Premium
Effects of propranolol on gastric microcirculation and acid secretion in portal hypertensive rats
Author(s) -
Piqué Josep M.,
Pizcueta Pilar,
Ayuso ROSA M. Pérez,
Bosch Jaime
Publication year - 1990
Publication title -
hepatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.488
H-Index - 361
eISSN - 1527-3350
pISSN - 0270-9139
DOI - 10.1002/hep.1840120305
Subject(s) - propranolol , pentagastrin , medicine , portal hypertension , gastric acid , basal (medicine) , endocrinology , blood flow , portal venous pressure , gastric mucosa , stomach , cirrhosis , insulin
Rats with chronic portal hypertension have an increased gastric mucosal blood flow and an impaired acid secretory response to pentagastrin stimulation. This study investigated the effects of propranolol, a drug widely used in the treatment of portal hypertension, on gastric mucosal blood flow and acid secretion in portal hypertensive rats with partial portal vein occlusion. In study I, gastric mucosal blood flow, measured by hydrogen gas clearance, and acid output were determined in basal conditions and after the administration of propranolol (0.3 mg/kg/min) or vehicle infusion in portal hypertensive and sham‐operated rats. Gastric mucosal blood flow was significantly higher (p < 0.005) in portal hypertensive rats than in sham‐operated rats, and it was significantly reduced (p < 0.05) after propranolol infusion in portal hypertensive rats (39 ± 2 vs. 35 ± 3 ml/min/100 gm). Basal acid output was not significantly modified with propranolol infusion, either in portal hypertensive or sham‐operated animals. In study II, acid output was measured in portal hypertensive rats in basal conditions, during pentagastrin (20 μ/kg/hr) infusion and after the combined infusion of pentagastrin and propranolol (or vehicle). Pentagastrin infusion significantly increased (p < 0.001) acid output, but propranolol did not modify stimulated gastric acid secretion. In conclusion, propranolol induced a slight but significant reduction in gastric mucosal blood flow and did not change basal or stimulated gastric acid secretion. (H EPATOLOGY 1990;12:476–480).