We have previously shown that experimental
peritonitis secondary to fecal bacteria plus
barium sulfate suppresses delayed cutaneous
hypersensitivity (DCH) in rats. We examined herein the role of
barium sulfate. In a series of experiments presensitized rats were simultaneously skin tested with intradermal
keyhole limpet hemocyanin and given an
intraperitoneal injection of either (1) a mixture of four fecal bacteria in their nutrient broths, (2) bacteria and broths plus
barium sulfate, (3) sterile broths plus
barium, (4) sterile
barium alone, (5) nutrient broths, or (6) saline. In rats given sterile
barium we measured phagocyte delivery to subcutaneous
polyvinyl alcohol sponges. We found that (1) the coadministration of
barium sulfate was necessary for rats given bacteria to die (P = 0.03) or develop
abdominal abscesses (P less than 0.005), (2) suppression of DCH occurred in 70% of rats receiving sterile
barium sulfate vs 0% in saline controls (P = 0.0001), (3) early suppression of DCH was associated with subsequent death and
abscess formation in rats given bacteria plus
barium (P = 0.00002) and with intraabdominal
barium collections in rats given
barium alone (P less than 0.02), (4)
barium sulfate administration caused suppression of phagocyte delivery to subcutaneous sponges: 23.2 X 10(6) cells/site vs 43.1 X 10(6) cells/site in saline controls (P less than 0.005). We conclude that
barium sulfate itself has profound systemic effects in the rat model of intraabdominal
sepsis. Early suppression of DCH is associated with a poor outcome in septic rats.