Key points are not available for this paper at this time.
Arterial-site vasoconstriction predominates in canine hypoxic and serotonergic pulmonary hypertension; leaves open translation to human mechanisms.
Pulmonary arterial pressure increases in dogs exposed to alveolar hypoxia or intravascular in-fusion of 5-hydroxytryptamine (serotonin). Al-though most investigators believe that this increase in pressure reflects a vasoconstriction in the pul-monary vascular bed, the site of vasoconstriction, whether venular, capillary, or arteriolar, is con-troversial. Interpretations have been based previ-ously upon measurements of pressure and flow at various sites in the pulmonary circulation and have been handicapped by the inability to measure the volumes of the segments under study (1-3). The development of an ether plethysmographic technique to measure pulmonary arterial blood vol-ume in vivo (4) prompted us to reassess the site of vasoconstriction produced by hypoxia or sero-tonin. To accomplish this, we used cardiac cath-eters to measure pulmonary arterial and left atrial pressures, dye dilution curves to measure pulmo-nary blood volume and cardiac output, and the ether plethysmographic method to calculate pul-monary arterial blood volume. These parameters were measured in dogs during 1) a control pe-riod, and then during 2) respiration of a low con-centration of oxygen, or 3) slow intravenous infu-sion of a solution of 5-hydroxytryptamine. We shall attempt to show that alveolar hypoxia and 5-hydroxytryptamine produced a form of pulmo-nary vasoconstriction in which there was increased smooth muscle tone of a major portion of the pul-monary arterial tree. * Submitted for publication June 23, 1965; accepted
No takes yet. Share an insight, caveat, or question.
Sackner et al. (1966) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: