(Circulation. 1996;94:3263-3270.)
© 1996 American Heart Association, Inc.
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the Cardiovascular Division, Department of Medicine (A.J.B., H.W., K.M., R.S., S.H.K.), and the Department of Biomedical Engineering (J.E.H.), University of Minnesota, Minneapolis.
Correspondence to Alan J. Bank, MD, Cardiovascular Division, Department of Medicine, University of Minnesota Medical School, Box 508 UMHC, 420 Delaware St SE, Minneapolis, MN 55455. E-mail bankx001@maroon.tc.umn.edu.
Background The contributions of collagen, elastin, and smooth muscle to arterial mechanical properties in the in vivo human artery are not known.
Methods and Results We used a recently developed intravascular ultrasound technique to measure total brachial artery wall stress and incremental elastic modulus (Einc) in seven normal human subjects at baseline and after intra-arterial norepinephrine (1.2 µg) and nitroglycerin (100 µg). Then we applied a modified Maxwell model to estimate the elastic modulus of elastin (EE); the recruitment of collagen fibers supporting wall stress; and the differential contributions of collagen, elastin, and smooth muscle to wall stress and Einc over a wide range of pressure and smooth muscle tone. With this model, EE was 3x106 dynes/cm2. Collagen fibers were recruited increasingly as transmural arterial pressure increased and reached a value of
5% to 6% at 100 mm Hg under each of the conditions studied. Isobaric smooth muscle contraction resulted in a small decrease in total wall stress and no significant change in total Einc while shifting the predominant element contributing to these mechanical parameters from collagen in parallel with the smooth muscle to collagen in series with the smooth muscle. In contrast, isometric smooth muscle contraction produced large increases in total wall stress (from 0.11x106 dynes/cm2 after nitroglycerin administration to 1.35x106 dynes/cm2 after norepinephrine administration) and Einc (from 3.84x106 dynes/cm2 after nitroglycerin administration to 57.8x106 dynes/cm2 after norepinephrine administration) entirely as a result of the additional contribution of the smooth muscle and its associated series collagen.
Conclusions This study describes a technique for determining arterial elastic properties and a model that can be used to estimate a number of mechanical parameters of the human brachial artery in vivo. This technique may be useful in studies of the arterial elastic properties of arteries in patients with vascular pathology.
Key Words: arteries elasticity mechanics muscle, smooth vasodilation
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