Physiopathogenic hypothesis of alcoholic pancreatitis: supranormal ecbolic stimulation of the "pancreon" units secondary to the loss of the negative component of pancreas innervation.

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.