The Effect of Granulomatous Pulmonary Disease in Dogs on the Response of the Pulmonary Circulation to Hypoxia

R. S. Irwin; J. Martinez-Gonzalez-Rio; H. M. Thomas; H. W. Fritts

doi:10.1172/JCI108885

The Effect of Granulomatous Pulmonary Disease in Dogs on the Response of the Pulmonary Circulation to Hypoxia

R. S. Irwin, J. Martinez-Gonzalez-Rio, H. M. Thomas III, and H. W. Fritts Jr.

Published December 1, 1977 - More info

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Abstract

We studied the effect of diffuse granulomatous pulmonary disease on the reponse of the pulmonary circulation to hypoxia in two series of experiments in intact dogs. First, in animals with unilateral disease, vasoconstriction in the diseased lung was compared to that in the contralateral control lung. Second, in animals with bilateral disease, the vasoconstriction of pulmonary shunt pathways was compared to that of the rest of the pulmonary vasculature. We assessed vasoconstriction in each study by measuring the distribution of pulmonary blood flow between the test and control set of vessels during 21 and 12% oxygen breathing. In the first set of experiments, we measured apportionment of the blood flow between the two lungs by bronchospirometry and the krypton bolus method. In normal dogs, hypoxia did not shift blood flow systematically from one lung to the other. In 10 dogs with unilateral disease, general hypoxia increased the proportion of blood flow to the diseased lung. The mean percent of blood flow to the left lung in eight dogs with disease in that lung rose from 29% during air breathing to 32% (P < 0.001). In the second set of experiments, we measured apportionment of the blood flow between shunt pathways and gas-exchanging pathways by a constant infusion of radio-active krypton and the standard shunt formula. In eight dogs with bilateral disease, hypoxia consistently increased the flow through shunt pathways, from a mean value of 10% of pulmonary blood flow to 14% (P < 0.005).

Thus, diffuse granulomatous disease causes a decreased vasoconstrictive response to hypoxia both in diseased, gas-exchanging regions and in shunt pathways. In proliferative interstitial pulmonary disease, generalized hypoxia causes shifts in pulmonary blood flow which do not ameliorate but rather worsen the hypoxemia of systemic arterial blood.