Gaseous diffusion from alveoli into pulmonary arteries

Abstract

In 40 patients, during right heart catheterization a catheter with a platinum tip electrode was wedged in a branch of the pulmonary artery. With the electrode acting as part of a potentiometer, signals were recorded following single inhalations of hydrogen. Similarly signals were recorded following inhalations of oxygen with the electrode acting as part of a polarograph. With either gas, signals were recorded appearing in less than 1 sec after the gas entered the nose. The signals paralleled the changes in the alveolar concentration of the gas. The infusion of dextrose through the wedged catheter or the withdrawal of the catheter a short distance from the wedged position, did not significantly affect the results. The inhaled gas was also shown to appear at the tip of the wedged catheter significantly before it appeared in the descending aorta. It is concluded that the observations made are evidence of diffusion of the inhaled gases from the alveoli directly into the pulmonary arteries. platinum/hydrogen anode; oxygen polarograph; alveolo-arterial oxygen diffusion; alveolo-arterial hydrogen diffusion Submitted on May 29, 1963

Hypoxia and Pulmonary Vascular Resistance. The Relative Effects of Pulmonary Arterial and Alveolar PO2

“…But this curve is unlikely to be correct as shown by data on gas penetration in pulmonary vessels (Sobol et al 1963, Jameson 1964. Oxygenized blood is found in pulmonary arteries of considerable size (Staub 1961).…”

Hypoxic Pulmonary Vasoconstriction

“…Perfusion of isolated cat lungs with a constant flow of partially deoxygenated blood during ventilation with air did not alter P PA , but ventilation with hypoxic gas mixtures increased inflow pressure during both forward and reverse perfusion, suggesting that HPV occurred in vessels that exchanged O 2 (447). Such vessels obviously included capillaries, but pul- monary arteries can also exchange gas (331, 881,1811).…”

Exercise-induced Arteriovenous Intrapulmonary Shunting in Dogs

“…Indeed, we would suggest that the magnitude of the exercise-induced anatomic arteriovenous shunting in the human may be greater than in the dog (32), because of the larger relative increases in cardiac output, pulmonary vascular pressures, and (a-a)Do 2 typically observed in humans with exercise. The lack of right-to-left shunt documented during exercise by gas exchange-dependent techniques, despite solid evidence of an anatomic I-P shunt, is controversial and may be explained by either gas exchange occurring proximal to (34) or within (35) arteriovenous anastomotic vessels (36). Notably, a substantial range in shunt fraction (range, 0.2-3.1% of cardiac output) was found in the three exercising dogs for which shunt fraction could be calculated.…”