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骨骼肌毛细血管化减少和葡萄糖不耐受。

Reduced skeletal muscle capillarization and glucose intolerance.

作者信息

Prior Steven J, McKenzie Michael J, Joseph Lyndon J, Ivey Frederick M, Macko Richard F, Hafer-Macko Charlene E, Ryan Alice S

机构信息

Baltimore Geriatric Research, Education and Clinical Center, VA Maryland Health Care System, Baltimore, Maryland 21201, USA.

出版信息

Microcirculation. 2009 Apr;16(3):203-12. doi: 10.1080/10739680802502423. Epub 2009 Feb 16.

Abstract

OBJECTIVE

Reduced capillarization in hemiparetic skeletal muscle of chronic stroke patients can limit insulin, glucose, and oxygen supply to muscle, thereby contributing to impaired glucose metabolism and cardiovascular deconditioning. We hypothesized that compared to sedentary controls, stroke subjects have reduced skeletal muscle capillarization that is associated with glucose intolerance and reduced peak oxygen consumption (Vo(2peak)).

METHODS

Twelve chronic stroke subjects (ages, 62.1+/-2.8 years), and matched sedentary controls with impaired (n=12) or normal (n=12) glucose tolerance underwent oral glucose tolerance tests, exercise tests, and vastus lateralis biopsies.

RESULTS

Stroke subjects had lower capillarization in hemiparetic muscle than in nonparetic muscle and normal glucose tolerant controls ( approximately 22 and approximately 28%, respectively; P<0.05) and had similar bilateral capillarization, compared to controls with impaired glucose tolerance. Capillary density in hemiparetic muscle inversely correlated with 120-minute glucose (r=-0.70, P<0.01) and glucose area under the curve (r=-0.78, P<0.01). Vo(2peak) was approximately 40% lower in stroke subjects, compared to controls (P<0.001), but did not correlate with capillarization (P=n.s.).

CONCLUSIONS

Hemiparetic muscle capillarization is reduced after stroke, and reduced capillarization is associated with glucose intolerance in stroke and control subjects. Interventions to increase skeletal muscle capillarization may prove beneficial for improving glucose metabolism in chronic stroke patients.

摘要

目的

慢性中风患者偏瘫骨骼肌的毛细血管化减少会限制胰岛素、葡萄糖和氧气向肌肉的供应,从而导致葡萄糖代谢受损和心血管功能失调。我们假设,与久坐不动的对照组相比,中风患者的骨骼肌毛细血管化减少,这与葡萄糖不耐受和峰值耗氧量(Vo₂peak)降低有关。

方法

12名慢性中风患者(年龄62.1±2.8岁)以及匹配的久坐不动的葡萄糖耐量受损(n = 12)或正常(n = 12)的对照组进行口服葡萄糖耐量试验、运动试验和股外侧肌活检。

结果

中风患者偏瘫侧肌肉的毛细血管化低于非偏瘫侧肌肉和葡萄糖耐量正常的对照组(分别约为22%和约28%;P<0.05),与葡萄糖耐量受损的对照组相比,双侧毛细血管化相似。偏瘫侧肌肉的毛细血管密度与120分钟血糖(r = -0.70,P<0.01)和曲线下血糖面积(r = -0.78,P<0.01)呈负相关。与对照组相比,中风患者的Vo₂peak约低40%(P<0.001),但与毛细血管化无关(P无统计学意义)。

结论

中风后偏瘫侧肌肉的毛细血管化减少,毛细血管化减少与中风患者和对照组的葡萄糖不耐受有关。增加骨骼肌毛细血管化的干预措施可能对改善慢性中风患者的葡萄糖代谢有益。

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