Some Physical Properties of the Pulmonary Arterial Bed Deduced from Pulsatile Arterial Flow and Pressure

Abstract

Changes of vascular compliance and resistance of the proximal and the peripheral pulmonary arterial vessels when vascular smooth muscle was stimulated was quantified. These vascular characteristics were derived from registrations of pulsatile pressure and flow in the pulmonary artery (PA). An in situ cat lung preparation was used, with the right heart by-passed by a pulsatile blood pump. Vascular input impedance was derived from PA pulsatile pressure and flow recordings, and impedance characteristics were used for calculation of the variables of a simple lumped analog representation of the arterial bed. PA smooth muscle was stimulated by infusions of collagen suspension, by general hypoxia and by noradrenaline [norepinephrine] injections. Collagen caused 40% reduction of vascular compliance (C), no changes in proximal arterial resistance (R1) and 180% increase in peripheral vascular resistance (R2). Hypoxia caused 50% reduced C, 20% increased R1 and 70% increased R2. Noradrenaline caused 20% reduced C and 30% increased R1 and R2. These results, together with results derived from simulation of the observed impendance changes in a computer model of the lung arterial bed, indicated that collagen infusion elicited contraction of small and medium-sized arteries, with increased arterial volume as a result of increased distending pressure. Hypoxia and noradrenaline both seemed to cause contraction of the total arterial bed, this effect being most pronounced during hypoxia.