Experimental Studies Of Early Enteral Nutrition In The Prophylaxis Of Acute Gastric Mucosal Lesions After Severe Brain Injury In Rats

Acute gastric mucosal lesion(AGML), one of the most common visceral complication following severe brain injury, has been a potential lethal threat against critically ill patients, and has great impact on treatment effectiveness and clinical prognosis. Literatures have reported some mechanisms of AGML occurring and treatment means, most of the investigation on AGML have focused on prenvention of durg, but have seldom explored the effect of selected early enteral nutrition on AGML induced by severe brain injury. An investigation, therefore, is needed to clarify whether or not can early enteral nutrition (EEN) further effectively protect gastric mucosa, play a role in preventing AGML , and serve as a major measure for the AGML prophylaxis and treatment in the early after severe brain injury. Objectives:To investigate the protective effects of early enteral nutrition on gastric mucosal after severe brain injury to provide the basis for clinical practice. Methods:Male Wistar rats were randomly divided into 3 groups: early enteral nutrition group(A), severe brain injury group(B) , control group(C). The severe brain injury of rats was produced by gas percussion. The concent of endogenous prostaglandin E2(PGE2),gastric mucosal blood flow(GMBF),the changes of ulcer index and the size of adenylic acid pool(ATP,ADP,AMP) in gastric mucosa tissue or mitochondria at postinjury 0,6,12,24,48,72h. Rat gastric mucosa was removed and mitochondria were isolated by centrifugation. The size of adenylic acid pool(ATP,ADP,AMP) in gastric mucosa tissue or mitochondria were separated, measured by high performance liquid chromatography(HPLC) and energy charge were calculated according to formula. The ultrastructure of gastric mucosa was observed by transmission electron microscopy transmission electron microscopy. Results :(1). AGML model of severe brain injury rats is established successfully. (2). In B group, ulcer index(UI) of remarkably higher than that in C group, the damage of gastric mucosal was serious under transmission electron microscope, GMBF,the size of ATP and total anenine nucleotide pool in gastric mucosa tissue or mitochondria, and contents of PGE2 in gastric mucosa were apparently lower than those in the C group(P<0.05~0.01). There was no significant differences in the changes of EC in gastric mucosa tissue between B group and C group(P>0.05), but in the changes of EC in gastric mucosa mitochondria decreased significantly postinjury 6h and 72h. (3). In A group, UI was decreased significantly compared with B group, accordingly the damage of gastric mucosal was slight. GMBF, the size of ATP and total anenine nucleotide pool in gastric mucosa tissue or mitochondria, and contents of PGE2 in gastric mucosa increased significantly(P<0.05~0.01). There was no significant differences in the level of EC in gastric mucosa tissue between A group and B group(P>0.05), but in gastric mucosa mitochondria increased significantly only postinjury 72h(P<0.01). (4). In the A group, the GMBF positively correlated with contents of PGE2,the size of adenylic acid pool and total anenine nucleotide pool in gastric mucosa mitochondria(P<0.01), but negatively correlated with the UI (P<0.01). Contents of ATP in mitochondria,PGE2 negatively correlated with UI(P<0.05,0.01). Conclusion: â’ˆSevere brain injury could induce remarkable pathological and pathopysiological changes in gastric mucosa. Such acute gastric mucosal lesions not only occurred early but also progressed rapidly. It was severe in degree and considerede to be a high-yield impairment among internal organ damages in the early phase of severe brain injury. â’‰Ischemia of gastric mucosa was the leading factor in the pathogenesis of AGML in the early after severe brain injury. EEN could effectively attenuate stress response and increase gastric mucosa blood flow. â’ŠSevere brain injury could induce the disturbance of energy metabolism in gastric mucosa tissue or mitochondria, indicating that it is possible one of the important mechanisms to AGML after severe brain injury. EEN has cytoprotective effect of gastric mucosa by increasing the energy reserve and alleviating the catabolism of energy-rich phosphates. â’‹EEN had notable prophylactico-therapeutic effects on AGML in the early after severe brain injury. Through this study, we believe that EEN can effectively lessen the degree of AGML in the early after severe brain injury.