Response of the main pulmonary artery of dogs to neuronally released versus blood-borne norepinephrine.

Abstract

The effects of sympathetic nerve stimulation and of norepinephrine infusions on the dynamic elastic properties of the main pulmonary artery were studied in 20 anesthetized, open-chest dogs. Pulmonary arterial pressure and diameter were linearly related between 5 to 45 mm Hg and at heart rates of 40 to 200 beats/min. Sympathetic nerve stimulation changed the stiffness (pressure-diameter slope) of the pulmonary artery by +35%; infusion of norepinephrine (0.25 µg/kg/min) by only +14%. Diameter intercepts, determined by extrapolation of the linear pressure-diameter line, were unchanged during stimulation, but decreased significantly during the infusion of norepinephrine. Local application of norepinephrine to the wall duplicated the changes produced by sympathetic nerve stimulation. Histologically, the arrangement of smooth muscle in the outer layers of the media of the artery suggested linkage of smooth muscle with continuous elastic fibers, whereas smooth-muscle cells of the deeper layers of the media appeared to connect with each other, and elastic fibers were discontinuous. The topical application of elastase to the outer wall effected a loss of elastic fibers in the outer layers of the media. After elastase, neither stimulation nor norepinephrine infusions increased stiffness; diameter intercepts decreased with both. The observations are consistent with the idea that stiffening of this artery during nerve stimulation is produced by contraction of smooth muscle attached to elastic fibers and that the anatomical arrangement for stiffening is located in the outer layer of the media, where the sympathetic nerve endings are located. In contrast, blood-borne norepinephrine stimulates predominantly the inner layers.