Gas Supply, Demand and Middle Ear Gas Balance

天然气供需与中期天然气平衡 根据对猴子的研究结果，我们开发了一个多层次的、交互的反馈模型来描述 中耳(ME)压力调节的效率和失调的病理生理后果。 该模型只需要系统几何和所表示的物理化学性质的知识 气体和组织来预测ME压力的行为和有利于在 正常和病理状态。如果有效，该模型允许测试先前建议的ME的机制 压力调节，确定导致ME压力失调(MEPD)/中耳炎的因果序列 与渗出(OME)有关，并确定可通过治疗来预防或“治愈”的中介联系 MEPD相关疾病的表现。该型号尚未根据人类ME的规格进行校准 它的任何具体预测也没有对临床疾病的适用性进行测试。这些实验包括 在这个翻译研究项目中，开发了一个经验数据库，用于测试模型的预测 单个组件的级别，以及完全组装时的级别。具体地说，我们将描述 影响ME压力的三条主要途径的气体交换，即被动交换 鼓膜(TM)和中耳粘膜(MEM)与咽鼓管的主动/被动交换 管子(ET)。因为用于测试人类ET功能(ETF)的协议通常仅限于耳部不完整 ，我们计划扩展现有的测试，并开发新的协议来测试完整的TM的耳朵 压力室的受控环境。此外，我们还将评估与我们的 病毒上呼吸道感染(VURI)期间MEPD介导的OM表达的描述；即1) 宪法ETF定义了VURI期间耳科并发症的风险；2)TransMEM惰性气体交换是 局部神经源性炎症增加；3)MEM炎症、水肿和积液在特定的 临界ME负压约为-200 mm H2O，4)跨MEM惰性气体交换增加 内膜发炎。

GAS SUPPLY, DEMAND AND MIDDLE EAR GAS BALANCE From the results of studies in monkeys, we developed a multi-level, interactive, feedback model to describe the efficiency of middle ear (ME) pressure-regulation and the pathophysiological consequences of disregulation. That model requires knowledge only of system geometry and the physiochemical properties of represented gases and tissues to predict the behavior of ME pressure and the conditions that favor transitions between normal and pathological states. If valid, the model allows for testing previously suggested mechanisms of ME pressure-regulation, defining the causal sequences leading to ME pressure disregulation (MEPD)/otitis media with effusion (OME) and identifying mediational links that could be targeted by treatments to prevent or "cure" MEPD related disease expressions. That model has not been calibrated to the specifications of the human ME nor have any of its specific predictions been tested for applicability to clinical disease. The experiments included in this translational research project develop an empirical database for testing the predictions of the model at the levels of individual components and when fully assembled. Specifically, we will characterize the properties of gas exchange across the three main pathways that affect ME pressure, i.e. passive exchange across the tympanic membrane (TM) and middle ear mucosa (MEM), and active/passive exchange across the Eustachian tube (ET). Because protocols for testing ET function (ETF) in humans are generally limited to ears with a nonintact TM, we plan to expand existing tests and to develop new protocols for testing ears with an intact TM in the controlled environment of a pressure-chamber. Also, we will evaluate four hypotheses relevant to our description of MEPD mediated OM expression during a viral upper-respiratory tract infection (vURI); i.e. 1) constitutional ETF defines the risk of otological complications during a vURI; 2) transMEM inert gas exchange is increased by local, neurogenic inflammation; 3) MEM inflammation, edema and effusion develop at a specific critical ME underpressure of approximately -200 mmH2O, and 4) transMEM inert gas exchange is increased by MEM inflammation.