Isometric smooth muscle contraction via norepinephrine increased brachial artery wall stress to 1.35 x 10^6 dynes/cm2 and elastic modulus to 57.8 x 10^6 dynes/cm2 versus nitroglycerin.
How do collagen, elastin, and smooth muscle contribute to in vivo human brachial artery wall stress and elastic modulus at baseline and after vasoactive agents?
This study demonstrates a novel intravascular ultrasound technique and mathematical model to quantify the in vivo mechanical contributions of collagen, elastin, and smooth muscle to human arterial elastic properties.
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 micrograms) and nitroglycerin (100 micrograms). 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 3 x 10(6) dynes/cm2. Collagen fibers were recruited increasingly as transmural arterial pressure increased and reached a value of approximately 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 0.11 x 10(6) dynes/cm2 after nitroglycerin administration to 1.35 x 10(6) dynes/cm2 after norepinephrine administration) and Einc (from 3.84 x 10(6) dynes/cm2 after nitroglycerin administration to 57.8 x 10(6) 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.
Bank et al. (Sun,) conducted a other in Normal human subjects (n=7). Intra-arterial norepinephrine and nitroglycerin vs. Baseline was evaluated on Total brachial artery wall stress and incremental elastic modulus (Einc). Isometric smooth muscle contraction via norepinephrine increased brachial artery wall stress to 1.35 x 10^6 dynes/cm2 and elastic modulus to 57.8 x 10^6 dynes/cm2 versus nitroglycerin.