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1 Department of Physiology, Northeastern Ohio Universities College of Medicine, Rootstown, Ohio 44272; and 2 Department of Biology, Westminster College, New Wilmington, Pennsylvania 16172
Endogenous epinephrine has been found to increase
alveolar liquid clearance (ALC) in several pulmonary edema
models. In this study, we infused epinephrine
intravenously for 1 h in anesthetized rats to produce plasma
epinephrine concentrations commonly observed in this species under
stressful conditions and measured ALC by mass balance. Epinephrine
increased ALC from 31.5 ± 3.2 to 48.9 ± 1.1 (SE)% of the
instilled volume (P < 0.05). The
increased ALC was prevented by either propranolol or amiloride. To
determine whether ALC returns to normal after plasma epinephrine
concentration normalizes, we measured ALC 2 h after stopping an initial
1-h epinephrine infusion and found ALC to be at baseline values.
Finally, to determine whether desensitization of the liquid clearance
response occurs, we evaluated the effects of both repeated 1-h
infusions and a continuous 4-h infusion of epinephrine on ALC and found no reduction in ALC under either condition. We conclude that
epinephrine increases ALC by stimulating 
-adrenoceptors and sodium
transport, that the increase is reversible once plasma epinephrine
concentration normalizes, and that desensitization of the ALC response
does not appear to occur after 4 h of continuous epinephrine exposure.
pulmonary edema; lung fluid balance; alveolar epithelium; 2-adrenergic agonist; homologous desensitization; downregulation
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