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长期习惯性打鼾合并阻塞性睡眠呼吸暂停患者的腭肌中线粒体结构和氧化活性异常。

Abnormal mitochondria organization and oxidative activity in the palate muscles of long-term snorers with obstructive sleep apnea.

机构信息

Department of Integrative Medical Biology, Section for Anatomy, Umeå University, Umeå, Sweden.

出版信息

Respiration. 2012;83(5):407-17. doi: 10.1159/000336040. Epub 2012 Mar 1.

Abstract

BACKGROUND

Histopathological alterations and a reduced number of capillaries have been observed in the palate muscles of snorers with obstructive sleep apnea syndrome (OSAS). These changes may create a substrate for decreased microcirculation, impaired aerobic metabolism and muscle dysfunction and contribute to upper airway obstruction during sleep.

OBJECTIVES

The aim was to analyze mitochondria distribution and oxidative enzyme activity in relation to capillary supply in the palate muscles of patients with a history of long-term snoring and OSAS.

METHODS

Palatopharyngeus (PP) and uvula (UV) muscle samples were obtained from 8 patients undergoing uvulopalatopharyngoplasty due to habitual snoring and OSAS. The muscles were analyzed with enzyme- and immunohistochemistry and morphometry.

RESULTS

Abnormalities in the internal organization of mitochondria and oxidative activity were observed in 39 ± 15% of the fibers in the PP and 4 ± 3% in the UV, but not in control samples. The majority of these fibers had a lobulated contour and trabecular internal organization of mitochondria. The number of capillaries around abnormal fibers (PP 0.9 ± 0.3, UV 0.4 ± 0.1) was lower than in fibers of a normal appearance in both patients (PP 1.4 ± 0.6, UV 1.2 ± 0.3) and references (PP 2.7 ± 0.7, UV 1.9 ± 0.9) (p < 0.05).

CONCLUSIONS

Abnormal mitochondrial distribution, a low capillary supply and signs of impaired oxidative activity suggest that muscle dysfunction of the palate muscles in long-term snorers may contribute to the upper airway obstruction during sleep. The cause of these abnormalities remains unclear, but local muscle and nerve trauma due to vibration and stretch is a possible etiology.

摘要

背景

阻塞性睡眠呼吸暂停综合征(OSAS)患者的腭肌中已经观察到组织病理学改变和毛细血管数量减少。这些变化可能为微循环减少、有氧代谢受损和肌肉功能障碍创造基质,并导致睡眠期间上气道阻塞。

目的

分析有长期打鼾和 OSAS 病史的患者腭肌中线粒体分布和氧化酶活性与毛细血管供应的关系。

方法

从 8 例行悬雍垂腭咽成形术的习惯性打鼾和 OSAS 患者中获取腭帆提肌(PP)和悬雍垂(UV)肌肉样本。使用酶和免疫组织化学以及形态计量学对肌肉进行分析。

结果

在 PP 中,39±15%的纤维和在 UV 中,4±3%的纤维出现线粒体内部结构和氧化活性异常,但在对照组样本中没有。这些纤维中的大多数具有分叶状轮廓和小梁状内部线粒体组织。异常纤维周围毛细血管的数量(PP 0.9±0.3,UV 0.4±0.1)低于患者(PP 1.4±0.6,UV 1.2±0.3)和参考值(PP 2.7±0.7,UV 1.9±0.9)中正常外观纤维的数量(p<0.05)。

结论

异常的线粒体分布、低毛细血管供应和氧化活性受损的迹象表明,长期打鼾患者腭肌的肌肉功能障碍可能导致睡眠期间上气道阻塞。这些异常的原因尚不清楚,但由于振动和拉伸导致的局部肌肉和神经损伤是一种可能的病因。

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