Pulmonary capillary blood flow (Qc) and apparent CO diffusing capacity (Dl) were calculated from the rates of disappearance of small alveolar concentrations of inspired acetylene and carbon monoxide during breath holding. Such measurements were performed simultaneously in four normal subjects at rest, during exercise and while performing Valsalva or Mueller maneuvers; they were also made at more than one alveolar oxygen tension so that true membrane diffusing capacity (Dm) and pulmonary capillary blood volume (Vc) could be calculated by the method of Roughton and Forster. Dl, Dm and Vc were closely correlated with Qc (r = 0.92, 0.71 and 0.92, respectively), indicating that both volume and effective surface of the pulmonary capillary bed changed along with corresponding directional changes in blood flow. During transients after starting or after stopping exercise, changes in Dl lagged slightly behind the associated changes in Qc; both parameters tended to reach steady values, however, after about 1 minute of steady exercise. The average time spent by red cells in the pulmonary capillaries at rest was estimated to be 0.79 second, falling to about 0.5 second at levels of exercise at which volume flow through the capillary bed was approximately tripled. Submitted on September 18, 1959
Eight patients with acute respiratory failure secondary to chronic bronchitis were studied for up to 5 consecutive days following admission; cardiac output and intravascular pressures, blood volume, arterial blood gas tensions, and body weight were measured. These observations were also compared with further measurements made some weeks later just before the patient was discharged. The effects of oxygen and acetylcholine on the pulmonary circulation were also studied. Pulmonary arterial pressure was raised in all patients during their acute illness and had fallen substantially after recovery. The pulmonary arterial pressure throughout the study correlated directly with the arterial carbon dioxide and inversely with the arterial oxygen tensions. The inhalation of 24% and 28% oxygen and the infusion of acetylcholine into the pulmonary artery resulted in a fall in pulmonary arterial pressure, often to levels close to those subsequently seen after recovery from the acute illness. No significant change in cardiac output was observed. It is suggested that the acute pulmonary hypertension seen in these patients is due primarily to pulmonary vasoconstriction resulting from hypoxia.
ADDITIONAL KEY WORDS hypoxic pulmonary vasoconstriction chronic bronchitis acetylcholine oxygen• Cournand and his colleagues have demonstrated that patients with acute respiratory and congestive failure secondary to chronic bronchitis and emphysema have, in general, a higher pulmonary arterial pressure than similar patients who are not in congestive failure (1). This pulmonary hypertension is associated with a lower oxygen saturation and an increased carbon dioxide tension in arterial blood. However, when these patients recover from their acute illness, the pulmo-
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