Vascular recruitment increases evidence of lung injury

Objective: Changes in pulmonary blood flow rate can alter the site of the p erfused pulmonary capillary surface area. We tested the hypothesis that ful l recruitment of the pulmonary vascular bed may decrease evidence of lung i njury by recruiting less injured capillaries, We also tested the hypothesis that endothelial ectoenzyme activity is an earlier indicator of lung injur y than are permeability measures. Design: Isolated canine lung robes were perfused with autologous blood at c onstant blood flows of either 2.05 +/- 0.04 L/min (SEM) thigh flow, full re cruitment, n =12) or 0.600 +/- 0.004 L/min (tow flow, 33% full recruitment, n = 12) after lung injury to determine the eff ect of vascular recruitment on measures of injury. Setting: Research laboratory at a medical university. Subjects: Lung lobes were obtained from 36 mongrel dogs of either gender. Interventions: Lung injury was induced by adding phorbol myristate acetate (PMA) to the blood perfusing the isolated lung. Measurements and Main Results: Indicator dilution methods were used to meas ure single pass hydrolysis of (3)[H]-benzoyl-Phe-Ala-Pro, a synthetic subst rate for angiotensin converting enzyme, and calculate the modified first or der kinetic parameter corresponding to the ratio of a normalized maximal en zymatic conversion rate (A(max)) to the Michaelis-Menten constant (K-m), i. e., A(max)/K-m, before and after PMA. At a given flaw rate, the decrease in A(max)/K-m serves as an index of vascular injury. PMA decreased A(max)/K-m , percent metabolism, and fractional substrate utilization, and increased p ermeability, vascular resistance, and vascular pressures regardless of flow rate. The decrease in enzyme activity was detected earlier than the increa se in permeability. Conclusions: The greater percentage decrease in percent metabolism and frac tional substrate utilization and the earlier appearance of increased permea bility during high flow indicates that increasing blood flow three-fold rec ruited injured vessels and/or increased vascular injury by Increasing vascu lar perfusion pressures.