Physiopathogenic Hypothesis of Alcoholic Pancreatitis

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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.

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