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1 Department of Cardiovascular Physiology, Okayama University Graduate School of Medicine and Dentistry, Okayama, Japan; Department of Physical Therapy, Suzuka University of Medical Science, Suzuka, Japan
2 Department of Cardiovascular Physiology, Okayama University Graduate School of Medicine and Dentistry, Okayama, Japan; Department of Food and Nutrition, Okayama Gakuin University, Kurashiki, Japan
3 Department of Physical Therapy, Suzuka University of Medical Science, Suzuka, Japan
4 Department of Cardiovascular Physiology, Okayama University Graduate School of Medicine and Dentistry, Okayama, Japan
* To whom correspondence should be addressed. E-mail: fujino{at}suzuka-u.ac.jp.
Little is known about the mechanisms responsible for the adaptation and changes in the capillary network of hindlimb unweighting (HU)-induced atrophied skeletal muscle, especially the coupling between functional and structural alterations of intercapillary anastomoses and tortuosity of capillaries. We hypothesized that muscle atrophy by HU leads to the apoptotic regression of the capillaries and intercapillary anastomoses with their functional alteration in hemodynamics. To clarify the three-dimensional (3-D) architecture of the capillary network, contrast medium-injected rat soleus muscles were visualized clearly using a confocal laser scanning microscope, and sections were stained by terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL) and with anti-von Willebrand factor. In vivo, the red blood cell velocity of soleus muscle capillaries were determined with a pencil-lens intravital microscope brought into direct contact with the soleus surface. After HU, the total muscle mass, myofibril protein mass and slow type myosin heavy chain content were significantly lower. The number of capillaries paralleling muscle fiber and red blood cells velocity were higher in atrophied soleus. However, the mean capillary volume and capillary luminal diameter were significantly smaller after HU than in the age-matched control group. In addition, we found the number of anastomoses and the tortuosity were significantly lower and TUNEL-positive endothelial cells were observed in atrophied soleus muscles, especially the anastomoses and/or tortuous capillaries. These results indicate that muscle atrophy by hindlimb unweighting generates structural alterations in the capillary network, and apoptosis appears to occur in the endothelial cell of the muscle capillaries.
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