The distribution function of pulmonary transit times (fPTT) defines co
ntact time between blood and vascular bed, which affects gas exchange
and endothelial metabolic functions. This study was undertaken to asse
ss effects of abnormal pulmonary inflow (($) over bar P-PA) and outflo
w pressures (P-LA) on fPTT. Three groups were studied: five patients w
ith elevated P-LA and passive pulmonary hypertension (LVD-Ab), eight w
ith normal P-LA (LVD-Nl), and six with pulmonary disease and various l
evels of ($) over bar P-PA (PD). Empirical complex exponential functio
ns were convoluted on right and left ventricular indicator-dilution cu
rves to derive fPTT; mean transit time (Mo-1), standard deviation (Sm2
), and cube root of the third moment about Mo-1 (Sm3) were calculated
by standard equations. A single linear regression of Sm3 and Sm2 on Mo
-1 was observed for all patients, regardless of disease process. Inver
se relations between Mo-1, Sm2, and Sm3 and blood flow were highly sig
nificant, but dispersion volumes (DV = Mo-1 X flow) were higher in pat
ients with elevated ($) over bar P-PA. Significant linear regressions
of fPTT parameters on ($) over bar P-PA, derived in LVD-Nl and LVD-Ab
patients, failed to predict Mo-1, Sm2, and Sm3 for the PD group, where
as linear regressions on P-LA accurately predicted Mol, Sm2, and Sm3 i
n the PD group. Relations between fPTT parameters and P-LA were equall
y well fit by exponential equations in all 19 patients, consistent wit
h an asymptotic pressure-volume relation of distensible vessels. Micro
vascular pressure (P-MV), combining ($) over bar P-PA, and P-LA, was n
ot a better predictor of fPTT parameters in LVD-NL and LVD-Ab patients
but provided a slightly closer estimate of relative dispersion and sk
ewness in PD patients. We conclude that, under conditions of this stud
y, P-LA is a major determinant of fPTT, somewhat modified by elevated
P ($) over bar(PA) and cardiac output in patients with lung disease.