PP032-SUN: Observation of Changes of Intestinal Barrier Function in Critically Ill Patients along with Enteral Nutrition

2014 ◽  
Vol 33 ◽  
pp. S31
Author(s):  
B. Ouyang ◽  
C. Qiu ◽  
Z. Tang
2020 ◽  
Vol 158 (6) ◽  
pp. S-1160-S-1161
Author(s):  
Kaiyue Gao ◽  
Si Chen ◽  
Jing Zheng ◽  
Lijie Wang ◽  
Haijia zhang ◽  
...  

2019 ◽  
Vol 17 ◽  
pp. 205873921982721 ◽  
Author(s):  
Ying-Jie Chen ◽  
Yao-Dong Zhuang ◽  
Zhe Cai ◽  
You-Ni Zhang ◽  
Sen-Ren Guo

The main objective of this study was to explore the effect of enteral nutrition on serum pro-inflammatory cytokines, tumor necrosis factor, and intestinal barrier function in patients with acute severe pancreatitis. A total number of 140 patients were recruited and divided randomly into parenteral nutrition (PN) and enteral nutrition (EN) groups. They received parenteral nutrition and enteral nutrition, respectively. The levels of serum total protein (TP) and albumin (ALB) in peripheral blood were detected in the two groups. Interleukin-1β (IL-1β), interleukin-6 (IL-6), and tumor necrosis factor alpha (TNFα) in the two groups were comparatively analyzed. The levels of pro-inflammatory factors (IL-1β, IL-6, and TNFα) for both groups were same, and there was no significant difference ( P < 0.05) between the two groups before treatment. However, after treatment, a significant reduction was found in EN group which were 31.16 ± 1.95, 36.09 ± 9.44, and 29.21 ± 3.85 ng/L, respectively, showing significant lower values as compared to PN group. The levels of TP and ALB in EN group were 64.46 ± 3.77 and 27.19 ± 1.56 g/L, respectively, after treatment, showing significantly ( P < 0.05) elevated values than PN group. The incidence rates of pancreatic necrosis and pancreatic abscess in EN group were 28.57% and 11.43%, respectively, which were found to be lower significantly than PN group. Enteral nutrition is found to be more effective than parenteral nutrition in the treatment of severe acute pancreatitis, which can significantly reduce the level of pro-inflammatory factors as well as the degree of systemic inflammatory response and protect the intestinal barrier function; thus, this study is worthy for awareness and application in clinical practice.


2021 ◽  
Author(s):  
Yupeng Qi ◽  
Wenjing Ma ◽  
Yingya Cao ◽  
Qun Chen ◽  
Qiancheng Xu ◽  
...  

Abstract Background: Gastrointestinal failure accounts for death in critically ill patients. This study aimed to explore the effect and mechanism of dexmedetomidine (DEX) in intestinal barrier function in critically ill patients undergoing gastrointestinal surgery.Methods: Patients undergoing gastrointestinal surgery were randomized into a DEX group (n=21) or an MID group (n=21). Sufentanil was used in both groups for analgesia. In the DEX group, DEX was loaded (1 µg/kg) before sedation and was infused (0.7 µg/kg/h) during sedation. The mean arterial pressure (MAP), heart rate (HR), borborygmus resumption time (BRT), first defecation time (FDT), stay of ICU and hospital were observed. The DAO, D-LAC, TNF-α, IL-6 and α7nAChR levels in plasma or haemocytes were detected before the start of the sedation (0 h) and after the sedation (24 h).Results: There were no significant differences in age, sex, BMI, APACHE II score, SOFA (P>0.05). The MAP between 0 and 24 h presented no significant difference between the groups (P > 0.05), but HR was significantly slower in the DEX group (P=0.042). The recovery time of bowel sounds was significantly earlier in the DEX group (P=0.034). Both of the stay of ICU (P=0.016) and hospital (P=0.031) were significantly shorter in the DEX group. The expression of α7nAChR in the DEX group was significantly higher at 24 h than at 0 h (P=0.002). The D-LAC decreased significantly in the DEX group than MID group at 24 h (P=0.016).Conclusions: DEX maintained the integrity of the intestinal barrier in patients undergoing gastrointestinal surgery through the cholinergic anti-inflammatory pathway.Trial registration:ChiCTR1900024367. Registered 7 July 2019-Retrospectively registered, http://www.chictr.org.cn/showproj.aspx?proj=40832


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