Pulmonary vasomotion and the distribution of vascular resistance in a dog lung lobe

Abstract

The influence of stellate ganglion stimulation, hypoxia and the infusion of norepinephrine, PGF2.alpha. [prostaglandin F2.alpha.] serotonin and histamine on the longitudinal distribution of vascular resistance and intravascular pressures in an isolated left lower lobe of the dog lung was examined using the low-viscosity bolus technique. Sympathetic stimulation, norepinephrine, serotonin, PGF2.alpha. and hypoxia increased total pulmonary vascular resistance by increasing the resistance, primarily on the arterial or upstream side of the volume midpoint, whereas histamine increased the resistance near the venous end of the lobar vascular bed. Hypoxia increased the volume upstream from the site of maximum resistance, suggesting that the larger lobar arteries were distended by the elevated lobar artery pressure. Sympathetic stimulation, norepinephrine, PGF2.alpha. and serotonin had little effect on the volume upstream from the maximum resistance, suggesting that these vasomotor stimuli prevented distension of the larger arteries.