Distribution of pulmonary vascular resistance during lactic acid infusion in dogs

1990 ◽  
Vol 68 (4) ◽  
pp. 1328-1336 ◽  
Author(s):  
K. W. Presberg ◽  
J. I. Sznajder ◽  
J. Melendres ◽  
T. Lewis ◽  
C. Abrahams ◽  
...  
Keyword(s):  
Lactic Acid ◽  
Lactic Acidosis ◽  
Pulmonary Vascular Resistance ◽  
Vascular Resistance ◽  
Light And Electron Microscopy ◽  
Balloon Occlusion ◽  
Longitudinal Distribution ◽  
Acid Infusion ◽  
Systemic Artery ◽  
Systemic Vein

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.

Capillary filtration coefficient, vascular resistance, and compliance in isolated mouse lungs

1999 ◽  
Vol 87 (4) ◽  
pp. 1421-1427 ◽  
Author(s):  
James C. Parker ◽  
Mark N. Gillespie ◽  
Aubrey E. Taylor ◽  
Sherri L. Martin
Keyword(s):  
Pulmonary Vascular Resistance ◽  
Vascular Resistance ◽  
Vascular Function ◽  
Vascular Occlusion ◽  
Filtration Coefficient ◽  
Longitudinal Distribution ◽  
Mouse Lung ◽  
Control Group ◽  
Capillary Filtration ◽  
Capillary Filtration Coefficient

Although many recently produced transgenic mice possess gene alterations affecting pulmonary vascular function, there are few baseline measurements of vascular resistance and permeability. Therefore, we excised the lungs of C57/BL6 mice and perfused them with 5% bovine serum albumin in RPMI-1640 culture medium at a nominal flow of 0.5 ml/min and ventilated them with 20% O2-5% CO2-75% N2. The capillary filtration coefficient, a sensitive measurement of hydraulic conductivity, was unchanged over 2 h (0.33 ± 0.03 ml ⋅ min−1 ⋅ cmH2O−1 ⋅ 100 g−1) in a control group ventilated with low peak inflation pressures (PIP) but increased 4.3-fold after high PIP injury. Baseline pulmonary vascular resistance was 6.1 ± 0.4 cmH2O ⋅ ml−1 ⋅ min ⋅ 100 g−1 and was distributed 34% in large arteries, 18% in small arteries, 14% in small veins, and 34% in large veins on the basis of vascular occlusion pressures. Baseline vascular compliance was 5.4 ± 0.3 ml ⋅ cmH2O−1 ⋅ 100 g−1 and decreased significantly with increased vascular pressures. Baseline pulmonary vascular resistance was inversely related to both perfusate flow and microvascular pressure and increased to 202% of baseline after infusion of 10−4 M phenylephrine due to constriction of large arterial and venous segments. Thus isolated mouse lung vascular permeability, vascular resistance, and the longitudinal distribution of vascular resistance are similar to those in other species and respond in a predictable manner to microvascular injury and a vasoconstrictor agent.

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