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J B Glazier

Publications and source records attributed to J B Glazier.

At least 19 recordsLinked to original sources

Sites of pulmonary vasomotor reactivity in the dog during alveolar hypoxia and serotonin and histamine infusion.

In order to evaluate separately changes in vascular tone occurring in arteries and veins, we measured pulmonary capillary red blood cell (RBC) concentration under zone II (waterfall) conditions in isolated dog lungs rapidly frozen with Freon 12. The lungs were frozen while being perfused from artery to vein and from vein to artery breathing normal and hypoxic gas mixtures and during infusions of serotonin and histamine. Changes in capillary RBC concentration which occurred during the experimental conditions indicated an alteration in vascular resistance upstream from the capillaries. Alveolar hypoxia caused a significant decrease in capillary RBC concentration during forward perfusion, but no change from the control values during reverse perfusion. Serotonin infusion caused a decrease in RBC concentration during forward perfusion comparable with that of hypoxia and a small but significant decrease during reverse perfusion. Histamine infusion caused no change in RBC concentration from control values during forward perfusion, but a large decrease during reverse perfusion. We conclude that vasoconstriction occurs (a) exclusively in arteries during alveolar hypoxia, (b) predominantly in arteries but to a lesser extent in veins during serotonin infusion, and (c) exclusively in veins during histamine infusion.

Animals↗

Effects of acetylcholine on regional pulmonary blood flow in patients with mitral stenosis.

The effect of acetylcholine was studied on the region of increased vascular resistance at the lung bases in patients with mitral stenosis. The patients had moderate elevations of pulmonary artery pressure. The distribution of blood flow and ventilation were measured in both lungs of 10 patients using radioactive xenon-133 and a scanning technique. Acetylcholine was then infused into one main pulmonary artery, and the distribution of blood flow and ventilation were measured again. One lung served as a control during the drug infusion. There was a small but significant increase in perfusion to the dependent lung zone during the drug infusion without a change in pulmonary artery pressure indicating localized vasodilation. Relative underperfusion was still present during the acetylcholine administration which indicated that increased vasomotor tone was not the principal pathophysiological mechanism for the increased vascular resistance. There was a decrease in ventilation to the lower zone of the lung receiving acetylcholine.

Acetylcholine↗