The Effect of Atropine and Duct Decompression on the Evolution of Diazinon™-Induced Acute Canine Pancreatitis

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Abstract
Three groups of 8 dogs each were studied to evaluate the early evolution of the hyperamylasemia, hyperlipasemia and acinar cell pathology at the light microscopic and EM levels during acute Diazinon-induced pancreatitis. Two more groups of 5 dogs each were evaluated for the effects of cholinergic receptor blockade with atropine and ductal decompression on the evolution of serum enzyme changes and acinar cell pathology. Group 1 dogs received a secretion infusion of 2 U/kg per h and a Diazinon infusion of 75 mg/kg, and demonstrated significant increases in serum amylase and lipase at 1, 2, and 3 h. Light microscopy revealed acinar cell vacuolization and progressive interstitial edema. EM revealed the formation of large intracytoplasmic vacuoles filled with flocculent material, the fusion of these vacuoles with basolateral membrane and the formation of interstitial edema. In both Group 2 dogs (that received secretin alone) and Group 3 dogs (that received atropine, 200 .mu.g/kg i.v. prior to secretin and Diazinon), the serum enzyme levels and histologic results were normal. In Group 4 dogs, pancreatic duct cannulation to prevent hypertension prevented the hyperamylasemia and hyperlipasemia, but not the acinar cell vacuolization and interstitial edema. This model for acute interstitial pancreatitis is apparently cholinergic-receptor mediated, the serum enzyme elevations are due primarly to ductal hypertension and the acinar cell pathology is primarily due to cholinergic stimulation and occurs independent of ductal hypertension.