Pharmacologic modulation of pulmonary vascular permeability during air embolism

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Pharmacologic modulation of pulmonary vascular permeability during air embolism

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dc.contributor.author Huang, KL en_US
dc.contributor.author Lin, YC en_US
dc.date.accessioned 2006-08-23T01:10:55Z
dc.date.available 2006-08-23T01:10:55Z
dc.date.issued 1997 en_US
dc.identifier.other Undersea Hyperb Med en_US
dc.identifier.uri PMID: 9444063 en_US
dc.identifier.uri http://archive.rubicon-foundation.org/2259
dc.description Undersea and Hyperbaric Medical Society, Inc. (http://www.uhms.org ) en_US
dc.description.abstract Pulmonary air embolism induces the generation of vasoactive and cytotoxic substances leading to lung injury. In the present study we investigated, in isolated and perfused rat lungs, the involvement of arachidonic acid metabolites in the alterations of vascular pressure, lung water content, and the filtration coefficient (Kf). We also tested the effects of a beta-agonist, a calcium channel blocker, and a cyclo-oxygenase inhibitor on the hemodynamic and the permeability changes following pulmonary air embolism. The artificially ventilated rat lungs were removed en bloc and suspended in a humidified chamber at 37 degrees C. The salt and buffered perfusate contained 4% Ficoll as albumin substitute for osmotic balance. We introduced air bubbles through the pulmonary artery. Air embolism increased pulmonary arterial resistance and caused pulmonary hypertension. Lungs receiving air infusion contained 88.6 +/- 0.6% water, which was significantly greater than the lung water content in the control groups (81.9 +/- 0.4%). Air embolism increased Kf by 145 +/- 19% from the baseline value. Pretreatment with indomethacin, isoproterenol, or nifedipine significantly reduced post-air-embolism lung water content to 85.8 +/- 0.5%, 84.1 +/- 0.4%, and 86.5 +/- 04%, respectively, and reduced the Kf increase to 17 +/- 8%, 1 +/- 9%, and 72 +/- 8%, respectively. These interventions did not alter the hemodynamic responses, except for the isoproterenol infusion, which shortened the half-time (T1/2) for pressure recovery after ending air infusion compared to the group with air embolism alone. Our results showed that indomethacin prevented vascular permeability increase and reduced pulmonary edema, suggesting that the cyclo-oxygenase products partially mediate the lung injury following air embolism. Furthermore, isoproterenol and nifedipine prevented or reduced the permeability increase, suggesting that alterations of the intracellular cAMP and cytosolic Ca2+ level play an important role in the pathophysiology of pulmonary air embolism. en_US
dc.format.extent 1857028 bytes
dc.format.mimetype application/pdf
dc.language.iso en_US
dc.rights Undersea and Hyperbaric Medical Society, Inc. (http://www.uhms.org ) en_US
dc.source.uri null en_US
dc.subject pulmonary en_US
dc.subject animal en_US
dc.subject rat en_US
dc.subject embolism en_US
dc.subject AGE en_US
dc.subject Pharmacologic en_US
dc.subject air en_US
dc.subject.mesh Animals Capillary Permeability/drug effects* Cyclooxygenase Inhibitors/pharmacology* Hypertension, Pulmonary/drug therapy Hypertension, Pulmonary/etiology Indomethacin/pharmacology Isoproterenol/pharmacology Lung/blood supply Lung/drug effects* Lung/physiopathology Male Nifedipine/pharmacology Pulmonary Artery/drug effects Pulmonary Artery/physiopathology Pulmonary Embolism/complications Pulmonary Embolism/physiopathology* Rats Rats, Wistar Vascular Resistance/drug effects Substances: Cyclooxygenase Inhibitors Nifedipine Indomethacin Isoproterenol en_US
dc.title Pharmacologic modulation of pulmonary vascular permeability during air embolism en_US

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