Endogenous catecholamine stimulates alveolar fluid clearance in rats with acute pancreatitis

Abstract

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. 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. 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. Endogenous catecholamine stimulates alpha-adrenoceptors and increases alveolar fluid clearance in rats with acute pancreatitis.