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J Appl Physiol 105: 381, 2008; doi:10.1152/japplphysiol.90301.2008
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: Because of their accessibility, cutaneous microvessels are suitable for mechanistic studies on vascular dysfunction. These examinations are associated with negligible discomfort for the study person and could perhaps, in the future, be used for cardiovascular risk determination. The studies of deficits in thermoregulatory function presented here are good examples on how such studies can be performed (4). The cutaneous vessels are effector organs for thermoregulation. The situation becomes more complicated when the skin is used as a surrogate circulatory bed. The underlying assumption is then that vascular dysfunction is a general phenomenon in a systemic disease process. This needs not always be true and the relevance of the surrogate needs to be critically examined. The impairment might not to be uniformly distributed (2) and there could also be changes over time; for example we have found that patients with advanced atherosclerotic manifestations do not always have cutaneous vascular impairment.

As the authors point out, the vascular reactivity is an integrated net response induced by a number of pathways. In many cases dysfunction is tightly associated with inflammation (1, 3). This gives both problems and opportunities since the characteristics of inflammation are variable. It could thus be that not all inflammatory conditions might be associated with vascular dysfunction and that some cases (inflammation not associated with increased cardiovascular risk) will temporarily reduce the vascular reactivity. It is our belief that there is a need to compare with several other vascular beds to make a general statement.

FOOTNOTES


Address for reprint requests and other correspondence: L. Edvinsson, Dept. of Medicine, Univ. Hospital, Lund, Sweden 22185 (e-mail: lars.edvinsson{at}med.lu.se)

REFERENCES

  1. Andersson SE, Edvinsson ML, Edvinsson L. Cutaneous vascular reactivity is reduced by aging and by heart failure; relation to inflammatory activity and endothelial function. Clin Sci 105: 699–707, 2003.[CrossRef][Web of Science][Medline]
  2. Baggia S, Perkins K, Greenberg B. Endothelium-dependent relaxation is not uniformly impaired in chronic heart failure. J Cardiovasc Pharmacol 29: 389–396, 1997.[CrossRef][Web of Science][Medline]
  3. Hingorani AD, Cross J, Kharbanda RK, Mullen MJ, Bhagat K, Taylor M, Donald AE, Palacios M, Griffin GE, Deanfield JE, MacAllister RJ, Vallance P. Acute systemic inflammation impairs endothelium-dependent dilatation in humans. Circulation 102: 994–999, 2000.[Abstract/Free Full Text]
  4. Holowatz LA, Thompson-Torgenson 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]

Lars Edvinsson
Sven E. Andersson
Institute of Clinical Science, Lund University Hospital, Lund, Sweden





This Article
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