Objective: To evaluate the role of gastric mucosa apoptosis in the stress of ischemic stroke, and to discuss the relationship between gastric mucosa apoptosis and gastric barrier.
Methods: Ten dogs were artificially made ischemic stroke by operation (IS group), and another 10 shamly-operated dogs were served as control group. Sucrose permeability were measured after the operation. All dogs were sacrificed 24 hours after operation to measure the gastric mucosal apoptosis index, gastric gross classification, and histological score.
Results: The gastric mucosal apoptosis index in the IS group were significantly higher than in the control group (14.83 +/- 4.41 vs. 5.60 +/- 2.61, P < 0.05). The gastric mucosal apoptosis index were correlated with the sucrose permeability (r = 0. 89, P < 0.05) , gastric gross classification (r = 0. 87, P < 0.05), and histological score (r = 0.92, P < 0.05).
Conclusions: Although ischemic stroke will not cause the obvious damage in the respiratory and circulatory system, it is responsible for the apoptosis of epithelial cell in the gastric mucosa and gastric barrier dysfunction. The apoptosis index is closely correlated with the damage of the function and morphology of the gastric barrier, indicating that the epithelial cell apoptosis acceleration in the gastric mucosa may result in the damage of gastric barrier function.