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Arch Inst Cardiol Mex ; 69(3): 207-13, 1999.
Article in Spanish | MEDLINE | ID: mdl-10529853

ABSTRACT

UNLABELLED: Alveolar hypoxia is the most powerful pulmonary vasoconstrictor. In a previous work, we did not demonstrate significant changes in vascular reactivity and edema formation in an isolated canine lobe model during alveolar hypoxia. The purpose of this study is to define vascular pulmonary reactivity and edema formation after induction of pulmonary vasoconstriction using a prostaglandin inhibitor like tiaprofenic acid and alveolar hypoxia. Six isolated canine pulmonary lobules were instrumented and studied, all of them under two conditions (normoxia FIO2 21% and hypoxia FIO2 5%) four starting in normoxia condition and 2 starting in hypoxia condition. RESULTS: No significant changes in filtration rate were found, normoxia 0.42 +/- 0.41, hypoxia 0.37 +/- 0.51 ml/min/100 g pulmonary tissue P = NS. The arterial pressure in basal conditions was 25.1 +/- 6.21, and during hypoxia increased to 37 +/- 7.19 cm H2O (Delta 12.0 +/- 1.2 cm H2O). P < 0.001. CONCLUSION: Hypoxia vascular reactivity was significantly increased in tiaprofenic acid pretreated isolated canine lobes, no changes in pulmonary permeability was found nor increased rate in edema formation.


Subject(s)
Propionates/pharmacology , Prostaglandin Antagonists/pharmacology , Pulmonary Artery/drug effects , Pulmonary Edema/etiology , Pulmonary Veins/drug effects , Animals , Calibration , Dogs , Female , Hypoxia/physiopathology , In Vitro Techniques , Male , Pulmonary Alveoli/drug effects , Pulmonary Alveoli/physiopathology , Pulmonary Artery/physiopathology , Pulmonary Edema/physiopathology , Pulmonary Veins/physiopathology , Vasoconstriction/drug effects , Vasoconstriction/physiology
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