title: Catecholamine clearance from alveolar spaces of rat and human lungs.
abstract: BACKGROUND
  Although aerosolized beta-adrenergic agonists have been used as a therapy for the resolution of pulmonary edema, the mechanisms of catecholamine clearance from the alveolar spaces of the lung are not well known.
  
  
  OBJECTIVE
  To determine whether catecholamine clearance from the alveolar spaces is correlated with the fluid transport capacity of the lung.
  
  
  METHODS
  Albumin solution containing epinephrine (10(-7)M) or norepinephrine (10(-7)M) was instilled into the alveolar spaces of isolated rat and human lungs. Alveolar fluid clearance rate was estimated by the progressive increase in the albumin concentration over 1 h. Catecholamine clearance rate was estimated by the changes in catecholamine concentration and alveolar fluid volume over 1 h.
  
  
  RESULTS
  The norepinephrine clearance rate was faster than the epinephrine clearance rate in the rat and human lungs. In the rat lungs, amiloride (a sodium channel blocker) caused a greater decrease in alveolar fluid clearance and epinephrine clearance rate than propranolol (a nonselective beta-adrenergic antagonist). Although propranolol and phentolamine (an alpha-adrenergic antagonist), and 5-(N-ethyl-N-isoprophyl)amiloride (a Na+/H+ antiport blocker) changed neither the alveolar fluid clearance nor the norepinephrine clearance rate, amiloride and benzamil (a sodium channel blocker) decreased both clearance rates. As in the rat lungs, amiloride decreased alveolar fluid and norepinephrine clearance rates in the human lungs.
  
  
  CONCLUSIONS
  These results indicate that the catecholamine clearance rate from the alveolar spaces is correlated with alveolar fluid clearance in rat and human lungs.
authors.affiliation: Thoracic Surgery, Kanazawa Medical University, Uchinada, Ishikawa, Japan. sakuma-t@kanazawa-med.ac.jp
authors.forename: Tsutomu
authors.initials: T
authors.lastname: Sakuma
authors.forename: Xiu
authors.initials: X
authors.lastname: Gu
authors.forename: Makoto
authors.initials: M
authors.lastname: Sugita
authors.forename: Motoyasu
authors.initials: M
authors.lastname: Sagawa
authors.forename: Maki
authors.initials: M
authors.lastname: Sakuda
authors.forename: Hirohisa
authors.initials: H
authors.lastname: Toga
mesh_terms: D000316:Adrenergic alpha-Agonists / Q000008:administration & dosage / Q000493:pharmacokinetics; D000317:Adrenergic alpha-Antagonists / Q000008:administration & dosage / Q000493:pharmacokinetics; D000318:Adrenergic beta-Agonists / Q000008:administration & dosage / Q000493:pharmacokinetics; D000584:Amiloride / Q000008:administration & dosage / Q000031:analogs & derivatives* / Q000493:pharmacokinetics; D000818:Animals; D002395:Catecholamines / Q000008:administration & dosage / Q000493:pharmacokinetics*; D004837:Epinephrine / Q000008:administration & dosage / Q000493:pharmacokinetics; D045604:Extracellular Fluid / Q000378:metabolism; D006801:Humans; D066298:In Vitro Techniques; D007322:Instillation, Drug; D008297:Male; D009638:Norepinephrine / Q000008:administration & dosage / Q000493:pharmacokinetics; D010646:Phentolamine / Q000008:administration & dosage / Q000493:pharmacokinetics; D011433:Propranolol / Q000008:administration & dosage / Q000493:pharmacokinetics; D011650:Pulmonary Alveoli / Q000166:cytology / Q000378:metabolism*; D051381:Rats; D017207:Rats, Sprague-Dawley; D026941:Sodium Channel Blockers / Q000008:administration & dosage / Q000493:pharmacokinetics; D017923:Sodium-Hydrogen Exchangers / Q000037:antagonists & inhibitors
chemical_list: D000316:Adrenergic alpha-Agonists; D000317:Adrenergic alpha-Antagonists; D000318:Adrenergic beta-Agonists; D002395:Catecholamines; D026941:Sodium Channel Blockers; D017923:Sodium-Hydrogen Exchangers; D000584:Amiloride; D011433:Propranolol; C039614:ethylisopropylamiloride; D009638:Norepinephrine; D004837:Epinephrine; D010646:Phentolamine