Inflammation has been implicated in the development of cardiovascular disease and a
potential underlying mechanism in the pathogenesis of impaired vascular function. Two
different but complementary approaches were utilized to determine the role of
inflammation on vascular function. First, to evaluate the effect of acute inflammation, we
induced muscle damage to both small and large muscle mass and measured vascular
function every 24 hours for up to 5 days of recovery. Eccentric exercise-induced muscle
damage, in both small and large muscle mass, resulted in a transient increase in central
arterial stiffness. Next, patients with systemic lupus erythematosus (SLE) were studied
as a model of chronic inflammation. Measurements of vascular function were compared
in habitually-exercising and sedentary SLE patients, and age-matched healthy controls.
Individuals with SLE demonstrated lower vascular function than healthy controls. When SLE patients were grouped by exercise status, habitually-exercising SLE patients
exhibited similar vascular function to healthy controls, and lower overall disease activity
compared with sedentary SLE patients, supporting the beneficial effect of regular
exercise in this population. Inflammatory biomarkers were associated with measures of
macro- and microvascular function. In conclusion, acute muscle damage and chronic
disease-related inflammation have a potent effect on measures of vascular function,
suggesting that inflammation plays a role in the pathogenesis of vascular dysfunction and is an important biomarker for cardiovascular risk. / text
| Identifer | oai:union.ndltd.org:UTEXAS/oai:repositories.lib.utexas.edu:2152/6529 |
| Date | 14 October 2009 |
| Creators | Barnes, Jill Nicole |
| Source Sets | University of Texas |
| Language | English |
| Detected Language | English |
| Format | electronic |
| Rights | Copyright is held by the author. Presentation of this material on the Libraries' web site by University Libraries, The University of Texas at Austin was made possible under a limited license grant from the author who has retained all copyrights in the works. |
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