Functional and morphological changes of the gut barrier during the restitution process after hemorrhagic shock

Chang, Jian-xing; Chen, Shuang; Ma, Li-Ping; Jiang, Longyuan; Chen, Jianwen; Chang, Ruiming; Li, Wen; Wu, Wei; Jiang, Zhipeng; Huang, Zitong

doi:10.3748/wjg.v11.i35.5485

Cited by 100 publications

(71 citation statements)

References 26 publications

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“…The liberation of proteolytic enzymes, particularly cathepsina D, was higher than the proximal portions of the small intestine. These findings suggest a greater susceptibility of structural compromise of the small intestine in relations to the colon, as has been observed by other authors 13,14,8 . This way, colic anastomoses carried out under adverse conditions could be more resistant, becoming in just a few alterations into biomechanic parameters.…”

Section: Discussionsupporting

confidence: 76%

“…Therefore, the simultaneous occurrence of intestinal injuries in patients in critical condition, make it relevant and the anastomotic dehiscence contributes to the death rate. Besides this, the intestinal tract is one of the organs that precociously suffers the consequences of the mechanism of post-shock hemorrhagic ischemia 8 , causing the release of inflammatory cytokines, toxins and bacterial translocation with serious systemic repercussions and, it is believed, that these alterations can negatively influence intestinal anastomoses. 3 Considering ethical and practical aspects in the evaluation of this variable, the influence of the state of hemorrhagic shock in patients with intestinal anastomoses, a study model in animals has been elaborated.…”

Section: Discussionmentioning

confidence: 99%

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Hemorrhagic shock influence on colonic anastomoses in rats: evaluation of rupture by liquid distension resistance test

et al. 2008

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PURPOSE: To evaluate the effect of hemorrhagic shock in colonic anastomoses in rats, with a rupture by liquid distension resistance test. METHODS: Wistar lineage rats, averaging 90 days old and weighing from 310 to 380 grams were divided into two groups. In the first group (G1), 10 animals were submitted to colonic anastomoses in normovolemic terms and the second group (G2), of 10 animals, was submitted to colonic anastomoses in hypovolemic conditions. The shock was caused by half milliliter of blood withdrawn, every two minutes, until the value of average 50mmHg arterial pressure or a total volume corresponding 30% withdrawal of volemia was reached. Serum lactate dosages were carried out at the beginning and end of the procedure. The average serum lactate values at the end of the surgery were 1.91 mmol/l in G1 group and 3.69 mmol/l in G2 group (p<0.05). On the fifth postoperative day, the animals were euthanized. The anastomoses were evaluated with a rupture by liquid distension resistance test. RESULTS: In G1, the average value of colonic rupture was 160.7 mmHg whereas in G2 it was 152.1mmHg (p>0.05). CONCLUSION: Hemorrhagic shock, under the established conditions of this study, had no influence on colonic anastomoses in rats evaluated with the rupture by liquid distention resistance test.

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Section: Discussionsupporting

confidence: 76%

Section: Discussionmentioning

confidence: 99%

Hemorrhagic shock influence on colonic anastomoses in rats: evaluation of rupture by liquid distension resistance test

et al. 2008

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“…LPS introduced into the intraperitoneal cavity enters the systemic circulation via the portal vein and activates the immune system [5], which was confirmed by monitoring serum TNFa in our study. This mimics the clinical situation in cases of severe trauma when the gut barrier is impaired and gram negative bacteria containing LPS enter the blood stream [11,41]. Second, we focused mainly on the cells that have been shown to play an important role in the inflammatory, regenerative, and remodeling phases (1-6 weeks postoperative) of the repair process.…”

