PORTAL PRESSURES AND HEPATIC FIBROSIS AS MECHANISMS IN THE DEVELOPMENT OF ESOPHAGOGASTRIC ULCERS INDUCED IN SWINE BY INFECTIONS WITH ASCARIS SUUM GOEZE, 1782
Abstract
Esophagogastric (EG) ulceration of swine can be induced with two inoculations of 200,000 embryonated Ascaris suum eggs, administered two weeks apart. The objective of this project was to study the mechanisms involved in the ulcerogenesis. Following the second inoculation of ascarid eggs, severe hepatic perilobular fibrosis develops, resulting in resistance to intrahepatic portal venous flow, with consequent elevation of hydrostatic pressure in the portal vein trunk. This elevated pressure upsets the gradient necessary for venous drainage of the viscera, and in particular the EG area. Physiologically this could be a major factor in the ulcerogenesis, as well as a cause of the associated hemorrhage from collateral circulation that develops. Using direct manometry, portal venous pressures (PVP) were determined in pentobarbital anesthetized piglets. In a preliminary trail using hysterotomy-derived piglets, a significant difference (P < 0.05) was observed between the PVP group means of the A. suum infected group (x = 12.4 (+OR-) 3.1 cm saline) and the uninfected control group (x = 4.0 (+OR-) 1.4 cm saline). An experimental model was developed where resistance to hepatic portal flow was induced by intraportal inoculation of 1 x 10('6) polystyrene microspheres. The PVP and the development of EG lesions produced were similar to those in A. suum infected swine. The MSP-MSP group (n = 16) receiving two inoculations of microspheres, two weeks apart, had a mean PVP 11.2 (+OR-) 1.3 cm saline. The ASC-ASC (n = 14) administered two ascarid infections had a mean PVP 7.6 (+OR-) 0.6. The third treatment group ASC-MSP group (n = 13) receiving an inoculum of microspheres two weeks following ascarid infection had mean PVP 8.42 (+OR-) 1.6 cm saline. The uninoculated control group (n = 11) had a mean PVP of 5.4 (+OR-) 1.1 cm saline. In the ASC-ASC group, 85% of the animals and 56% of the MSP-MSP group had ulcerative or erosive EG lesions in the stomach; 61.5% of the animals ASC-MSP group had similar EG lesions. Of these groups 58%, 18.75%, and 23%, respectively, had severely ulcerated EG lesions. Where neither ulcerative or erosive EG lesions were evident, moderate to severe parakeratotic changes were present. Five of the 11 controls had mild hyperplasia of the EG area, but none had ulcers or ersosions. From the data presented, it appears that elevated PVP subsequent to hapatic fibrosis plays an important role in the development of EG ulcers induced in swine by infections with A. suum.
Degree
Ph.D.
Subject Area
Animal diseases
Off-Campus Purdue Users:
To access this dissertation, please log in to our
proxy server.