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Results for “PULMONARY CIRCULATION”

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At least 919 records · Page 51Linked to original sources
PubMed1992

Acute effects of increased intravascular volume and hypoxia on the pulmonary circulation: assessment with high-resolution CT.

High-resolution computed tomography (HRCT) was used to evaluate acute morphologic changes in the circulation of anesthetized miniature pigs (a) after volume loading and (b) after induction of hypoxia. Before and after each challenge, serial HRCT scans were obtained at a constant position in the caudal lobes of the lung. Scans were digitized and analyzed to determine the extent of changes in the cross-sectional area of vessels greater than 300 microns in diameter. Parenchymal background attenuation in anterior, middle, and posterior lung regions was used to assess volume changes in vessels less than 300 microns in diameter. Volume loading increased cross-sectional area by 25.2% +/- 4.3 in arteries and by 37.8% +/- 6.1 in veins and caused a gravity-dependent increase in parenchymal attenuation. Hypoxia decreased parenchymal attenuation, which was consistent with constriction of vessels smaller than 300 microns. Larger arteries and veins reacted heterogeneously. Vascular dilation during volume loading was predominantly passive, and hypoxia increased vascular tone throughout the circulation. HRCT represents a new in vivo approach to investigate vascular responses to various stimuli.

Acute Disease↗
PubMed1975

Metabolism of prostaglandin f 1 alpha in the pulmonary circulation.

3-H5,6-Prostaglandin F1alpha is largely eliminated from the circulation during a single passage through the pulmonary vascular bed. Its elimination requires cellular uptake. The volume of distribution and the mean transit time of the radioactivity are greater than those of an intravascular marker, blue dextran. The lungs retain 25-30% of the radioactivity, most in the form of a metabolite less polar that PGF1alpha itself. The pulmonary venous effluent contains the same metabolite along with some unmetabolized PGF1alpha. The metabolite can be distinguished from prostaglandins of the A, B, D, E and F series. It is reduced on reaction with borohydride, but reduction does not yield PGF1alpha. NaOH has no effect on the metabolite, a finding that rules out the presence of a beta-hydroxy-ketone configuration of the ring structure. The chromatographic behavior of the metabolite and its reaction with borohydride are those expected of 9,11-hydroxy-15-ketoprostanoic acid.

Animals↗
PubMed1991

Sustained effects of endothelin-1 on rabbit, dog, and rat pulmonary circulations.

Effects of endothelin-1 (10(-8) M) on the pulmonary vascular resistance-compliance profile were examined in isolated blood-perfused rabbit, dog, and rat lungs using occlusion techniques. Capillary permeability was assessed by filtration coefficient (Kfc). Cyclooxygenase products were assessed by radioimmunoassay. In rabbit lungs, endothelin-1 increased all resistances except large vein; ibuprofen reversed the constriction. Endothelin-1 decreased total vascular compliance (CT), which was reversed by ibuprofen. Cyclooxygenase products were unchanged by endothelin-1 or endothelin-1 plus ibuprofen. In dog lungs, large vein resistance increased after endothelin-1; ibuprofen increased large arterial resistance. Endothelin-1 decreased CT and middle compartment compliance, and endothelin-1 plus ibuprofen decreased large vessel compliance (CLV). Ibuprofen reversed the endothelin-1 increase in plasma 6-oxo-prostaglandin F1 alpha. In rat lungs, ibuprofen reversed the endothelin-1 increase in small arterial resistance. Endothelin-1 decreased CLV, and endothelin-1 plus ibuprofen returned the compliance to baseline values. Ibuprofen potentiated the endothelin-1 increase in plasma prostanoids. Endothelin-1 plus indomethacin increased vascular resistance and blocked prostaglandin production. Kfc was increased only in rat lung after endothelin-1 plus ibuprofen. In summary, endothelin-1 increased pulmonary vascular resistance, which was attenuated by prostacyclin in dogs and rats. In rabbits, the resistance increase was reversed by ibuprofen.

6-Ketoprostaglandin F1 alpha↗
PubMed1967

Experimental emphysema. Histologic changes and alterations in pulmonary circulation.

Detailed study of the pathogenesis of bullous emphysema has been hampered by lack of a suitable animal model of this disease. Prolonged exposure of rats and dogs to elevated partial pressures of oxygen produced a chronic obstructive disease in the lungs of these animals which anatomically resembles bullous emphysema in man. The disease was characterized by extensive bullae formation, alveolar septal destruction, airway obstruction and pronounced circulatory changes. It is suggested that this condition in laboratory animals may serve as a model for the study of pulmonary obstructive disease.

Animals↗