Experimental Studies of Early Enteral Nutrition in the Prophylaxis of Acute Gastric Mucosal Lesions after Severe Brain Injury in Rats

Acute gastric mucosal injury (AGML) is one of the most common visceral complications after severe traumatic brain injury, potentially fatal threat clinical patients in critical condition has a direct impact on the treatment effect and clinical prognosis. Therefore, for a head injury after the AGML the incidence reason, early prevention is to reduce the incidence and improve one of the important measures of severe traumatic brain injury treatment success rate. Literature AGML pathogenesis and prevention means there are a large number of reports, the majority of research has focused on the role of drugs on the AGML the brain injury prevention. But fewer experimental study reported on the AGML the early enteral nutrition (EEN) impact due to severe traumatic brain injury. And the change in the energy metabolism of the gastric mucosa after severe brain injury and the EEN its impact understanding is not perfect, especially from the angle of gastric mitochondrial energy synthesis to explore the impact of enteral nutrition after brain damage gastric mucosa, both at home and abroad have not been reported. In this study, due to severe traumatic brain injury the AGML model, aimed at implementation of early enteral nutrition in brain damage, and to explore the role of EEN the AGML in the prevention of severe traumatic brain injury, the animal experiments, for clinical science applications EEN prevention AGML the occurrence provide a theoretical basis. Experimental method in this study in healthy male Wistar rats were randomly divided into early enteral nutrition group (A), a simple injury group (B) and normal control group (C). Group A and Group B are used pneumatic impact injury device to create a model of severe traumatic brain injury, about two hours after injury gastrointestinal tract were fed the entire battalion prime and saline, respectively, after injury, 6, 12, 24, 48 5 and 72 hours time points to observe changes in the indicators of the gastric mucosa. Laser Doppler flowmetry detection of gastric mucosal blood flow (GMBF); the differential centrifugation extracted gastric mucosal mitochondria, high performance liquid chromatography (HPLC) separation and measurement the adenylyl within the gastric mucosa and its mitochondrial content; radioimmunoassay Determination of gastric mucosal prostaglandin E ₂ (of PGE ₂ ) content; transmission electron microscopy to observe the ultrastructural changes of gastric mucosa; count ulcer index changes. The main results. Successful establishment of a the AGML induced rat model of severe traumatic brain injury. Group B and group C comparison: significant increase in the ulcer index (UI), transmission electron microscopy gastric mucosal obvious damage, GMBF, gastric mucosa and mitochondrial ATP and total adenylate content of PGE ₂ content significantly decreased (P lt; 0.05 ^{0 .01), gastric mucosa energy charge (EC) no statistically significant test at the α = 0.05 level to the level of the gastric mucosa mitochondrial energy charge level in 6,72 hours after injury significantly decreased (P lt; 0.05, 0.01).}