The Effect of Preterm Birth and RLN Damage on Airway Protection and Maturation

空气消化系统各功能部件之间的协调，特别是 在吞咽和呼吸之间，是成功保护婴儿呼吸道的关键。 这种协调的破坏会导致呼吸道保护的失败，表现为肺性 渴望。早产是这种干扰和随后的渴望的原因之一。这些 问题可能会与喉返神经(RLN)受损而复杂化 因早产而必须进行的心血管修复。因为目前对 这些脆弱患者的病理很大程度上是基于非侵入性技术， 协调障碍与呼吸道保护之间的因果关系，包括如何 发展对这一系统的影响，是未知的。特别是，我们不知道生物力学 引起吸入的改变或生物力学中发生的纵向变化 这可能会促进呼吸道保护。我们建议调查 有或无RLN损伤的早产儿/足月儿的呼吸道保护成熟。它的用途 验证的早产动物模型将允许使用侵入性方法收集详细数据 不适合人类的方法，包括高速、双平面视频透视 病人。这里提出的工作将确定早产如何影响感觉运动。 成功的呼吸道保护基础上的相互作用以及RLN损伤如何影响 这些通过三个具体目标的相互作用：(SA1)决定了 对照仔猪出生时呼吸与吞咽的协调性 通过断奶；(SA2)确定纵向发展的协调性 早产后的呼吸和吞咽使用相当于人类分娩的猪 胎龄30-32周；(SA3)决定成熟之间的相互作用 (Sa3a)对照足月儿和(SA3b)早产儿的呼吸道保护和RLN损伤。 通过使用经过验证的、具有翻译重要性的动物模型，这项研究 将提供关于潜在的正常和病理生理机制的数据 导致早产儿呼吸道保护失败。这些数据是纵向收集的 并有足够的数量来评估内部的个体差异和个体发育变化 个人，将提供人类患者无法提供的洞察力。这些数据将改变我们的 了解康复的潜力和治疗建议。此外，这些 数据可以作为根据对数据的理解设计干预策略的基础 病理生理学的基本机制。

Coordination among the functional components of the aerodigestive system, particularly between swallowing and respiration, is critical for successful airway protection in infants. Disruption of this coordination can produce failure of airway protection, manifest as pulmonary aspiration. Preterm birth is one cause of this disruption and subsequent aspiration. These problems may be compounded with damage to the recurrent laryngeal nerve (RLN) resulting from cardiovascular repairs necessitated by prematurity. Because the current understanding of the pathologies in these fragile patients is based largely on non-invasive technologies, the causal relationship between disordered coordination and airway protection, including how development impacts this system, is unknown. In particular, we do not know the biomechanical alterations that cause aspiration nor what, if any, longitudinal changes occur in biomechanics that may promote airway protection. We propose to investigate the longitudinal course of maturation of airway protection in preterm/term infants, with and without RLN damage. The use of a validated preterm animal model will permit the collection of detailed data, using invasive methods, including high-speed, biplanar videofluoroscopy, that are not appropriate for human patients. The work proposed here will determine how preterm birth effects the sensorimotor interactions that underlie successful airway protection as well as how RLN damage impacts those interactions through three specific aims: (SA1) Determine the longitudinal development of coordination between respiration and swallowing in control infant pigs born at term from birth through weaning; (SA2) Determine the longitudinal development of the coordination between respiration and swallowing after preterm birth using pigs delivered at the equivalent of human gestational age of 30-32 weeks; (SA3) Determine the interaction between the maturation of airway protection and RLN injury in both (SA3a) control term infants and (SA3b) preterm infants. By working with a proven and validated animal model of translational importance, the study proposed here will provide data on the underlying normal and pathophysiologic mechanisms that cause failure of airway protection in preterm infants. These data, collected longitudinally and in sufficient quantity to assess within individual variation and ontogenetic changes within individuals, will provide insight not possible from human patients. Such data will change our understanding of the potential for recovery and treatment recommendations. Furthermore these data can be the basis for designing intervention strategies based on understanding of the mechanisms underlying the pathophysiology.