Gastric dysreflexia after spinal cord injury

脊髓损伤（SCI）后即刻的临床报告表明，胃肠道淤滞，或 肠梗阻，导致误吸和反流的并发症。胃喂养不耐受需要积极的 全胃肠外营养和偶尔的侵入性和GI手术干预（具有相关的风险， 并发症），以维持积极的能量和氮平衡。由此产生的误吸风险 伴有严重和长期胃郁滞的急性呼吸道感染需要气道的强化管理， 创伤后发病率和死亡率重要原因。不同程度的这种综合征可能会继续 在从最初的创伤稳定后很长时间内， SCI后的生活该项目的范围是使用脊柱挫伤的高胸椎（脊柱水平T3）模型 使用PI建立的技术对SCI后胃停滞进行研究。胃运动及 排空在很大程度上由副交感神经反射介导，副交感神经反射包括一般内脏传入输入， 通过迷走神经到达延髓胃运动的延髓控制通过迷走神经返回胃 传出神经这种迷走神经-迷走神经反射在SCI患者中保持解剖学完整。然而，受伤后 胃的发病率表明，脊髓介导的输入到髓质被破坏，导致兴奋 有充分证据证明延髓回路产生类似于迷走神经干切断术的痉挛性胃轻瘫。使用 将最大限度地减少脊髓中继胃内脏传入 信息DVC。在这样做时，将解决以下具体目标：1）T3挫伤病变将 产生痉挛性胃麻痹（即，胃排空、弹性和运动性降低）; 2）确定 脊髓孤束上行输入的丧失是脊髓损伤后胃反射改变的基础; 3）确定 脊髓孤束上行纤维和脑干的投射和神经化学表型 4）在轻度至中度SCI后，损伤后胃停滞将表现为 解剖恢复超时。该实验室的长期目标是建立一个后SCI模型， 包括胃肠道全长的胃肠道功能的改变，以减轻 人SCI患者中的GI功能障碍。Pi对SCI后远端肠（肠）消除反射的研究， 再加上Co-l对脑干调节胃功能的研究显然是互补的。

Clinical reports of the immediate post-spinal cord injury (SCI) phase indicate that gastrointestinal stasis, or ileus, results in complications from aspiration and reflux. Gastric feeding intolerance necessitates aggressive total parenteral nutrition and occasionally invasive and Gl surgical intervention (with associated risk of complications) for the maintenance of a positive energy and nitrogen balance. The resultant risk of aspiration that accompanies severe and prolonged gastric stasis requires intensive management of the airway and is a significant cause of post-trauma morbidity and mortality. Various degrees of this syndrome may continue long after stabilization from the initial trauma thus having profound negative effects on the patient's quality of life after SCI. The scope of the project is to use a high thoracic (spinal level T3) model of spinal contusion injury using established techniques by the PI to the study of post-SCI gastric stasis. Gastric motility and emptying is heavily mediated by parasympathetic reflexes that incorporate general visceral afferent input to the medulla via the vagus nerve. Medulary control of gastric motility returns to the stomach via vagal efferents. This vago-vagal reflex remains anatomically intact in the SCI patient. However, the post-injury gastric morbidity suggests that a spinally-mediated input to the medulla is disrupted, resulting in an excitation of well documented medullary circuits that produce a spastic gastroparesis similar to truncal vagotomy. Use of a high thoracic injury model will maximize the reduction in spinal relays for gastric visceral afferent information to the DVC. In so doing the following Specific Aims will be addressed 1) T3 contusion lesion will produce a spastic gastric paralysis (i.e., reduced gastric emptying, elastance, and motility); 2) Identify that the loss of ascending spinosolitary inputs is the basis for alterations in gastric reflexes after SCI; 3) Identify the projections and neurochemical phenotypes of the ascending spinosolitary fibers and the brainstem neurons upon which they act; 4) After mild to moderate SCI, post-injury gastric stasis will demonstrate anatomical recovery overtime. The long term goal of this laboratory is to establish a model of post-SCI alterations in gastrointestinal function that encompasses the entire length of the Gl tract in order to alleviate Gl dysfunction in human SCI patients. The Pi's research on distal gut (bowel) eliminative reflexes after SCI, coupled with the Co-l's research on brainstem regulation of gastric function is clearly complementary.