In Vivo Assessment of Pulmonary Vascular Integrity in Experimental Pulmonary Edema

Abstract

During single pass indicator studies across the lungs [¹⁴C]urea remains in the vascular compartment, but its molecular size and solubility suggest it might escape abnormally permeable vessels. To test the hypothesis that [¹⁴C]urea might be used to distinguish pulmonary edema due to acutely increased intravascular pressure from that due to vascular damage by alloxan, we studied [⁵¹Cr]erythrocytes (r), [¹²⁵I]albumin (a), [¹⁴C]urea (u), and tritiated water as dilution indicators in the pulmonary circulation of anesthetized dogs. In addition, the adequacy of albumin as an intravascular indicator was evaluated. Indicator curves, blood gases, hematocrit, and vascular pressures were determined during a base-line period and repeated 30 and 60 min after treatment in five groups of dogs: (a) saline control. (b) alloxan edema. (c) epinephrine infusion, (d) volume overload, and (e) left atrial (LA) balloon obstruction. Groups b, d, and e developed a similar degree of edema judging by wet/dry lung weights and histology. Groups a and c did not develop edema. In alloxan edema, differences between the mean transit time volume of u and r (V_v-r) increased over base line at 30 (P < 0.001) and 60 min (P < 0.02); the differences between the mean transit time volume of a and r (V_e-r) increased slightly at 30 (P < 0.03) and 60 min (P < 0.02); and V_u-r significantly exceeded V_a-r at 30 (mean difference = 9 ml, P < 0.02) and 60 min (mean difference = 11, P < 0.04). In none of the other groups did V_u-r significantly exceed V_a-r. Thus, comparison of V_u-r with V_a-r may permit distinction between “high pressure” and “increased permeability” pulmonary edema. Albumin was not a consistently reliable indicator of intravascular volume as compared with composite red cell and albumin curve.