McGuire Michelle, MacDermott Mary, Bradford Aidan
Department of Physiology, Royal College of Surgeons in Ireland, St. Stephen's Green, Dublin 2, Ireland.
Chest. 2002 Oct;122(4):1400-6. doi: 10.1378/chest.122.4.1400.
Obstructive sleep apnea (OSA) is caused by episodes of upper airway (UA) obstruction due to an inability of UA muscles such as the geniohyoids and sternohyoids to maintain airway patency. This results in chronic episodic hypercapnic hypoxia. Chronic continuous hypoxia and episodic hypocapnic hypoxia affect skeletal muscle structure and function, but the effects of chronic episodic hypercapnic hypoxia on UA muscle structure and function are unknown.
Rats breathed air and hypercapnic hypoxic gas twice per minute for 8 h/d for 5 weeks in order to mimic the intermittent hypercapnic hypoxia of OSA in humans. Isometric contractile properties were determined using strips of isolated geniohyoid and sternohyoid muscles in physiologic saline solution at 30 degrees C. Fiber-type distribution was determined by adenosine triphosphatase staining.
For both muscles, chronic episodic hypercapnic hypoxia had no significant effect on twitch or tetanic tension, twitch/tetanic tension ratio, and tension-frequency relationship. There was a significant (p < 0.05) increase in geniohyoid fatigue (50.5 +/- 6.6% vs 43.6 +/- 5.8% of initial tension), but sternohyoid fatigue was reduced (31.5 +/- 5.2% vs 37.8 +/- 6.0% of initial tension). Geniohyoid type 1 fibers were reduced and type 2B fibers increased, whereas sternohyoid muscle had an increase in type 1 and 2A fibers and a decrease in type 2B fibers.
Chronic episodic hypercapnic hypoxia alters UA muscle structure and function, changes that may affect the regulation of UA patency.
阻塞性睡眠呼吸暂停（OSA）是由于颏舌骨肌和胸骨舌骨肌等上气道（UA）肌肉无法维持气道通畅，导致上气道阻塞发作所致。这会导致慢性间歇性高碳酸血症性缺氧。慢性持续性缺氧和间歇性低碳酸血症性缺氧会影响骨骼肌的结构和功能，但慢性间歇性高碳酸血症性缺氧对UA肌肉结构和功能的影响尚不清楚。
为模拟人类OSA的间歇性高碳酸血症性缺氧，大鼠每天呼吸空气和高碳酸血症性缺氧气体两次，每次持续1分钟，共持续8小时，持续5周。在30℃的生理盐溶液中，使用分离的颏舌骨肌和胸骨舌骨肌条带测定等长收缩特性。通过三磷酸腺苷酶染色确定纤维类型分布。
对于这两块肌肉，慢性间歇性高碳酸血症性缺氧对抽搐或强直张力、抽搐/强直张力比值以及张力-频率关系均无显著影响。颏舌骨肌疲劳显著增加（初始张力的50.5±6.6%对43.6±5.8%），但胸骨舌骨肌疲劳减轻（初始张力的31.5±5.2%对37.8±6.0%）。颏舌骨肌1型纤维减少，2B型纤维增加，而胸骨舌骨肌1型和2A型纤维增加，2B型纤维减少。
慢性间歇性高碳酸血症性缺氧会改变UA肌肉的结构和功能，这些变化可能会影响UA通畅性的调节。
