Projektakademie Medizintechnik - simulation of obstructive sleepapnea syndrome (OSAS) in a mouse model using "LivingLab"

背景：阻塞性睡眠呼吸暂停综合征(OSAS)在西方工业国家的发病率呈上升趋势。睡眠障碍自主地代表着高血压、动脉硬化以及最近的2型糖尿病的风险因素。低氧是由睡眠中的呼吸暂停阶段(每小时15到100次)引起的，在这一过程中起着主要作用。这一现象已经通过慢性间歇性低氧(CIH)在小鼠模型中模拟。然而，CIH小鼠模型还不能完全显示和解决病理生理学问题，特别是胰岛素抵抗作为2型糖尿病的主要因素的发生，即使经过几周的OSAS模拟，也不能得到可靠的证实。一个决定性因素可能是模型骨骼肌中微循环的差异。初步研究首次表明，在大多数OSAS患者中，骨骼肌毛细管化显著减少，而在CIH小鼠模型中，骨骼肌毛细血管显著增加。这方面可能是以前的CIH小鼠模型的关键弱点。本项目的目的：真实和完整地复制OSAS中骨骼肌的巨大代谢和血管风险，最终并首次以现实的方式评估病理生理学和(如果可能的话)治疗方法。

Background: The incidence of obstructive sleep apnea syndrome (OSAS) is rising in western industrial nations. The sleep disorder autonomously represents a risk factor for high blood pressure, arteriosclerosis and lately also type 2 diabetes. Hypoxia, which is caused by apnea phases during sleep (15 to >100/h) plays a major role in this process. This phenomenon has been simulated in a mouse model through chronic intermittent hypoxia (CIH). However, the CIH mouse model has not been able to show and solve pathophysiology entirely.Especially the occurrence of insulin resistance as a main factor for type 2 diabetes could not be reliably verified, even after several weeks of OSAS simulation. A determining factor could be differences in microcirculation in the models skeletal muscles. Preliminary studies showed for the first time that capillarization of the skeletal muscle significantly decreases in the majority of OSAS patients, whereas it significantly increases in the CIH mouse model. This aspect could be the crucial weak point of the previous CIH mouse model.Aim of the project: To realistically and entirely reproduce the massive metabolic and vascular risks of the skeletal muscle in OSAS to eventually and for the first time evaluate pathophysiology and (if possible) therapeutic approaches in a realistic way.