Gastric dysreflexia after spinal cord injury

脊髓损伤(SCI)后即刻阶段的临床报告表明，胃肠道停滞，或 肠梗阻，导致吸入和反流的并发症。胃饲不耐受导致攻击性 完全肠外营养，偶尔有侵入性和Gl手术干预(有相关风险 并发症)，以维持正能量和氮平衡。由此产生的抱负风险 伴随着严重和长期的胃淤滞需要加强对呼吸道的管理，这是一种 创伤后发病率和死亡率的重要原因。这种综合征可能会持续不同程度 从最初的创伤中稳定下来很长时间，因此对患者的质量有深刻的负面影响 SCI后的生活。该项目的范围是使用脊柱挫伤的高胸(脊柱水平T3)模型。 采用已建立的损伤技术，通过PI来研究脊髓损伤后胃淤滞。胃动力和胃动力 排空在很大程度上受到副交感反射的调节，这种反射结合了一般的内脏传入信息 通过迷走神经的延髓。延髓对胃运动的控制通过迷走神经回到胃 传出物。脊髓损伤患者迷走-迷走神经反射在解剖学上保持完好。然而，受伤后 胃病提示脊髓介导的延髓传入受到干扰，导致兴奋。 有文献记载的延髓环路会导致类似于迷走神经干切断术的痉挛胃瘫。使用 高位胸部损伤模型的建立将最大限度地减少胃内脏传入的脊髓中继 给DVC的信息。在这样做的过程中，将解决以下具体目标1)T3挫伤将 导致痉挛胃瘫(即胃排空、弹性和运动能力降低)；2)确定 脊髓损伤后胃反射改变的基础是失去上行的脊髓屏障输入；3)辨认 上行脊髓致密纤维和脑干的投射和神经化学表型 4)轻、中度脊髓损伤后，损伤后胃停滞。 解剖学恢复加班。本实验室的长期目标是建立一个后脊髓损伤模型。 胃肠道功能的改变，包括整个胃肠道，以缓解 人类脊髓损伤患者的GL功能障碍。PI对脊髓损伤后远端肠(肠)排空反射的研究， 再加上L对脑干调节胃功能的研究显然是相辅相成的。

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.