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Mechanisms responsible for acute pancreatitis‐stimulated alveolar fluid clearance capacity in rat lungs
Author(s) -
Sakuma Tsutomu,
Xu Jin,
Wang Zheng,
Maeda Sumiko,
Sugita Makoto,
Sagawa Motoyasu,
Shimazaki Miyako,
Ueda Yoshimichi
Publication year - 2006
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.20.4.a745
Subject(s) - acute pancreatitis , pancreatitis , medicine , endocrinology , yohimbine , prazosin , antagonist , chemistry , receptor
We determined whether acute pancreatitis affected alveolar fluid clearance in rat lungs. Acute pancreatitis was induced by a retrograde injection of 5% taurocholate sodium (0.2 ml) into the common bile duct. Alveolar fluid clearance was estimated by the increase of the alveolar albumin concentration in the isolated rat lungs 4, 24, and 48 hrs after pancreatitis. Effects of endogenous catecholamine on alveolar fluid clearance and expression of sodium channel and Na,K‐ATPase mRNA were determined. We found that acute pancreatitis increased epinephrine and norepinephrine levels in blood and stimulated alveolar fluid clearance by 180 and 120% at 4 and 24 hrs after pancreatitis, respectively. Prazosin (α 1 ‐antagonist), yohimbine (α 2 ‐antagonist), and adrenalectomy, but not propranolol (β‐antagonist), inhibited pancreatitis‐stimulated alveolar fluid clearance in part. A combination of prazosin and yohimbine abolished the effect of pancreatitis. Pancreatitis also increased the expression of α‐, β‐, γ‐ENaC mRNA and α 1 ‐, β 1 ‐Na,K‐ATPase mRNA. In conclusion, acute pancreatitis increases alveolar fluid clearance via α‐adrenoceptors‐mediated mechanism. (Grant from Kanazawa Medical University H2005‐7, Grand‐in‐Aid for Scientific Research from MEXT Japan 17591492)