| Objectives. Stress ulcer bleeding is a major acute cerebrovascular disease, and many of the most common complications of traumatic brain injury, one of the event is difficult to control, high mortality. Therefore, the gastric mucosal injury and protection is the eternal theme. Gastrointestinal lesions caused by acute cerebral vascular disease involving numerous pathophysiological process, although the mechanism of its occurrence on doing a lot of research, but its exact mechanism is still not very clear. The purpose of the present study is to determine gastric histological and histochemical changes and the effect of blood flow of stomach on stress-induced gastric mucosal lesions caused by acute cerebrovascular disease.Methods1. Forty-eight adult male Wistar rats (280-320g, body weight) were randomly divided into4groups:(1) middle cerebral artery occlusion (MCAO) and reperfusion group (MCAO group);(2) MCAO sham-operated group (MCAO-sham group);(3) gastric ischemia-reperfusion (GI-R) group;(4) GI-R sham-operated group (GI-R-sham group). Twelve rats were involved in each group. Focal cerebral ischemia and reperfusion rat model was established with left middle cerebral artery occlusion by using thread inserting. After consciousness regaining from anaesthesia, the rats were scored according to Zea longa5score system. Animals with scores1-3were Included in the experiment. Sham-operated animals were stimulated only by the operation without occluding the middle cerebral artery. Reperfusion was given to the rats after2hours’ischemia. The GI-R rat model was established by clamping the celiac artery. Reperfusion was given to the rats after30mins. Sham-operated animals were stimulated only by the operation without occluding the bloodstream. Respectively after48hours of the reperfusion, the samples were taken out. Gastric mucosa injury index was calculated by Guth method. Mucosal damage was evaluated with macroscopic study and histopathologically. Immunohistochemical methodology was used to detect the expression of Gas and SST. Six rats were examined for each index. One-way analysis of variance was used for statistical analysis. Difference between two groups was compared with q-test.2. Fifty adult male Wistar rats (280～320g, body weight) were randomly divided into5groups:sham group;NS group;CGRP low-dose group;CGRP middle-dose group;CGRP high-dose group. Ten rats were involved in each group. Gastric mucosal blood flow before and after cerebral infarction was detected by laser Doppler flowmetry in rat, cyclely detected three times. Observe the changes of gastric mucosal blood flow was observed in rats after acute cerebral infarction. Different doses exogenous CGRP was intraperitoneally administrated after reperfusion in the rats of cerebral ischemia, and simultaneously gastric blood flow changes were detected, cyclely tested3times. Immunohistochemical methodology was used to detect the expression of CD31.Results1. Focal cerebral ischemia and reperfusion rat①The injury index of gastric mucosa decreased in CGRP group as compared with that in NS group (P<0.01).②nder light microscope, gastric mucosa histopathological alterations of NS group was more obvious than that of CGRP group.③Gas expression in gastric antrum mucosa was lower in CGRP group than that in NS group(P<0.01); SST expression in gastric antrum mucosa was higher in CGRP group than that in NS group(P<0.01). 2. Doppler flowmeter test results showed that, gastric mucosal blood flow decreased after cerebral infarction, and exogenous CGRP could increase gastric mucosal blood flow. CD31expression in gastric antrum mucosa was lower in NS group than that in CGPP group and sham group(P<0.05)Conclusions. The decrease of blood flow of stomach is the primary cause on gastric mucosal lesions after acute cerebrovascular disease, Microcirculation central link in the gastric mucosa to stress injury; One of the important mechanism to protect the ischemic gastric mucosal injury of CGRP is increasing gastric mucosal blood flow irrigation, improve the microcirculation of gastric. |
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