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J Appl Physiol 105: 376, 2008; doi:10.1152/japplphysiol.90345.2008
8750-7587/08 $8.00
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LETTER TO THE EDITOR

Commentary on Viewpoint: The human cutaneous circulation as a model of generalized microvascular function

TO THE EDITOR: the increasing prevalence of chronic disease states (diabetes, cardiovascular disease) is a global epidemic, and these pathologies have adverse effects on vascular and endothelial function. The Viewpoint by Holowatz and colleagues (2) accurately points to the need for non- to minimally invasive techniques by which to investigate, and better understand, the effect of chronic disease on vascular and endothelial function. In human skin, laser-Doppler flowmetry combined with intradermal microdialysis is a powerful technique by which to perform in vivo mechanistic studies in both health and disease. Using these techniques, our understanding of the effect of disease on the (micro)vascular response to various stimuli has been greatly advanced, which may lead to an improved ability to treat and manage the associated vascular/endothelial dysfunction.

Although investigations using the cutaneous vasculature afford several advantages, it may be prudent to use cautious optimism when extrapolating findings from human skin to other vascular beds, be it conduit vessels or microvasculature. For example, postocclusive reactive hyperemia (PORH) in conduit arteries appears to be NO dependent (3), whereas, in human skin, PORH appears to be NO independent (5). In addition, cutaneous and skeletal muscle responses during PORH may demonstrate different dynamics (1), suggesting the possibility of different control features. Inasmuch as PORH in the skin appears to be NO independent while the cutaneous vascular response to local heating contains a large NO-dependent component (4), one must further determine whether the cutaneous vascular response under question represents microvascular or endothelial function. Nevertheless, the ability to perform minimally invasive in vivo mechanistic studies in human skin could have a profound influence on our understanding of how disease states adversely affect vascular/endothelial function.

FOOTNOTES


Address for reprint requests and other correspondence: B. J. Wong, Dept. of Kinesiology, 1A Natatorium, Kansas State Univ., Manhattan, KS 66506 (e-mail: bwong{at}ksu.edu)

REFERENCES

  1. Addor G, Delachaux A, Dischl B, Hayoz D, Liaudet L, Waeber B, Feihi F. A comparative study of reactive hyperemia in human forearm skin and muscle. Physiol Res. In press.
  2. Holowatz LA, Thompson-Torgerson CS, Kenney WL. Viewpoint: The human cutaneous circulation as a model of generalized microvascular function. J Appl Physiol; doi:10.1152/japplphysiol.00858.2007.[Free Full Text]
  3. Joannides R, Haefeli WE, Linder L, Richard V, Bakkali E, Thuillez C, Lüscher TF. Nitric oxide is responsible for flow-dependent dilatation of human peripheral conduit arteries in vivo. Circulation 91: 1314–1319, 1995.[Abstract/Free Full Text]
  4. Minson CT, Berry LT, Joyner MJ. Nitric oxide and neutrally mediated regulation of skin blood flow during local heating. J Appl Physiol 91: 1619–1626, 2001.[Abstract/Free Full Text]
  5. Wong BJ, Wilkins BW, Holowatz LA, Minson CT. Nitric oxide synthase inhibition does not alter the reactive hyperemic response in the cutaneous circulation. J Appl Physiol 95: 504–510, 2003.[Abstract/Free Full Text]

Thomas J. Barstow
Brett J. Wong
 Department of Kinesiology, Kansas State University, Manhattan, Kansas





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