DIFFERENTIAL-EFFECTS OF EXPERIMENTALLY-INDUCED CHRONIC-PANCREATITIS ON NEUROPEPTIDE IMMUNOREACTIVITIES IN THE FELINE PANCREAS

The distribution and concentration of calcitonin gene-related peptide (CGRP), substance P (SP), vasoactive intestinal polypeptide (VIP), neu ropeptide Y (NPY), and gastrin-releasing peptide (GRP) immunoreactivit ies in the pancreas of cats with experimentally induced chronic pancre atitis and of age- and sex-matched controls were investigated. By narr owing the main pancreatic duct between the head and the body to approx imately 25% of its normal diameter, we induced within 5 weeks chronic pancreatitis restricted to the body and tail. In control animals, pept ide immunoreactive nerves were distributed to the islets, acini, and d ucts; the latter were predominantly innervated by fibers immunoreactiv e for NPY, VIP, or CGRP. The vasculature received an abundant supply o f NPY-, CGRP-, and, to a lesser extent, SP-containing axons. Within in trapancreatic ganglia, peptide immunoreactivities were identified in f ibers and ganglion cells, with the exception of CGRP and SP immunostai ning, which could be visualized only in fibers. In animals with chroni c pancreatitis, the innervation pattern of each peptidergic system was comparable to that described in controls. However, there was a remark able increase in the density and staining intensity of VIP and NPY imm unoreactive fibers in the exocrine parenchyma and fibrous septa of the body and tail, where chronic pancreatitis developed. Fibers immunorea ctive for CGRP and SP also were moderately denser than in controls, wh ereas those containing GRP immunoreactivity did not show any detectabl e changes. In addition, a marked increase of the immunostaining for VI P and, to a much lesser extent, for NPY and GRP, was observed in neuri tes supplying the head of the pancreas, which appeared devoid of histo logically detectable pathological alterations. Radioimmunoassay analys is confirmed the immunohistochemical observations. The increased densi ty of distinct peptidergic nerves in the pancreas with induced chronic pancreatitis might be the result of compensatory phenomena in respons e to the inflammatory process.