Abstract

The dynamics of CO(2) exchange in the lungs of man was studied by observing the rate of disappearance of a stable isotope of CO(2) ((13)CO(2)) from the alveolar gas during breath holding. Over 50% of the inspired isotope disappeared within the first 3 sec followed by a moderately rapid logarithmic decline in which one-half of the remaining (13)CO(2) disappeared every 10 sec. The large initial disappearance of (13)CO(2) indicated that alveolar (13)CO(2) equilibrated in less than 3 sec with the CO(2) stored in the pulmonary tissues and capillary blood. The volume of CO(2) in the pulmonary tissues calculated from this initial disappearance was 200 ml or 0.33 ml of CO(2) per milliliter of pulmonary tissue volume. The alveolar to end-capillary gradient for (13)CO(2) was calculated by comparing the simultaneous disappearance rates of (13)CO(2) and acetylene. At rest and during exercise this gradient for (13)CO(2) was either very small or not discernible, and diffusing capacity for CO(2) (D(LCO2)) exceeded 200 ml/(min x mm Hg). After the administration of a carbonic anhydrase inhibitor the rate of disappearance of (13)CO(2) decreased markedly. D(LCO2) fell to 42 ml/(min x mm Hg) and at least 70% of the exchange of (13)CO(2) with the CO(2) stores in the pulmonary tissues and blood was blocked by the inhibitor. These changes were attributed to impairment of exchange of (13)CO(2) with the bicarbonate in the pulmonary tissues and blood. The pH of the pulmonary tissues (V(tis)) was determined by a method based on the premise that the CO(2) space in the pulmonary tissues blocked by the inhibitor represented total bicarbonate content. At an alveolar P(CO2) of 40 mm Hg pH of V(tis) equalled 6.97 +/- 0.09.

Full Text
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