We had recently reported that linalool odor exposure induced significant analgesic effects in mice and that the effects were disappeared in olfactory-deprived mice in which the olfactory epithelium was damaged, thus indicating that the effects were triggered by chemical senses evoked by linalool odor exposure. However, the peripheral neuronal mechanisms, including linalool receptors that contribute toward triggering the linalool odor-induced analgesia, still remain unexplored. In vitro studies have shown that the transient receptor potential ankyrin 1 (TRPA1) responded to linalool, thus raising the possibility that TRPA1 expressed on the trigeminal nerve terminal detects linalool odor inhaled into the nostril and triggers the analgesic effects. To address this hypothesis, we measured the behavioral pain threshold for noxious mechanical stimulation in TRPA1-deficient mice. In contrast to our expectation, we found a significant increase in the threshold after linalool odor exposure in TRPA1-deficient mice, indicating the analgesic effects of linalool odor even in TRPA1-deficient mice. Furthermore, intranasal application of TRPA1 selective antagonist did not alter the analgesic effect of linalool odor. These results showed that the linalool odor-induced analgesia was triggered by a TRPA1-independent pathway in mice.

Linalool odor exposure induces an analgesic effect in mice. This effect disappeared in the anosmic model mice, indicating that olfactory input evoked by linalool odor triggered this effect. Furthermore, hypothalamic orexinergic neurons play a pivotal role in this effect. However, the neuronal circuit mechanisms underlying this effect have not been fully addressed. In this study, we focused on the descending orexinergic projection to the spinal cord and examined whether this pathway contributes to the effect. We assessed the effect of intrathecal administration of orexin receptor antagonists on linalool odor-induced analgesia in the tail capsaicin test. We found that the selective orexin type 1 receptor antagonist, but not the selective orexin type 2 receptor antagonist, prevented the odor-induced analgesic effect. Furthermore, immunohistochemical analyses of c-Fos expression induced by the capsaicin test revealed that neuronal activity of spinal cord neurons was suppressed by linalool odor exposure, which was prevented by intrathecal administration of the orexin 1 receptor antagonist. These results indicate that linalool odor exposure drives the orexinergic descending pathway and suppresses nociceptive information flow at the spinal level.

Objective: To examine the relationship between the method of anesthesia for alveolar bone graft surgery and postoperative nausea and vomiting (PONV) based on the difference in surgical timing and to assess factors related to the postoperative quality of life. Design: Retrospective observational study. Setting: Hospital. Participants: Patients with cleft lip and palate who underwent alveolar bone graft surgery under general anesthesia. The subjects were divided into two groups based on surgical timing: secondary bone graft (SBG) and late secondary bone graft (LSBG) groups. Main Outcome Measures: Relationship between time to recovery of feeding and the types of anesthesia, PONV, and postoperative pain period. Results: The mean patient age was 9.97 ± 1.33 years in the SBG group and 15.39 ± 0.31 years in the LSBG group. In the SBG group, patients who were administered fentanyl or remifentanil had significantly higher incidence of PONV than those who were not administered these drugs. In the SBG group, the time to recovery of feeding was significantly longer in patients experiencing PONV within 2 hours or that lasted for 24 hours than in those without PONV. In the LSBG group, there was no significant difference regarding any of the above factors. Conclusions: Our results suggest that the occurrence of PONV within 2 hours or lasting for 24 hours postoperatively in school-age children prolonged the time to recovery of feeding. This indicates that the time to recovery of feeding can be predicted based on the occurrence of PONV within the first 2 hours.

We performed general anesthesia for a lip repair and palatoplasty in a patient with left ventricular hypoplasia following a Glenn procedure. Preoperative examination revealed hemorrhagic diathesis, hypoxemia, and secondary polycythemia. After completion of the palatoplasty, hypoxemia and intraoral bleeding were observed, and reintubation was required. The bleeding risk was likely increased in this patient due to several factors including the surgical procedure and concurrent antithrombotic therapy. In conclusion, the risks associated with hypoxemia and increased bleeding must be considered for the safe provision of general anesthesia during palatoplasty procedures in patients with cyanotic heart disease.