Literature DB >> 22726882

Human skeletal muscle feed arteries: evidence of regulatory potential.

S J Ives1, R H I Andtbacka, S-Y Park, A J Donato, J R Gifford, R D Noyes, L A Lesniewski, R S Richardson.   

Abstract

AIM: Recently, it has been recognized that human skeletal muscle feed arteries can be harvested during exploratory surgery for melanoma. This approach provides vessels for in vitro study from a wide spectrum of relatively healthy humans. Although, the regulatory role of skeletal muscle feed arteries in rodent models has been documented, whether such vessels in humans possess this functionality is unknown.
METHODS: Therefore, skeletal muscle feed arteries (~950 μm OD) from 10 humans (48 ± 4, 27-64 years) were studied using pressure myography. Vessel function was assessed using potassium chloride (KCl), phenylephrine (PE), acetylcholine (ACh) and sodium nitroprusside (SNP) concentration-response curves (CRCs) to characterize non-receptor and receptor-mediated vasoconstriction as well as endothelium-dependent and independent vasodilation respectively. To understand the physiological relevance of the diameter changes as a result of pharmacological stimulation, the estimated conductance ratio (CR) was calculated.
RESULTS: Vessel function protocols revealed significant vasoconstriction in response to PE and KCl (35 ± 6; 43 ± 9%vasoconstriction, respectively) and significant vasodilation with ACh and SNP (85 ± 7; 121 ± 17% vasodilation, respectively). Both PE and KCl significantly reduced the CR (0.26 ± 0.05 and 0.23 ± 0.07, respectively), whereas ACh and SNP increased the CR (2.56 ± 0.10 and 5.32 ± 1.3, respectively).
CONCLUSION: These novel findings provide evidence that human skeletal muscle feed arteries are capable of generating significant diameter changes that would translate into significant changes in vascular conductance. Thus, human skeletal muscle feed arteries likely play a significant role in regulating vascular conductance and subsequently blood flow in vivo.
© 2012 The Authors Acta Physiologica © 2012 Scandinavian Physiological Society.

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Year:  2012        PMID: 22726882      PMCID: PMC4722951          DOI: 10.1111/j.1748-1716.2012.02464.x

Source DB:  PubMed          Journal:  Acta Physiol (Oxf)        ISSN: 1748-1708            Impact factor:   6.311


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