title: Physiopathogenic hypothesis of alcoholic pancreatitis: supranormal ecbolic stimulation of the "pancreon" units secondary to the loss of the negative component of pancreas innervation.
abstract: In the rat, basal pancreatic secretion is generated and modulated by positive and negative duodeno-pancreatic reflexes. The former activates secretion, the latter acts as a "brake". Impairment of this brake plays a crucial role in the pathogenesis of alcoholic pancreatitis by causing elevation of pancreatic cholinergic tone and inducing increased pancreon ecbolic response to CCK-PZ stimulation. Both factors lead to pancreatic damage by supranormal stimulation of the pancreon.
authors.affiliation: Gastroenterology Section, Clinicas Hospital, University of Buenos Aires.
authors.forename: O M
authors.initials: OM
authors.lastname: Tiscornia
authors.forename: D A
authors.initials: DA
authors.lastname: Dreiling
mesh_terms: D000208:Acute Disease; D000437:Alcoholism / Q000150:complications*; D000818:Animals; D001341:Autonomic Nervous System / Q000503:physiopathology; D004285:Dogs; D004386:Duodenum / Q000294:innervation; D006801:Humans; D010179:Pancreas / Q000294:innervation* / Q000378:metabolism; D010195:Pancreatitis / Q000209:etiology / Q000503:physiopathology*; D051381:Rats