Studies on the pulmonary hemodynamics in pulmonary tuberculosis. III. Effects of unilateral hypoxia on pulmonary blood flow in patients with pulmonary tuberculosis

Abstract

It is well known that the hypoxia causes the pulmonary arterial pressure to rise, and many investigators ascribed this to the constriction of pulmonary blood vessels. Acoording to Kato who subjected the patients with pulmonary tuberculosis to 14% O2 gas, the observed rise in the pulmonary arterial pressure was due to an increase in the pulmonary vascular resistance owing to the contraction of pulmonary blood vessels. A different opinion has been recently voiced by Fishman who subjected a unilateral lung, of man, to the ambient air, and next, to 10% O2 gas, while subjecting the contralateral lung to 25-33 O2 gas and who found no change in the rate of blood flow through the hypoxic lung and pulmonary artery blood pressure. Thus he was led to a conclusion opposed to the view of V. Euler that the hypoxia acted directly on the pulmonary blood vessels. A previous report was made by the present author on the differential pulmonary blood flow in patients with pulmonary tuberculosis. This paper aims to report a study where the affected lung was subjected to a 10% O2 gas and where the effect of such maneuvre on the blood flow through the hypoxic lung was studied. MATERIALS AND METHODS Materials used were 5 cases out of the previously reported series and one new case, bringing the total to 6. They were subjected to the right heart catheterization, broncho-spirometry and arterial cannulation simultaneously. First, the healthy lung was subjected to a high O2 gas, while subjecting the affected lung to the ambient air, and the differential blood flow was measured under this circum-stance as the control observation. Next, the air-way to the affected lung was switched to a source of 10-12% O2 gas and another determination of the differential pulmonary blood flow was made after allowing a certain period of time. In this way the effect of unilateral hypoxla on the affected lung was studied. At different stages of the experiment arterial blood samples were withdrawn and analysed for O2 tension (PaO2) and CO2 tension (PaCO2) and hematocrit (Hta) ; pH of the arterial blood was calculated from Singer and Histings' nomogram90).