the length of tube fixation as (height/10) + 1 + DM for nasal intubation and (height/10) − 3 + DM for oral intubation. In conclusion, the estimation formulas of (height/10) − 3 + DM and (height/10) + 1 + DM for oral and nasal intubation, respectively, are within almost 1 cm error in most cases.

Background: Postoperative fluid retention is a factor that causes delay in recovery and unexpected adverse events. It is important to prevent intraoperative fluid retention, which is putatively caused by intraoperative release of stress hormones, such as ADH (anti-diuretic hormone) or others. We hypothesized that intraoperative analgesia may prevent pathological fluid retention. We retrospectively explored the relationship between analgesics and in-out balance in surgical patients from anesthesia records. Methods: Anesthetic records of 80 patients who had undergone orthognathic surgery were checked in this study. Patients were anesthetized with either TIVA (propofol and remifentanil) or inhalational anesthesia (sevoflurane and remifentanil). During surgery, acetated Ringer's solution was infused for maintenance at a rate of 3-5 ml/kg/h at the discretion of the anesthetist. The perioperative parameters, including the amount of crystalloid and colloid infused, and the amount of urine and bleeding were checked. Furthermore, we checked the amount and administration rate of remifentanil during the surgical procedure. The correlation coefficient between the remifentanil dose and the in-out balance or the urinary output was analyzed using the Pearson correlation coefficient. The contributing factor to fluid retention, including urinary output, was statistically examined by means of multivariate logistic regression analysis. Results: A significant positive correlation was found between remifentanil dose and urinary output. Urinary output less than 0.04 ml/kg/min was suggested to cause positive fluid balance. Although in-out balance approaches zero balance with increase in remifentanil administration rate, no contributing factor for near-zero fluid balance was statistically picked up. The remifentanil administration rate was statistically picked up as the significant factor for higher urinary output (> 0.04 ml/kg/min) (OR, 2,644; 95% CI, 3.2-2.2 × 10 6) among perioperative parameters. Conclusions: In conclusion, remifentanil contributes in maintaining the urinary output during general anesthesia. Although further prospective study is needed to confirm this hypothesis, it was suggested that fluid retention could be avoided through suppressing intraoperative stress response by means of appropriate maintenance of remifentanil infusion rate.

Congenital bronchial atresia is a relatively rare malformation that causes a segmental obstruction of the bronchus during the fetal period. The peripheral lung distal from the obstructed bronchus becomes hyperinflated because of the unidirectional flow through collateral check-valve entry. Positive pressure ventilation during general anesthesia may cause a rupture of the bulla, resulting in pneumothorax. An 8-year-old girl, who had to undergo oral surgery, was diagnosed as having congenital bronchial atresia and one-fifth of her lung was poorly ventilated. We planned to perform general anesthesia under spontaneous respiration using a laryngeal mask, which was well tolerated.