Undersea Hyperbar M
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Undersea Hyperbar M · Jan 1997
Pharmacologic modulation of pulmonary vascular permeability during air embolism.
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. ⋯ 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.