title: Endogenous catecholamine stimulates alveolar fluid clearance in rats with acute pancreatitis.
abstract: OBJECTIVE
  Acute pancreatitis causes pulmonary oedema with the accumulation of fluid in the alveolar spaces, possibly due to reduced clearance. This study tested the hypothesis that acute pancreatitis decreases alveolar fluid clearance in a rat model of pulmonary oedema during acute pancreatitis.
  
  
  METHODS
  Acute pancreatitis was induced by a retrograde injection of 5% taurocholate sodium (0.2 mL) into the common bile duct. The lungs were isolated 4, 24 and 48 h after the induction of acute pancreatitis and alveolar fluid clearance was measured in the absence of pulmonary perfusion.
  
  
  RESULTS
  Alveolar fluid clearance increased to 31.0 +/- 3.5% of instilled volume/h in rats with acute pancreatitis for 4 h compared with 17.3 +/- 1.0% of instilled volume/h in sham rats (P < 0.01), then returned to the control level 48 h after acute pancreatitis (16.0 +/- 4.1% of instilled volume/h). In contrast, the lung water to dry lung weight ratio decreased maximally 24 h after acute pancreatitis (P < 0.01), then returned to the control level 48 h after acute pancreatitis. The plasma epinephrine levels increased to 25-fold higher in rats with acute pancreatitis for 4 h than in sham rats without acute pancreatitis. Prazosin (an alpha(1)-adrenergic antagonist, 10(-4) mol/L), yohimbine (an alpha(2)-adrenergic antagonist, 10(-4) mol/L) or a bilateral adrenalectomy inhibited the increase in part, a combination of prazosin (10(-4) mol/L) and yohimbine (10(-4) mol/L) completely inhibited the increase in alveolar fluid clearance in rats after acute pancreatitis for 4 h, whereas propranolol (a beta-adrenergic antagonist, 10(-4) mol/L) had no effect.
  
  
  CONCLUSIONS
  Endogenous catecholamine stimulates alpha-adrenoceptors and increases alveolar fluid clearance in rats with acute pancreatitis.
authors.affiliation: Thoracic Surgery, Kanazawa Medical University, Uchinada, Ishikawa, Japan.
authors.forename: Jin
authors.initials: J
authors.lastname: Xu
authors.forename: Zheng
authors.initials: Z
authors.lastname: Wang
authors.forename: Gang
authors.initials: G
authors.lastname: Ma
authors.forename: Motoyasu
authors.initials: M
authors.lastname: Sagawa
authors.forename: Miyako
authors.initials: M
authors.lastname: Shimazaki
authors.forename: Yoshimichi
authors.initials: Y
authors.lastname: Ueda
authors.forename: Tsutomu
authors.initials: T
authors.lastname: Sakuma
mesh_terms: D000208:Acute Disease; D000315:Adrenalectomy; D000316:Adrenergic alpha-Agonists / Q000097:blood; D000317:Adrenergic alpha-Antagonists / Q000494:pharmacology / Q000627:therapeutic use; D000818:Animals; D001992:Bronchoalveolar Lavage Fluid; D002395:Catecholamines / Q000378:metabolism*; D004195:Disease Models, Animal; D004837:Epinephrine / Q000097:blood; D053503:Epithelial Sodium Channels / Q000378:metabolism; D008297:Male; D010195:Pancreatitis / Q000139:chemically induced / Q000150:complications* / Q000378:metabolism*; D011224:Prazosin / Q000494:pharmacology / Q000627:therapeutic use; D011654:Pulmonary Edema / Q000188:drug therapy / Q000209:etiology* / Q000378:metabolism*; D012333:RNA, Messenger / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D011942:Receptors, Adrenergic, alpha / Q000187:drug effects / Q000378:metabolism; D013656:Taurocholic Acid / Q000009:adverse effects; D015016:Yohimbine / Q000494:pharmacology / Q000627:therapeutic use
chemical_list: D000316:Adrenergic alpha-Agonists; D000317:Adrenergic alpha-Antagonists; D002395:Catecholamines; D053503:Epithelial Sodium Channels; D012333:RNA, Messenger; D011942:Receptors, Adrenergic, alpha; D015016:Yohimbine; D013656:Taurocholic Acid; D011224:Prazosin; D004837:Epinephrine