Journal of Applied Physiology, Vol 68, Issue 4 1328-1336, Copyright © 1990 by American Physiological Society
Distribution of pulmonary vascular resistance during lactic acid infusion in dogs
K. W. Presberg, J. I. Sznajder, J. Melendres, T. Lewis, C. Abrahams and L. D. Wood
Section of Pulmonary and Critical Care Medicine, University of Chicago, Illinois.
We sought to determine the longitudinal distribution of pulmonary vascular
resistance (PVR) in acute lactic acidosis utilizing pulmonary artery and
vein balloon occlusion techniques (Holloway et al. J. Appl. Physiol. 54:
840-851, 1983). In anesthetized dogs, both a systemic vein (I-V) infusion
and systemic artery (I-A) infusion of L-lactic acid were studied to control
for potential effects of factors other than pH on PVR. During progressive
I-A infusion (n = 9) to a pH of 6.94 +/- 0.06 there was no significant
change in PVR or its distribution. In contrast, I-V infusion (n = 9) to a
pH of 7.08 +/- 0.09 increased median PVR from 3.6 to 21.7 mmHg.1(-1).min (P
less than 0.001), due to an increase in middle segment resistance (0.0-15.4
mmHg.1(-1).min, P less than 0.02). Examination by light and electron
microscopy demonstrated pulmonary capillary obstruction with hemolyzed
erythrocyte (RBC) membranes with I-V infusion, but representative I-A
animals did not demonstrate these findings. Conceivably, the systemic
vascular bed filtered the fragmented RBC membranes in the I-A model, but
this microvascular obstruction with altered RBCs and RBC fragments caused
the pulmonary hypertension observed in the I-V infusion. We conclude that
lactic acidosis does not increase pulmonary vascular tone in dogs, a
finding compatible with most previous studies in which observed increases
in PVR may be attributed to other effects from I-V acid infusion on
circulating blood elements.
