Intra-arterial nitroglycerin increased brachial artery area by 22% and decreased pulse-wave velocity from 15.1 to 13.2 m/s (P<0.05), while norepinephrine decreased area by 17%.
Absolute Event Rate: 13.2% vs 15.1%
p-value: p=<0.05
Abstract The direct effect of smooth muscle relaxation on arterial elastic properties is controversial. Studies in animals show both a decrease and an increase in elastic modulus. In human subjects, the contribution of smooth muscle to arterial elastic mechanics has been limited by difficulty in separating the direct effects of a vasodilator drug on the arterial wall from the indirect effects due to reduced blood pressure. The purpose of the present study was to assess the direct contribution of vascular smooth muscle to brachial artery elastic mechanics in normal human subjects in vivo. We measured brachial artery compliance and incremental elastic modulus (E inc ) in eight normal subjects (age, 22 to 51 years) by using intravascular ultrasound. A 3.5F 30-MHz intravascular ultrasound catheter was placed through a sheath into the brachial artery, and intra-arterial pressure, cross-sectional area, and wall thickness were measured simultaneously under baseline conditions and after the administration of intra-arterial nitroglycerin (100 μg) and norepinephrine (1.2 μg). A pressurized cuff surrounding the brachial artery was inflated to reduce transmural brachial artery pressure. Using this technique, we were able to measure the following arterial characteristics for the first time in human subjects in vivo: (1) the effective unstressed arterial radius and (2) the pressure-area, stress-strain, and pressure-E inc relations over a wide pressure range (0 to 100 mm Hg). Intra-arterial nitroglycerin increased brachial artery area by 22% and intra-arterial norepinephrine decreased brachial artery area by 17% at 100 mm Hg transmural pressure ( P <.001 versus baseline). Nitroglycerin produced a significant ( P <.01) nonparallel upward shift of the compliance pressure curve compared with baseline, and norepinephrine produced a smaller downward shift of the compliance-pressure curve. Pulse-wave velocity was decreased from 15.1±1.1 m/s at baseline to 13.2±0.7 m/s at 100 mm Hg after the administration of nitroglycerin ( P <.05). Nitroglycerin and norepinephrine also significantly shifted the brachial artery stress-strain and E inc -strain curves in opposite directions. However, nitroglycerin did not significantly change E inc under isobaric conditions. This study describes and validates a new technique for determining brachial artery elastic properties in vivo over a wide pressure range. At constant pressure, nitroglycerin-induced smooth muscle relaxation increased brachial artery compliance and decreased pulse-wave velocity without significantly altering E inc .
Bank et al. (Wed,) conducted a other in Normal subjects (n=8). Intra-arterial nitroglycerin and norepinephrine vs. Baseline conditions was evaluated on Pulse-wave velocity at 100 mm Hg (p=<0.05). Intra-arterial nitroglycerin increased brachial artery area by 22% and decreased pulse-wave velocity from 15.1 to 13.2 m/s (P<0.05), while norepinephrine decreased area by 17%.