HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) All Versions of this Article: 293/1/H1    most recent 00063.2007v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Web of Science (14) Citing Articles via Google Scholar Google Scholar Articles by Safar, M. E. Articles by Lacolley, P. Search for Related Content PubMed PubMed Citation Articles by Safar, M. E. Articles by Lacolley, P.

INVITED REVIEW

Disturbance of macro- and microcirculation: relations with pulse pressure and cardiac organ damage

¹Paris-Descartes University, Faculty of Medicine; Hôtel-Dieu Hospital, Diagnosis Center Assistance Publique-Hôpitaux de Paris, Paris, France; and ²Faculté de Médecine de Nancy, Nancy University, Nancy, France

Whereas large arteries dampen oscillations resulting from intermittent ventricular ejection, small arteries steadily deliver optimal blood flow to various organs as the heart. The transition from pulsatile to steady pressure is influenced by several factors as wave travel, damping, and reflections, which are mainly determined by the impedance mismatch between large vessels and arteriolar bifurcations. The mechanism(s) behind the dampening of pressure wave in the periphery and the links between central and peripheral pulsatile pressure (PP) may determine cardiac damage. Active pathways participate to pulse widening and changes in pulse amplitude in microvessels. Steady and cyclic stresses operate through different transduction mechanisms, the former being focal adhesion kinase and the latter being free radicals and oxidative stress. Independently of mechanics, calcifications and attachment molecules contribute to enhance vessel wall stiffness through changes in collagen cross-links, proteoglycans, integrins, and fibronectin. Enhanced PP transmission may thus occur and precipitate organ damage at each time that autoregulatory mechanisms, normally protecting the heart from vascular injury, are blunted. Such circumstances, observed in old subjects with systolic hypertension and/or Type 2 diabetes mellitus, particularly under high-sodium diet, cause cardiac damage and explain why increased PP and arterial stiffness are significant predictors of morbidity and mortality in the elderly.

microvessels; end-organ damage

This article has been cited by other articles:

				G. F. Mitchell Effects of central arterial aging on the structure and function of the peripheral vasculature: implications for end-organ damage J Appl Physiol, November 1, 2008; 105(5): 1652 - 1660. [Abstract] [Full Text] [PDF]

				M. Rakobowchuk, S. Tanguay, K. A. Burgomaster, K. R. Howarth, M. J. Gibala, and M. J. MacDonald Sprint interval and traditional endurance training induce similar improvements in peripheral arterial stiffness and flow-mediated dilation in healthy humans Am J Physiol Regulatory Integrative Comp Physiol, July 1, 2008; 295(1): R236 - R242. [Abstract] [Full Text] [PDF]