Intravenous cannulation is an invasive procedure that causes stress, anxiety, and pain for many patients. A recent animal study found that exposure to green light induced antinociceptive and anxiolytic effects. This study examined whether green color exposure reduced stress, anxiety, and pain during peripheral intravenous cannulation (PIC) for sedation in dental patients. In this controlled clinical trial, 24 patients (mean age 40.9 years) were randomized to wear clear glasses or green-colored glasses for 15 min before PIC on two separate days in a cross-over manner. The primary outcome measures were salivary alpha-amylase (sAA) activity and stress-related hemodynamic changes, and the secondary outcome measures were the visual analog scale anxiety (VAS-A) and pain (VAS-P) scores during PIC. The sAA level in the clear group significantly increased during PIC compared with baseline, but did not increase in the green group. Median VAS-P scores during PIC were lower in the green group than in the clear group (VAS-P, 17.0 vs. 50.0). Green color exposure with glasses significantly reduced stress and pain during PIC without any adverse effects. This simple, safe, and effective method may be useful during painful medical procedures.

Postoperative pain and consequent inflammatory responses after tissue incision adversely affects many surgical patients due to complicated mechanisms. In this study, we examined whether activation of protease-activated receptor 2 (PAR-2), which is stimulated by tryptase from mast cells, elicits nociception and whether the PAR-2 antagonist could reduce incisional nociceptive responses in vivo and in vitro. The effects of a selective PAR-2 antagonist, N3-methylbutyryl-N-6-aminohexanoyl-piperazine (ENMD-1068), pretreatment on pain behaviors were assessed after plantar incision in rats. The effects of a PAR-2 agonist, SLIGRL-NH₂, on nociception was assessed after the injection into the hind paw. Furthermore, the responses of C-mechanosensitive nociceptors to the PAR-2 agonist were observed using an in vitro skin–nerve preparation as well. Intraplantar injection of SLIGRL-NH₂ elicited spontaneous nociceptive behavior and hyperalgesia. Local administration of ENMD-1068 suppressed guarding behaviors, mechanical and heat hyperalgesia only within the first few hours after incision. SLIGRL-NH₂ caused ongoing activity in 47% of C-mechanonociceptors in vitro. This study suggests that PAR-2 may support early nociception after incision by direct or indirect sensitization of C-fibers in rats. Moreover, PAR-2 may play a regulatory role in the early period of postoperative pain together with other co-factors to that contribute to postoperative pain.

Perioperative tachycardia and hypertension are often treated with esmolol, a short-acting β1-adrenoceptor antagonist. Besides its cardiac effect, esmolol is reported to exert antinociceptive effects. This study examined the efficacy of intrathecal (IT) esmolol on pain responses in a postoperative pain model. Male Sprague-Dawley rats (250-300 g) were anesthetized with sevoflurane and an IT catheter was implanted. Six days after catheter implantation, a postoperative pain model was established by plantar incision under sevoflurane anesthesia. Withdrawal latencies were assessed by applying a focused radiant heat source before plantar incision; 1 day after the incision (before esmolol administration); and 5, 10, and 15 minutes after bolus administration of IT esmolol. Plantar incision produced hypersensitivity in the postoperative pain model expressed as decreased withdrawal latency to heat stimulation (before incision: 13.9 ± 0.29 seconds and 1 day after incision: 6.3 ± 0.26 seconds). These decreased latencies caused by incision were significantly increased by esmolol administration (40 μg, 80 μg) at 5 minutes (10.7 ± 1.16 seconds, 10.5 ± 1.16 seconds). No postoperative antinociceptive effects of esmolol were observed at 10 or 15 minutes. IT administration of esmolol produced antinociceptive effects of short duration in a rat postoperative pain model. These results suggest that IT esmolol could offer a new strategy for managing perioperative pain, although an alternative approach is necessary to lengthen the duration of the analgesia.

Aims The molecular genetic mechanisms underlying postoperative nausea and vomiting (PONV) in the brain have not been fully elucidated. This study aimed to determine the changes in whole transcriptome in the nucleus of the solitary tract (NTS) in an animal model of PONV, to screen a drug candidate and to elucidate the molecular genetic mechanisms of PONV development. Methods Twenty-one female musk shrews were assigned into three groups: the Surgery group (shrew PONV model, n = 9), the Sham group (n = 6), and the Naive group (n = 6). In behavioral studies, the main outcome was the number of emetic episodes. In genetic experiments, changes in the transcriptome in the NTS were measured. In a separate study, 12 shrews were used to verify the candidate mechanism underlying PONV. Results A median of six emetic episodes occurred in both the Sham and Surgery groups. Whole-transcriptome analysis indicated the inhibition of the GABA(B) receptor-mediated signaling pathway in the PONV model. Baclofen (GABA(B) receptor agonist) administration eliminated emetic behaviors in the shrew PONV model. Conclusions Our findings suggest that the GABA(B) receptor-mediated signaling pathway is involved in emesis and that baclofen may be a novel therapeutic or prophylactic agent for PONV.