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Change of inspired oxygen concentration in low flow anesthesia
김지욱,Kang Donghee,Lee Hochul,Ryu Sungwon,Ryu Siejeong,Kim Doosik 대한마취통증의학회 2020 Anesthesia and pain medicine Vol.15 No.4
Background: There are several advantages of low flow anesthesia including safety, economics, and eco-friendliness. However, oxygen concentration of fresh gas flow and inspired gas are large different in low flow anesthesia. This is a hurdle to access to low flow anesthesia. In this study, we aimed to investigate the change in inhaled oxygen concentration in low flow anesthesia using oxygen and medical air.Methods: A total of 60 patients scheduled for elective surgery with an American Society of Anesthesiologist physical status I or II were enrolled and randomly allocated into two groups. Group H: Fresh gas flow rate (FGF) 4 L/min (FiO₂ 0.5). Group L: FGF 1 L/min (FiO₂ 0.5). FGF was applied 4 L/min in initial phase (10 min) after intubation. After initial phase FGF was adjusted according to groups. FGF continued at the end of surgery. Oxygen and inhalation anesthetic gas concentration were recorded for 180 min at 15 min interval.Results: The inspired oxygen concentration decreased by 5.5% during the first 15 min in the group L. Inspired oxygen decreased by 1.5% during next 15 min. Inspired oxygen decreased by 1.4% for 30 to 60 min. The inspired oxygen of group L is 35.4 ± 4.0% in 180 min. The group H had little difference in inspired oxygen concentration over time and decreased by 1.8% for 180 min.Conclusions: The inspired oxygen concentration is maintained at 30% or more for 180 min in patients under 90 kg. Despite some technical difficulties, low flow anesthesia may be considered.
Jeong, Jee-Yeong,Kim, Jiwook,Kim, Bokyoum,Kim, Joowon,Shin, Yusom,Kim, Judeok,Ryu, Siejeong,Yang, Yu-Mi,Song, Kyoung Seob Hindawi Publishing Corporation 2016 MEDIATORS OF INFLAMMATION Vol.2016 No.-
<P>Mucus secretion is often uncontrolled in many airway inflammatory diseases of humans. Identifying the regulatory pathway(s) of mucus gene expression, mucus overproduction, and hypersecretion is important to alleviate airway inflammation in these diseases. However, the regulatory signaling pathway controlling mucus overproduction has not been fully identified yet. In this study, we report that the ATP/P2Y<SUB>2</SUB> complex secretes many cytokines and chemokines to regulate airway inflammation, among which IL-1 receptor antagonist (IL-1ra) downregulates<I> MUC5AC</I> gene expression via the inhibition of G<I>α</I>q-induced Ca<SUP>2+</SUP> signaling. IL-1ra inhibited IL-1<I>α</I> protein expression and secretion, and vice versa. Interestingly, ATP/P2Y<SUB>2</SUB>-induced IL-1ra and IL-1<I>α</I> secretion were both mediated by PLC<I>β</I>3. A dominant-negative mutation in the PDZ-binding domain of PLC<I>β</I>3 inhibited ATP/P2Y<SUB>2</SUB>-induced IL-1ra and IL-1<I>α</I> secretion. IL-1<I>α</I> in the presence of the ATP/P2Y<SUB>2</SUB> complex activated the ERK1/2 pathway in a greater degree and for a longer duration than the ATP/P2Y<SUB>2</SUB> complex itself, which was dramatically inhibited by IL-1ra. These findings suggest that secreted IL-1ra exhibits a regulatory effect on ATP/P2Y<SUB>2</SUB>-induced<I> MUC5AC</I> gene expression, through inhibition of IL-1<I>α</I> secretion, to maintain the mucus homeostasis in the airway. Therefore, IL-1ra could be an excellent modality for regulating inflamed airway microenvironments in respiratory diseases.</P>
( Sang-su Kim ),( Cheol Hong Kim ),( Ji Wook Kim ),( Hsi Chiang Kung ),( Tae Woo Park ),( Yu Som Shin ),( Ju Deok Kim ),( Siejeong Ryu ),( Wang-joon Kim ),( Yung Hyun Choi ),( Kyoung Seob Song ) 생화학분자생물학회 2017 BMB Reports Vol.50 No.10
CLB<sub>2.0</sub>, a constituent of PM, induces secretion of multiple cytokines and chemokines that regulate airway inflammation. Specifically, IL-6 upregulates CLB<sub>2.0</sub>-induced MUC5AC and MUC1 expression. Interestingly, of the tight junction proteins examined, claudin-1 expression was inhibited by CLB<sub>2.0</sub>. While the overexpression of claudin-1 decreased CLB<sub>2.0</sub>-induced MUC5AC expression, it increased the expression of the anti-inflammatory mucin, MUC1. CLB<sub>2.0</sub>-induced IL-6 secretion was mediated by ROS. The ROS scavenger N-acetylcysteine inhibited CLB<sub>2.0</sub>-induced IL-6 secretion, thereby decreasing the CLB<sub>2.0</sub>-induced MUC5AC expression, whereas CLB<sub>2.0</sub>-induced MUC1 expression increased. CLB<sub>2.0</sub> activated the ERK1/2 MAPK via a ROS-dependent pathway. ERK1/2 downregulated the claudin-1 and MUC1 expressions, whereas it dramatically increased CLB<sub>2.0</sub>-induced MUC5AC expression. These findings suggest that CLB<sub>2.0</sub>-induced ERK1/2 activation acts as a switch for regulating inflammatory conditions though a ROS-dependent pathway. Our data also suggest that secreted IL-6 regulates CLB<sub>2.0</sub>-induced MUC5AC and MUC1 expression via ROS-mediated downregulation of claudin-1 expression to maintain mucus homeostasis in the airway. [BMB Reports 2017; 50(10): 516-521]