Abstract
Objective
To identify the cause and mechanisms of injury in gastroesophageal ulcer disease in market weight swine.
Design
Comparison of mechanisms of injury caused by HCI with those caused by short chain fatty acids (SCFA) in gastric mucosa.
Animals
Pigs weighing 30 to 40 kg.
Procedure
Gastric tissues were studied in Ussing chambers; short-circuit current (Isc) and electrical resistance (R) were recorded in response to treatment, and tissues were examined histologically.
Results
60 mM mucosal acetate abruptly (≤ 75 minutes) and irreversibly abolished Isc at pH ≤ 4.5, whereas R decreased more slowly. These data were associated with cell swelling and vesicle formation in mid-zonal layers, followed by sloughing of the outer barrier, erosion into deeper zones, and finally, ulceration. Mucosal HCI at pH > 1.5 was ineffective; however, at pH 1.5, HCI induced an abrupt decrease in R, followed by a slow decrease in Isc, an effect opposite to that caused by SCFA. Serosal addition of HCI rapidly abolished Isc suggesting a barrier to free H+ diffusion from the mucosal solution.
Conclusions
Undissociated SCFA rapidly penetrate the outer barrier and acidify underlying viable tissue. Cellular acidification inhibits Na pumping and osmoregulation, resulting in cell swelling and necrosis. In contrast, HCI induces an increase in outer barrier permeability before accessing the transporting cells, a much longer process (≥ 5 hours) requiring a lower pH. These studies suggest that microbial production of SCFA may be important in the pathogenesis of porcine gastric ulcers. (Am J Vet Res 1996;57:564-573)
