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Five patients with severe aortic regurgitation had their intraarterial radial pulse recorded simultaneously with the external radial artery deflection of the other wrist. Recordings were made with the arms horizontal and repeated after elevation of the wrists, until the arms were vertical. Elevating the arm of a patient with aortic regurgitation increased the pulsation recorded over the radial artery, lowered mean intraarterial pressure, and reduced the pulse pressure. The results suggest that elevation increases the compliance of the arterial wall, primarily by moving the artery to a lower position on its pressure-volume curve. The same changes occurred in 5 normal subjects but were less pronounced.

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Professor Cournand has a special interest in hypoxic pulmonary vasoconstriction, and Professor Richards, his colleague, had a special interest in hyperexis, two seemingly unrelated phenomena in physiology. But at the end of a series of studies on cardiac output, when younger members of the Laboratory were assessing the effect of granulomatous lung disease on the calculation of output by the Fick principle, the pulmonary vessels in the diseased lung showed behaviour consistent with hyperexis, and the individual interests of the two men unexpectedly converged.

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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.

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Measurements of gas exchange in dogs with granulomatous lung disease resembled those which have been made in similar disorders of man. The minute volume of ventilation was large, the oxygen extracted from each liter of ventilation was low, and the arterial blood oxygen saturation tended to be subnormal despite hyperventilation. When the diseased dogs breathed 21% oxygen and had alveolar oxygen tensions above 100 mm Hg, the pulmonary blood flows calculated from the Fick principle were significantly higher than those estimated by the dye-dilution method. By way of contrast, the two values agreed when the alveolar tensions were lowered. Whether the agreement of the flows is causally related to the alveolar tension remains an open question. A possible explanation may lie in the effect of alveolar tension on the oxygen consumed by the diseased lung.

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Intravenous injections of complete Freund's adjuvant, used by others to stimulate the reticuloendothelial system of small laboratory animals, produced granulomas resembling sarcoid in the lung of the dog. At the height of the disease, when granulomas occupied more than half of the alveolar tissues, transpulmonary arteriovenous (A-[unk]V) differences of lactate, pyruvate, and glucose were measured. When the diseased dogs breathed room air, the A-[unk]V differences of lactate and pyruvate were greater than normal; and when the dogs breathed an hypoxic mixture, the differences increased further. Hence the model affords the opportunity for studying the in vivo metabolism of diseased lungs. It may also prove useful for studying other aspects of granulomatous disease which cannot be easily approached in man.

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