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1.
J Clin Monit Comput ; 37(1): 139-145, 2023 02.
Article in English | MEDLINE | ID: mdl-35616797

ABSTRACT

Complications of the endotracheal tube (ETT) displacement during head and neck positional changes are related to not only the tip position but also the cuff pressure against the larynx. Here, we evaluated movement of the ETT cuff relative to laryngeal structures as well as tip displacement from the carina.Sixty-two patients scheduled for thyroidectomy were recruited. The distance from the cricoid cartilage to the upper margin of the cuff (CC) and that from the ETT tip to the carina (TC) were measured using ultrasonography and fiberoptic bronchoscopy, respectively, during flexion and extension. The total tracheal length (TTL) was defined as the combination of CC, TC, and the distance from the upper margin of the cuff to the tip.During flexion, the CC and TC were 1.5 ± 0.6 and 2.9 ± 1.0 cm respectively. Seven patients (11.7%) exhibited excessively deep intubation. After adjusting the cuff position under ultrasonography (CC = 0), the tip position was corrected in 96.7%. While the TC increased by 2.1 ± 1.0 cm after the positional change in extension, the CC decreased by 0.6 ± 0.7 cm because the TTL lengthened (1.4 ± 1.1 cm). Four patients (6.7%) exhibited excessive cuff displacement beyond the cricoid cartilage, which could have been corrected under ultrasonography.In conclusion, the ETT cuff displaced toward the larynx in a less degree than the tip did from the carina due to the tracheal lengthening during head and neck extension. Nevertheless, we suggest that ultrasonographic assessment of cuff position may avoid ETT misplacement. Trial registration https://cris.nih.go.kr/ (approval no. KCT0005319); registered on May 14, 2019.


Subject(s)
Intubation, Intratracheal , Trachea , Humans , Trachea/diagnostic imaging , Movement , Bronchoscopy , Bronchi
2.
Korean J Pain ; 34(1): 27-34, 2021 Jan 01.
Article in English | MEDLINE | ID: mdl-33380565

ABSTRACT

BACKGROUND: Chemotherapy-induced peripheral neuropathy (CIPN) is a major reason for stopping or changing anticancer therapy. Among the proposed pathomechanisms underlying CIPN, proinflammatory processes have attracted increasing attention. Here we assessed the role of prostaglandin D2 (PGD2) signaling in cisplatin-induced neuropathic pain. METHODS: CIPN was induced by intraperitoneal administration of cisplatin 2 mg/kg for 4 consecutive days using adult male Sprague-Dawley rats. PGD2 receptor DP1 and/or DP2 antagonists were administered intrathecally and the paw withdrawal thresholds were measured using von Frey filaments. Spinal expression of DP1, DP2, hematopoietic PGD synthase (H-PGDS), and lipocalin PGD synthase (L-PGDS) proteins were analyzed by western blotting. RESULTS: The DP1 and DP2 antagonist AMG 853 and the selective DP2 antagonist CAY10471, but not the DP1 antagonist MK0524, significantly increased the paw withdrawal threshold compared to vehicle controls (P = 0.004 and P < 0.001, respectively). Western blotting analyses revealed comparable protein expression levels in DP1 and DP2 in the spinal cord. In the CIPN group the protein expression level of L-PGDS, but not of H-PGDS, was significantly increased compared to the control group (P < 0.001). CONCLUSIONS: The findings presented here indicate that enhanced PGD2 signaling, via upregulation of L-PGDS in the spinal cord, contributes to mechanical allodynia via DP2 receptors in a cisplatin-induced neuropathic pain model in rats, and that a blockade of DP2 receptor activation may present a novel therapeutic target for managing CIPN.

3.
Korean J Pain ; 34(1): 58-65, 2021 Jan 01.
Article in English | MEDLINE | ID: mdl-33380568

ABSTRACT

BACKGROUND: Supraspinal delivery of neurotensin (NTS), which may contribute to the effect of a systemically administered agonist, has been reported to be either pronociceptive or antinociceptive. Here, we evaluated the effects of systemically administered NTSR1 agonist in a rat model of neuropathic pain and elucidated the underlying supraspinal mechanism. METHODS: Neuropathic pain was induced by L5 and L6 spinal nerve ligation in male Sprague-Dawley rats. The effects of intraperitoneally administered NTSR1 agonist PD 149163 was assessed using von Frey filaments. To examine the role of 5-HT neurotransmission, a serotonin (5-HT) receptor antagonist dihydroergocristine was pretreated intrathecally, and spinal microdialysis studies were performed to measure the change in extracellular level of 5-HT in response to PD 149163 administration. To investigate the supraspinal mechanism, NTSR1 antagonist 48692 was microinjected into the rostral ventromedial medulla (RVM) prior to systemic PD 149163. Additionally, the effect of intrathecal DHE on intra-RVM PD 149163 was assessed. RESULTS: Intraperitoneally administered PD 149163 exhibited a dose-dependent attenuation of mechanical allodynia. This effect was partially reversed by intrathecal pretreatment with dihydroergocristine and was accompanied by an increased extracellular level of 5-HT in the spinal cord. The PD 149163-produced antinociception was also blocked by intra-RVM SB 48692. Direct injection of PD 149163 into the RVM mimicked the maximum effect of the same drug delivered intraperitoneally, which was reversed by intrathecal dihydroergocristine. CONCLUSIONS: These observations indicate that systemically administered NTSR1 agonist produces antinociception through the NTSR1 in the RVM, activating descending serotonergic projection to release 5-HT into the spinal dorsal horn.

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