Observation on dynamic changes of gastrointestinal mucosal injury in rats with acute stage of cerebral infarction
10.3969/j.issn.1008-9691.2019.04.004
- VernacularTitle:脑梗死急性期大鼠胃肠黏膜损伤的动态变化观察
- Author:
Pengpeng AN
1
;
Jianing WANG
;
Zhizhen REN
;
Yi ZHANG
;
Liang DING
;
Ming TANG
Author Information
1. 青岛市海慈医疗集团
- Keywords:
Cerebral infarction acute phase;
Gastrin;
Gastrointestinal mucosal injury;
Dynamic changes
- From:
Chinese Journal of Integrated Traditional and Western Medicine in Intensive and Critical Care
2019;26(4):398-401
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the dynamic characteristic changes of gastrointestinal mucosa and its relationship with disease progression in rats with acute cerebral infarction. Methods Fifty-six male Wistar rats were selected as the study subjects, and they were divided into three groups: normal control, sham operation and cerebral infarction model groups by random number table method. The middle cerebral artery occlusion (MCAO) model was prepared by the modified Longa thread embolic method. The levels of gastrin (GAS) were monitored in each group after modeling for 24 hours, 4 days and 7 days; after the rats were killed, the sections of gastric antrum and small intestine were taken and stained with hematoxylin-eosin (HE) staining method, the histopathological changes of gastric and small intestinal mucosa were observed under light microscope, in the mean time the gastric and small intestinal mucosal pathological scores were also performed, and the differences of pathological scores among the three groups were compared. Results There were no statistical significant differences in GAS, gastrointestinal mucosa and small intestinal mucosal pathological scores between the normal control group and sham operation group at each time point (all P > 0.05); the GAS level in cerebral infarction model group was decreased gradually with time prolongation, reaching the lowest level 7 days after modeling, but the GAS level in cerebral infarction model group was significantly higher than that in normal group and shamoperation group (ng/L: 205.02±7.68 vs. 130.51±8.03, 145.29±7.68, both P < 0.05). The pathological scores of gastrointestinal mucosa and small intestinal mucosa in the cerebral infarction model group were increased first and then decreased with time prolongation, peaked on 4th day and decreased significantly on 7th day, the pathological scores of gastrointestinal mucosa and small intestinal mucosa in the cerebral infarction model group at each time point were significantly higher than those in the normal control group and sham-operated group (gastric mucosal pathological score: 82.50±2.95 vs. 21.38±1.57, 36.10±3.41; small intestinal mucosal pathological score: 62.00±2.78 vs. 18.25±1.39, 25.55±1.75, all P < 0.05). Under light microscopy, the normal control group showed complete normal morphological appearance, normal structure, orderly arrangement of villi and no infiltration of inflammatory cells; in shamoperation group, inflammatory cells infiltrated the lamina propria at each time point, and there were villi slightly uneven, enlarged stroma, congestion, edema occasionally seen and no obvious ulcer; in cerebral infarction model group, the various layers of gastrointestinal mucosal were not very clear, the glands were arranged irregularly and the capillaries dilated, and in part of tissues, congestion, hemorrhage, edema and inflammatory cell infiltration were seen obviously. Conclusion The injury of gastrointestinal mucosa in acute stage of cerebral infarction should be related to the stress stimulation and disease progress of cerebral infarction itself, not due to the abnormal secretion of GAS.
