The Changes Of Gastric Parietal Cellular Configuration In Rats Under Various Somatic Stressor

Stress ulcers(SU) occur mainly in the victims of severe trauma and sepsis. The pathogenesis of stress ulcers is not completely understood. There is an imbalance between protective and destructive factors.The presence of luminal acid is essential for the development of stress ulcerations. However, with the exception of sepsis and head-injury patients, there does not appear to be acid hypersecretion and in some patients there may actually be gastric acid hyposecretion. Some study shown that reduction of gastric mucosal blood flow caused by shock in experimental animals was almost always accompanied by a decrease in acid secretion. Thus, the precise role of acid in various somatic stress ulcerations remains to be established.In the nonsecreting of parietal cell, apical canalicular surfaces are lined with short, stubby microvilli. Throughout the cytoplasmic space there is an abundance of H+/K+-ATPase-rich tubulovesicles. Stimulated cells have dilated canalicular spaces, a dramatically expanded apical membrane surface with elongated microvilli, and diminution of cytoplasmic tubulo vesicles. Therefore, the activation of acid secretion of parietal cell can be assessed by its configuration changes with immunofioresence detection of gastric H+/K+-ATPase.Until now, stress ulcer induced by water immersion restraint(WRS) is the most common animal model, which cannot imitate entirely all of the SU induced by various stressor in clinical practice, but the study about complicated mechanism of SU is strongly limited by unique animal model. In this study, we assessed the changes of gastric parietal cellular configuration in rats under various somatic stressor and try to elucidate the mechanism of SU further.Materials and methods 1. Animal model of various somatic stressSprague-Dawley rats weighing 180-210g, were used in all experiments. Rats were housed in temperature-controlled rooms with free access to food and water. Before being exposed to stress, the rats were deprived of food for 24 hours and water 1h. Rats were randomly divided 9 groups with control, WRS 2 4h, burns 24>48h, sepsis 24 48h and brain injurys 24 48h groups.(1) WRS modelSprague-Dawley rats were exposed to stress by being fixed in a wooden board causing immobilization and immersed in 19+ 1C water to the rat's xyphoid process and killed at 2, or 4hours after WRS respectively.(2) Burns modelNaked back skin of rats were exposed to water of 100C 12 seconds until severe burn injurys of 30% total body skin area were developed, followed by 40ml/kg normal sodium being supplied intraperitoneally lh after injury and returned to its home cage with fasting and free accessing to water. The animals were killed at 24, or 48 hours after injury respectively.(3) Sepsis modelRats were anaesthetized by pentobarbital sodium and a midline laparotomy was performed, then the cecum was exposed with the medium of cecum was ligated followed by distal cecum being punctured, then the abdomen were closed. After 40ml/kg normal sodium being supplied intraperitoneally, the animal returned to its home cage with fasting and free accessing to water. The animals were killed at 24, or 48 hours after injury respectively.(4) Brain injurys modelRats were anaesthetized by pentobarbital sodium 24 hr before fluid percussion, the scalp sagittally incised, and soft tissue displaced. A 4.8-mm-diameter craniotomy was performed over the right parietal cortex. Two nickel-plated screws were placed in burr holes 1 mm rostral to bregma and 1 mm rostral to lambda/1 mm medial to the lateral ridge. A modified 20-gauge Leur-Loc syringe hub was placed over the exposed, intact dura mater and bonded to the skull with cyanoacrylate adhesive and dental acrylic, and the animal returned to its home cage. At 24 hr after surgical preparation, animals were anesthetized with aether. The hub of animal was connected to the fluid percussion injury device, and a moderate (182. 4 kPa) level of fluid percussion injury was delivered. The animals were killed at 4, or 8 hours after injury . 2. Evalu...