Acute and Critical Care

Original Articles

Basic science and research
The Anti-Inflammatory Effect of Arginine-Vasopressin on Lipopolysaccharide-Induced IκBα/Nuclear Factor-κB Cascade: Jisoo Park, Eun Young Eo, Kyoung-Hee Lee, Jong Sun Park, Jae-Ho Lee, Chul-Gyu Yoo, Choon-Taek Lee, Young-Jae Cho; Korean J Crit Care Med. 2015;30(3):151-157. Published online August 31, 2015; DOI: https://doi.org/10.4266/kjccm.2015.30.3.151

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Background
Arginine vasopressin (AVP) is widely used as a vasopressor agent. Some recent studies have suggested that AVP may exert an immunomodulatory effect. However, the mechanism about the anti-inflammatory effect of AVP is not well known. We investigated the effect of AVP on the ihibitor of kappa B (IκBα)/nuclear factor-kappa B (NF-κB) pathway in RAW 264.7 cells.
Methods
Cultured RAW 264.7 cells were pretreated with AVP and stimulated with lipopolysaccharide (LPS). To evaluate the effect of AVP on inflammatory cytokines, the concentration of interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) were assessed by an enzyme-linked immunosorbent assay technique. The expression of IκBα and nuclear translocation of NF-κB p65 were measured by Western blotting, and IκB kinase (IKK) activity was analyzed by an in vitro immune complex kinase assay. To confirm the AVP effect on IκBα/NF-κB cascade and via V2 receptor, we added tolvaptan (V2 receptor antagonist) after AVP pretreatment.
Results
The increase of IL-6 and TNF-α in LPS-stimulated RAW 264.7 cells was suppressed by a treatment with AVP. Pretreatment of AVP inhibited increasing of IKK activity and IκBα degradation induced by LPS in RAW 264.7 cells. Furthermore, LPS induced and NF-κB transcription was inhibited by AVP pretreatment. The observed changes in IKK activity, IκBα degradation and NF-κB transcription by AVP was abolished by tolvaptan treatment.
Conclusions
Our results suggest that AVP showed anti-inflammatory effect on LPS-induced IκBα/NF-κB cascade in mouse macrophages via V2 receptors.

Citations

Citations to this article as recorded by

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Alexandra Castillo-Ruiz, Carla D. Cisternas, Hannah Sturgeon, Nancy G. Forger
Brain, Behavior, and Immunity.2022; 104: 122. CrossRef
Comprehensive biology of antipyretic pathways
Prajitha N, Athira SS, Mohanan PV
Cytokine.2019; 116: 120. CrossRef
Oxytocin and Vasopressin Systems in Obesity and Metabolic Health: Mechanisms and Perspectives
Cherlyn Ding, Faidon Magkos
Current Obesity Reports.2019; 8(3): 301. CrossRef

Pharmacology
The Optimal Dose of Midazolam for Promoting Sleep in Critically Ill Patients: A Pilot Study: Se Joong Kim, Jisoo Park, Yeon Joo Lee, Jong Sun Park, Ho Il Yoon, Jae Ho Lee, Choon Taek Lee, Young Jae Cho; Korean J Crit Care Med. 2014;29(3):166-171. Published online August 31, 2014; DOI: https://doi.org/10.4266/kjccm.2014.29.3.166

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Abstract PDF

BACKGROUND
Many critically ill patients treated in the intensive care unit (ICU) experience sleep disruption. Midazolam is commonly used for the sedation of critically ill patients. This pilot study is aimed to identify the optimal dose of midazolam for achieving sound sleep in critically ill patients.
METHODS
This prospective study was conducted in the medical ICU of a tertiary referral hospital. Polysomnography recording was performed over 24 hours to assess the quantity and quality of sleep in patients sedated with midazolam.
RESULTS
A total of five patients were enrolled. Median total sleep time was 494.0 (IQR: 113.5-859.0) min. The majority of sleep was stage 1 (median 82.0 [IQR 60.5-372.5] min) and 2 (median 88.0 [60.5-621.0] min) with scant REM (median 10.0 [6.0-50.5] min) and no stage 3 (0.0 min) sleep. The median number of wakings in 1 hour was 16.1 (IQR: 7.6-28.6). The dose of midazolam showed a positive correlation with total sleep time (r = 0.975, p = 0.005).
CONCLUSIONS
The appropriate quantity of sleep in critically ill patients was achieved with a continuous infusion of 0.02-0.03 mg/kg/h midazolam. However, the quality of sleep was poor. Further study is required for the promotion of quality sleep in such patients.

Citations

Citations to this article as recorded by

Effect of prolonged sedation with dexmedetomidine, midazolam, propofol, and sevoflurane on sleep homeostasis in rats
Brian H. Silverstein, Anjum Parkar, Trent Groenhout, Zuzanna Fracz, Anna M. Fryzel, Christopher W. Fields, Amanda Nelson, Tiecheng Liu, Giancarlo Vanini, George A. Mashour, Dinesh Pal
British Journal of Anaesthesia.2023;[Epub] CrossRef
Reliability of the Korean version of the Richards-Campbell Sleep Questionnaire
Jae Kyoung Kim, Ju-Hee Park, Jaeyoung Cho, Sang-Min Lee, Jinwoo Lee
Acute and Critical Care.2020; 35(3): 164. CrossRef
Sedation in Critically Ill Patients
Mark Oldham, Margaret A. Pisani
Critical Care Clinics.2015; 31(3): 563. CrossRef

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