The impairment of alveolar gas exchange in pulmonary tuberculosis was investigated with special reference to the morphologic changes of pulmonary affection.
Twenty-four mature rabbits were used. Twenty rabbits were injected with 2mg/kg of Mycobacterium bovis intrapulmonarily. Ten rabbits out of all the infected animals were treated with 20mg/kg of Rifampicin and 10mg of Streptomycin from the sixth week after the infection and the treatment was continued for four to six weeks. The patho-physiological changes in each group were investigated.
The obtained conclusions were as follows.
1. The values of the arterial Po
2 began to decrease at the fourth week after the infection, and they were aggravated with the advancement of pulmonary affection. The values of the arterial PCO
2 werealso reduced with the appearance of hypoxemia, and hypercapnia was shown in three cases which died of the far-advanced pulmonary tuberculosis.
2. The increase in the venous-to-arterial shunt might be regarded as the most important factor o hypoxemia in tuberculosis cases without treatment. In this group, the alveolar walls were highly thickened with tuberculous inflammation and some alveolar spaces were destroyed by tuberculous, affection. It was suggested that the increase in the true shunt was originated from such morphologic changes.
In the treated group, two kinds of different patterns of the impairment of alveolar gas exchange were demonstrated. One of them was the uneven distribution of the ventilation and the other was the impairment of the alveolar gas diffusion. The former might be caused by the regional differences, in the compliance due to the uneven pulmonary affection. The latter depended on the decrease in the diffusion surface of alveoli. The difference of both patterns which were found in the treated group, however, was pooly understood from the viewpoint of the morphologic findings in the lung.
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