Section: Discussionmentioning

confidence: 99%

Defective Bone Repair in C57Bl6 Mice With Acute Systemic Inflammation

Behrends

Hui

Gao

et al. 2017

Clinical Orthopaedics &Amp; Related Research

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Background Bone repair is initiated with a local inflammatory response to injury. The presence of systemic inflammation impairs bone healing and often leads to malunion, although the underlying mechanisms remain poorly defined. Our research objective was to use a mouse model of cortical bone repair to determine the effect of systemic inflammation on cells in the bone healing microenvironment. Question/Purposes (1) Does systemic inflammation, induced by lipopolysaccharide (LPS) administration affect the quantity and quality of regenerating bone in primary bone healing? (2) Does systemic inflammation alter vascularization and the number or activity of inflammatory cells, osteoblasts, and osteoclasts in the bone healing microenvironment? Methods Cortical defects were drilled in the femoral diaphysis of female and male C57BL/6 mice aged 5 to 9 months that were treated with daily systemic injections of LPS or physiologic saline as control for 7 days. Mice were euthanized at 1 week (Control, n = 7; LPS, n = 8), 2 weeks (Control, n = 7; LPS, n = 8), and 6 weeks (Control, n = 9; LPS, n = 8) after surgery. The quantity (bone volume per tissue volume [BV/TV]) and microarchitecture (trabecular separation and thickness, porosity) of bone in the defect were quantified with time using microCT. The presence or activity of vascular endothelial cells (CD34), macrophages (F4/80), osteoblasts (alkaline phosphatase [ALP]), and osteoclasts (tartrate-resistant acid phosphatase [TRAP]) were evaluated using histochemical analyses.The institution of one or more of the authors (JEH, PAM) has received, during the study period, funding from the Fonds de recherche Santé Québec. The remaining authors certify that neither he or she, nor a member of his or her immediate family, has funding or commercial associations (consultancies, stock ownership, equity interest, patent/licensing arrangements, etc) that might pose a conflict of interest in connection with the submitted article. Results Only one of eight defects was bridged completely 6 weeks after surgery in LPS-injected mouse bones compared with seven of nine defects in the control mouse bones (odds ratio [OR], 0.04; 95% CI, 0.003-0.560; p = 0.007). The decrease in cortical bone in LPS-treated mice was reflected in reduced BV/TV (21% ± 4% vs 39% ± 10%; p\0.01), increased trabecular separation (240 ± 36 lm vs 171 ± 29 lm; p \ 0.01), decreased trabecular thickness (81 ± 18 lm vs 110 ± 22 lm; p = 0.02), and porosity (79% ± 4% vs 60% ± 10%; p \ 0.01) at 6 weeks postoperative. Defective healing was accompanied by decreased CD34 (1.1 ± 0.6 vs 3.4 ± 0.9; p\0.01), ALP (1.9 ± 0.9 vs 6.1 ± 3.2; p = 0.03), and TRAP (3.3 ± 4.7 vs 7.2 ± 4.0; p = 0.01) activity, and increased F4/80 (13 ± 2.6 vs 6.8 ± 1.7; p \ 0.01) activity at 2 weeks postoperative. Conclusion The results indicate that LPS-induced systemic inflammation reduced the amount and impaired the quality of bone regenerated in mouse femurs. The effects were associated with impaired revascularization, decreased bone turnover by osteoblasts...

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“…I/R has also been shown to induce apoptosis [20] . Bacterial translocation and mucosal barrier dysfunction have been implicated in the damage caused by I/R in the gut [21] . This damage is also related to an increase in circulating levels of proinflammatory cytokines such as interleukin-6 and tumor necrosis factor alpha (TNF-alpha), liberated by the intestine itself [22] .…”

Section: Discussionmentioning

confidence: 99%

Ketamine anesthesia reduces intestinal ischemia/reperfusion injury in rats

Cámara¹,

Guzmán²,

Barrera³

et al. 2008

WJG

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showed significantly less injury in rats that received ketamine than in rats that did not (2.35 ± 1.14 vs 4.58 ± 0.50, P < 0.0001). The distance traveled by a marker, expressed as percentage of total intestinal length, in rats that received pentobarbital sodium was 20% ± 2% in comparison with 25.9% ± 1.64% in rats that received ketamine (P = 0.017 INTRODUCTIONMesenteric ischemia is a clinical entity with a mortality rate between 60% and 100% that usually requires surgical resection of the necrotic intestinal segment [1] . Although there have been advancements in the treatment of ischemic injury, an ideal treatment has not been defined, and new options should be considered. A promising strategy is the use of anesthetic and sedative agents that might exert protective effects on the injured tissue. Ketamine is an agent that has been recommended for this purpose in clinical situations of sepsis, renal ischemia, cerebral ischemia and serious burn injuries [2][3][4] . The small intestine is very sensitive to ischemic insult [5] . Reperfusion causes additional damage through the release of free radicals, pro-inflammatory cytokines, leukotrienes and other related products [6] . Intestinal Abstract AIM: To investigate the effects of ketamine anesthesia on the motility alterations and tissue injury caused by ischemia/reperfusion in rats. METHODS: T h i r ty m a l e W i s t a r ra t s w e i g h i n g 200-250 g were used. Ischemia was induced by obstructing blood flow in 25% of the total small intestinal length (ileum) with a vascular clamp for 45 min, after which either 60 min or 24 h of reperfusion was allowed. Rats were either anesthetized with pentobarbital sodium (50 mg/kg) or ketamine (100 mg/kg). Control groups received sham surgery. After 60 min of reperfusion, the intestine was examined for morphological alterations, and after 24 h intestinal basic electrical rhythm (BER) frequency was calculated, and intestinal transit determined in all groups. RESULTS: The intestinal mucosa in rats that were anesthetized with ketamine showed moderate alterations such as epithelial lifting, while ulceration and hemorrhage was observed in rats that received pentobarbital sodium after 60 min of reperfusion. Quantitative analysis of structural damage using the Chiu scale

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Functional and morphological changes of the gut barrier during the restitution process after hemorrhagic shock

Cited by 100 publications

References 26 publications

Hemorrhagic shock influence on colonic anastomoses in rats: evaluation of rupture by liquid distension resistance test

Hemorrhagic shock influence on colonic anastomoses in rats: evaluation of rupture by liquid distension resistance test

Defective Bone Repair in C57Bl6 Mice With Acute Systemic Inflammation

Ketamine anesthesia reduces intestinal ischemia/reperfusion injury in rats

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