Background: Asthma and obstructive sleep apnea (OSA) are highly prevalent chronic conditions, and both are associated with systemic hypertension. Additionally, asthma and OSA reciprocally interact, mutually exacerbating each other. In this study, we tested the effect of allergen-induced lower airway inflammation and concurrent chronic intermittent hypoxia (CIH) on systemic blood pressure (BP), pulmonary function and pro-inflammatory cytokines, in a rat model. Methods: Brown Norway rats were exposed to 43 days of normoxia (NORM) or CIH, concurrent with weekly House Dust Mite (HDM) challenges. BP was measured 1 day after the last HDM challenge. On Day 44, pulmonary function was tested and blood for Th-2 and Th-1 cytokine levels was collected. Results: HDM significantly increased Mean (p= 0.002), systolic (p=0.003) and diastolic (p=0.004) BP, compared to saline-challenged controls. Higher mean BP significantly correlated to increased total respiratory system resistance (R² = 0.266, p=0.002), driven by an association with parenchymal tissue dampening (R² = 0.166, p=0.016). HDM relative to saline-challenged controls increased the expression of serum IL-6 (p=0.008), but no relationships of systemic BP with IL-6 or any other cytokines were found. CIH did not alter the allergen-induced responses on BP, although it tended to increase the expression of serum IL-6 (p=0.06) and MCP-1 (p=0.09), regardless of HDM challenge. Conclusions: Chronic allergen-induced airway inflammation results in systemic hypertension that is correlated to the degree of distal airway obstruction induced by the allergen. These effects do not appear to be explained by the associated systemic inflammation.

中文翻译：

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过敏性气道炎症和慢性间歇性低氧对全身血压的影响。

背景：哮喘和阻塞性睡眠呼吸暂停（OSA）是高度流行的慢性疾病，都与系统性高血压相关。此外，哮喘和OSA相互影响，相互加剧。在这项研究中，我们在大鼠模型中测试了变应原诱导的下呼吸道炎症和并发的慢性​​间歇性缺氧（CIH）对全身血压（BP），肺功能和促炎细胞因子的影响。方法：褐挪威大鼠暴露于常氧（NORM）或CIH的43天，同时每周进行一次室内除尘螨（HDM）攻击。最后一次HDM攻击后1天测量BP。在第44天，测试肺功能并收集血液中的Th-2和Th-1细胞因子水平。结果：HDM显着提高了均值（p = 0.002），收缩压（p = 0.003）和舒张压（p = 0.004）BP，与生理盐水挑战的对照组相比。较高的平均血压显着与总呼吸系统阻力增加相关（R² = 0.266，p = 0.002），是由与实质组织衰减相关的（R ² = 0.166，p = 0.016）驱动的。HDM相对于生理盐水挑战的对照组增加了血清IL-6的表达（p = 0.008），但未发现全身性BP与IL-6或任何其他细胞因子的关系。CIH不会改变对BP的过敏原诱导的反应，尽管它倾向于增加血清IL-6（p = 0.06）和MCP-1（p = 0.09）的表达，而与HDM挑战无关。结论：慢性变应原引起的气道炎症导致全身性高血压，其与变应原引起的远端气道阻塞程度有关。这些作用似乎不能由相关的全身性炎症解释。