Partitioning of pulmonary vascular resistance in dogs by arterial and venous occlusion.
We perfused in situ isolated left lower lung lobes at a steady flow rate in zone 3 condition. When the lobar arterial inflow was suddenly occluded, the arterial pressure (Pa) fell rapidly and then more slowly. When the lobar venous outflow was suddenly occluded, the venous pressure (Pv) rose rapidly and then continued to rise more slowly. The rapid changes in Pa and Pv with inflow and outflow occlusion, respectively, represent the pressure drops across the arterial (delta Pa) and venous (delta Pv) relatively indistensible vessels. The total arteriovenous pressure difference (delta Pt) minus delta Pa + delta Pv gives the pressure drop across the vessels in the middle (delta Pm) that are much more distensible. Serotonin and histamine infusion increased delta Pa and delta Pv, respectively, but left delta Pm unchanged. delta Pa and delta Pv, but not delta Pm, increased as flow rate was increased. The studies with varying flow rate and venous pressures suggested that the arteries and veins became resistant to distension when their transmural pressures exceeded 10--5 Torr, respectively. Under the conditions studied, the middle nonmuscular segment contributed a major fraction of the vascular compliance and less than 16% of the total resistance. The muscular arteries and veins contributed equally to the remaining resistance. We conclude that the arterial and venous occlusion method is a useful technique to describe the resistance and compliance of different segments of the pulmonary vasculature.
D000818:Animals; D001794:Blood Pressure / Q000187:drug effects; D003250:Constriction; D004285:Dogs; D006632:Histamine / Q000494:pharmacology; D008168:Lung / Q000098:blood supply*; D010477:Perfusion; D011651:Pulmonary Artery / Q000502:physiology; D011652:Pulmonary Circulation; D011667:Pulmonary Veins / Q000502:physiology; D012701:Serotonin / Q000494:pharmacology; D014655:Vascular Resistance
D012701:Serotonin; D006632:Histamine