Issn Print: 0885-3177
Publication Date: 2006/11/01
THE TRYPSINOGEN ACTIVATOR ENTEROKINASE PROMOTES PANCREATIC INFLAMMATORY PAIN
Eugene P. Ceppa; Sarah W. Grahn; Lorna Divino; Kimberly S. Kirkwood
+ Author Information
Author Information: Department of Surgery, Duke University Medical Center, Durham, NC;
Excerpt
Premature activation of trypsin within the pancreatic acinar cells is an early event in acute pancreatitis which results in pancreatic parenchymal auto-digestion. Intrapancreatic injection of exogenous trypsin produces pain by potentiating capsaicin-induced activation of TRPV1, an ion channel specialized to integrate noxious inflammatory stimuli. Expression of fos protein in laminae I and II of the dorsal horn of the spinal cord is a validated measure of pancreatic nociception in the rat. Although the possibility that pancreatic trypsin promotes pain has been suggested by studies using exogenous trypsin, the significance of this finding depends upon the ability of endogenous trypsin to promote TRPV1activation and nociception. We hypothesized that injection of enterokinase into the pancreas would promote inflammation and activate pancreatic pain pathways via a mechanism involving TRPV1.