Suppr超能文献

大鼠比目鱼肌离心运动后的微循环:硝苯地平的作用

Microcirculation in rat soleus muscle after eccentric exercise: the effect of nifedipine.

作者信息

Heap S J, Fulgenzi G L, Hudlicka O

机构信息

Department of Physiology, Division of Medicine, University of Birmingham Medical School, Birmingham, B15 2TT, UK.

出版信息

Eur J Appl Physiol. 2006 Aug;97(6):687-94. doi: 10.1007/s00421-006-0239-0. Epub 2006 Jun 13.

Abstract

This paper explores the role of the calcium entry blocker nifedipine in the explanation of eccentric exercise-induced fibre damage by changes in skeletal muscle microcirculation. Eccentric exercise (EE) was induced by indirect stimulation of rat soleus muscle in its lengthening phase during cycling. Muscle damage was assessed by histology, electron microscopy and muscle tension 48 h later. Diameters of arterioles and venules, their response to dilator and constrictor stimuli and pattern of capillary flow were measured in epiiluminated muscles using intravital microscopy. Tetanic tension developed by EE muscles was lower (8.60 +/- 1.02, means +/- SEM, n = 8 N g(-1) wet weight compared to 12.25 +/- 0.56 in controls, P < 0.01). Electron microscopy showed changes similar to those in muscles exposed to EE by downhill running (Z line streaming, disruption of sarcolemma, swollen tubules). A total of 16% of muscle fibres were damaged, and fibre areas and interstitial space were enlarged. Capillary red blood cell flow showed tendency to a greater intermittency. Large venules were narrower, but arterioles and smaller venules had diameters similar to control muscles. Vessel dilatation to topically applied 10(-4) M adenosine was attenuated. Daily administration of calcium entry blocker nifedipine by gavage (2 mg/kg/day in two equal doses) removed the narrowing of venules, restored the dilator response of all vessels to adenosine and increased capillary:fibre ratio. The percentage of damaged fibres decreased to 4.7 and the size of the interstitial space and fibre areas was normalized. Thus muscle damage caused by eccentric exercise was attenuated by nifedipine due to its beneficial effect on muscle microcirculation, which was impaired by eccentric exercise.

摘要

本文探讨了钙通道阻滞剂硝苯地平在解释离心运动引起的纤维损伤中所起的作用,该损伤是由骨骼肌微循环变化导致的。通过在大鼠比目鱼肌处于骑车过程中的拉长阶段进行间接刺激来诱发离心运动(EE)。48小时后,通过组织学、电子显微镜和肌肉张力评估肌肉损伤情况。使用活体显微镜在落射光照明的肌肉中测量小动脉和小静脉的直径、它们对扩张剂和收缩剂刺激的反应以及毛细血管血流模式。EE肌肉产生的强直张力较低(8.60±1.02,均值±标准误,n = 8 N g⁻¹湿重,而对照组为12.25±0.56,P < 0.01)。电子显微镜显示的变化与下坡跑导致的暴露于EE的肌肉中的变化相似(Z线流、肌膜破坏、小管肿胀)。总共16%的肌纤维受损,纤维面积和间隙增大。毛细血管红细胞血流显示出更大的间歇性趋势。大静脉变窄,但小动脉和小静脉的直径与对照肌肉相似。局部应用10⁻⁴ M腺苷时血管扩张减弱。通过灌胃每日给予钙通道阻滞剂硝苯地平(2 mg/kg/天,分两等份剂量)可消除静脉的变窄,恢复所有血管对腺苷的扩张反应,并增加毛细血管与纤维的比例。受损纤维的百分比降至4.7%,间隙和纤维面积的大小恢复正常。因此,硝苯地平可减轻离心运动引起的肌肉损伤,这是由于其对肌肉微循环具有有益作用,而离心运动会损害该微循环。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验