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Enterococcus faecium strain R30 increases red blood cell velocity and prevents capillary regression in the soleus of hindlimb‐unloaded rats via the eNOS / VEGF pathway
Author(s) -
Hirayama Yusuke,
Nakanishi Ryosuke,
Tategaki Airo,
Maeshige Noriaki,
Kondo Hiroyo,
Ishihara Akihiko,
Roy Roland R.,
Fujino Hidemi
Publication year - 2017
Publication title -
microcirculation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.793
H-Index - 83
eISSN - 1549-8719
pISSN - 1073-9688
DOI - 10.1111/micc.12356
Subject(s) - enos , vegf receptors , strain (injury) , enterococcus faecium , hindlimb , angiogenesis , chemistry , biology , microbiology and biotechnology , anatomy , endocrinology , biochemistry , nitric oxide , cancer research , nitric oxide synthase , antibiotics
Objective A chronic decrease in neuromuscular activity results in atrophy and capillary regression in skeletal muscles. The purposes of this study were to determine the effects of Enterococcus faecium strain R30 (R30) administration on (i) the hemodynamics of the rat soleus muscle, and (ii) the capillary regression normally associated with HU . Methods Experiment 1: The V RBC was measured for up to 1 hour after administration of R30 with or without the β‐blocker propranolol. Experiment 2: R30 was administered daily to control and HU rats for 2 weeks. Mean capillary luminal diameter, volume, and the levels of eNOS and VEGF protein were measured. Results Experiment 1: V RBC was faster 20, 40, and 60 minutes after than before the administration of R30: This effect was suppressed by propranolol administration. Experiment 2: R30 administration during HU increased capillary luminal diameter and volume and eNOS and VEGF protein levels in the soleus of HU rats. Conclusions The results suggest that R30 increases V RBC in the soleus muscle via muscle sympathetic nerve activity (Experiment 1) and that R30 supplementation lessens the capillary regression normally associated with HU via the eNOS / VEGF pathway (Experiment 2).