The neuronal system that controls respiration creates plasticity in response to physiological changes. Chronic sustained hypoxia causes neuroplasticity that contributes to ventilatory acclimatization to hypoxia (VAH). The purpose of this study is to explain the potential roles of the VAH mechanism developing because of chronic sustained hypoxia on respiratory neuroplasticity of vascular endothelial growth factor (VEGF) receptor activation on the nucleus tractus solitarius (NTS) and phrenic nerve. In this study 24 adult male Sprague–Dawley rats were used. Subjects were separated into four groups, a moderate-sham (mSHAM), severed-sham (sSHAM), moderate chronic sustained hypoxia (mCSH), and severed chronic sustained hypoxia (sCSH). Normoxic group (mSHAM and sSHAM) rats were exposed to 21% O₂ level (7 days) in the normobaric room while hypoxia group (mCSH and sCSH) rats were exposed to 13% and 10% O₂ level (7 days). Different protocols were applied for normoxic and hypoxia groups and ventilation, respiratory frequency, and tidal volume measurements were made with whole-body plethysmography. After the test HIF-1α, erythropoietin (EPO), and VEGFR-2 expressions on the NTS region in the medulla oblongata and phrenic nerve motor neurons in spinal cord tissue were analyzed using the immunohistochemical stain method. Examinations on the medulla oblongata and spinal cord tissues revealed that HIF-1α, EPO, and VEGFR-2 expressions increased in hypoxia groups compared to normoxic groups while a similar increase was also seen when respiratory parameters were assessed. Consequently, learning about VAH-related neuroplasticity mechanisms developed as a result of chronic continuous hypoxia will contribute to developing new therapeutical approaches to various diseases causing respiratory failure using brain plasticity without recourse to medicines.

中文翻译：

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慢性持续缺氧后大鼠孤束核和膈神经血管内皮生长因子受体依赖性神经可塑性的研究

控制呼吸的神经元系统会根据生理变化产生可塑性。慢性持续缺氧导致神经可塑性，有助于通气适应缺氧 (VAH)。本研究的目的是解释由于慢性持续缺氧而发展的 VAH 机制对孤束核 (NTS) 和膈神经上血管内皮生长因子 (VEGF) 受体激活的呼吸神经可塑性的潜在作用。在这项研究中，使用了 24 只成年雄性 Sprague-Dawley 大鼠。受试者被分为四组，中度假（mSHAM）、切断假（sSHAM）、中度慢性持续缺氧（mCSH）和切断慢性持续缺氧（sCSH）。常氧组（mSHAM 和 sSHAM）大鼠在常压室暴露于 21% O2 水平（7 天），而缺氧组（mCSH 和 sCSH）大鼠暴露于 13% 和 10% O2 水平（7 天）。对常氧组和缺氧组应用不同的方案，并通过全身体积描记法进行通气、呼吸频率和潮气量测量。试验后采用免疫组化染色法分析延髓NTS区和脊髓组织膈神经运动神经元中HIF-1α、促红细胞生成素(EPO)和VEGFR-2的表达。对延髓和脊髓组织的检查显示，与常氧组相比，缺氧组的 HIF-1α、EPO 和 VEGFR-2 表达增加，而在评估呼吸参数时也观察到类似的增加。最后，