Volume 13, Issue 2 (Summer 2009)                   Physiol Pharmacol 2009, 13(2): 199-208 | Back to browse issues page

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Abstract:   (12005 Views)
Introduction: Acute respiratory disorders such as obstructive pulmonary diseases and hypoventilation may lead to alveolar hypoxia and hypercapnia which their effects on pulmonary vascular beds are controversial. The aim of this study was to establish the isolated perfused lung setup and investigate the effects of alveolar hypoxia and hypercapnia on pulmonary vascular resistance. Methods: White New Zealand rabbits anaesthetized and anticoagulated with heparin and trachea cannulated. Then the lung exposed and perfused with Krebs solution through pulmonary artery cannula. The ventilated-perfused lung was carefully excised from the chest and the healthy lungs were randomly divided into three groups (n=7 for each). Ventilation performed for 30 min with normoxic-normocapnic , or hypoxic-normocapnic, or hypoxic-hypercapnic gas mixtures. The percent changes of pulmonary vascular resistance per min (%PVR) and their maximum values were evaluated. Results: Hypoxic-normocapnic ventilation resulted in an initial sharp rise in PVR that after 8 min of exposure reversed to a slow decline. After 12 min of exposure a second steady rise in PVR occurred and continued until the end of the experiment. The rate of rise of PVR during hypoxic-hypercapnia was steeper (17.3±2.4% /min) compared to hypoxic-normocapnia (8.86±1.6% /min), but the maximum increases observed in PVR were similar in both conditions. Conclusion: In the isolated ventilated perfused lung, acute alveolar hypoxia had a complex influence on PVR and combination of hypoxia with hypercapnia transiently strengthened PVR without affecting its maximum level.
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