ArticleExperimental and therapeutic medicine2018
Characterization and evolution of intestine injury at the anhepatic phase in portal hypertensive rats.
Article in Experimental and therapeutic medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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2 citing papers in PubMed, 4 citations in OpenAlex.
- The advantages of duct-to-duct biliary reconstruction in pediatric living donor liver transplantation.Pediatric surgery international · 2023Article
- Remote ischemic post‑conditioning alleviates ischemia/reperfusion‑induced intestinal injury via the ERK signaling pathway‑mediated RAGE/HMGB axis.Molecular medicine reports · 2021Article
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The aim of the present study was to investigate the characteristics and progression of intestinal injury at the anhepatic phase in portal hypertensive rats. A total of 120 healthy male Wistar rats were purchased, with 15 rats in the normal control group and 105 rats were assigned to establish a prehepatic portal hypertension model. The 105 model rats were further divided into seven treatment groups following ischemia-reperfusion. Meanwhile, portal vein pressure, the area of lower esophageal mucosal vein, endotoxin levels in portal vein blood and the level of malondialdehyde (MDA) and superoxide dismutase (SOD) were measured. Morphology changes of the intestine were observed using optical microscopy and transmission electron microscopy. A portal hypertension rat model was successfully established. Furthermore, endotoxin, MDA and SOD level reached a peak at 12-24 h following reperfusion and then decreased gradually to normal levels at 1 week following reperfusion. However, cytological damage did not recover to preoperative level within 1 week. These findings suggest that intestinal injury was most severe within 12-24 h following ischemia-reperfusion and most indicators recovered to almost normal levels. Therefore, further study on the intestinal mucosal damage is required, with the aim to reduce the production of intestinal endotoxin.
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