Effects of traumatic brain injury on intestinal contractility

Abstract

Patients with traumatic brain injury (TBI) often suffer from gastrointestinal dysfunction including intolerance to enteral feedings. However, it is unclear how TBI affects small intestinal contractile activity. The purpose of this study was to determine if TBI affects intestinal smooth muscle function. Sprague-Dawley rats were subjected to controlled cortical impact injury (TBI). Sham animals underwent a similar surgery but no injury (SHAM). Animals were sacrificed 1, 3, and 7days after TBI and intestinal smooth muscle tissue was collected for measurement of contractile activity and transit, NF-kB activity, and cytokine levels. Brains were collected after sacrifice to determine volume loss due to injury. Contractile activity decreased significantly in ileum, but not jejunum, in the TBI group 7days after injury compared with SHAM. Brain volume loss increased significantly 7days after injury compared with 3days and correlated significantly with the contractile activity 1day after injury. In the intestinal smooth muscle, NF-kB activity increased significantly in the TBI group 3 and 7days after injury vs SHAM. Wet to dry weight ratio, indicating edema, also increased significantly in the TBI group. Interleukin-1α, -1β, and -17 increased significantly in the TBI group compared with SHAM. Traumatic brain injury causes a delayed but significant decrease in intestinal contractile activity in the ileum leading to delayed transit. The decreased intestinal contractile activity is attributed to secondary inflammatory injury as evidenced by increased NF-kB activity, increased edema, and increased inflammatory cytokines in the intestinal smooth muscle.