BACKGROUND: Despite emergence of markers of intestinal mucosal damage such as intestinal fatty-acid binding protein (i-FABP), there are no specific markers of damage extending into the muscle layers. We hypothesized that smooth muscle actin (SMA) released from the intestinal muscularis would be detectable in plasma after severe intestinal injury. MATERIALS AND METHODS: Serial blood samples were collected from rats (n = 10) undergoing intestinal ischemia-reperfusion injury (IRI) and controls (n = 5). Additionally, admission and/or preoperative plasma samples were collected from twelve neonates with necrotizing enterocolitis (NEC), and five age- and weight-matched controls. Plasma ileal fatty-acid binding protein (rat) or i-FABP (human) were measured by enzyme-linked immunosorbent assay, and plasma SMA was detected by western blotting. RESULTS: Plasma ileal fatty-acid binding protein was low in both the control group and IRI at baseline, but became rapidly elevated in the IRI group even during ischemia. SMA was detected in reperfusion plasma samples of all IRI rats, but in none of the control samples. Plasma i-FABP was higher in infants with NEC than age- and weight-matched controls. Although i-FABP was higher in infants with severe surgical disease compared with focal disease, there was no difference between the operative and nonoperative groups. SMA was detected in the plasma of all four neonates with severe surgical NEC, but not in those with focal disease or those who were successfully conservatively managed. CONCLUSIONS: SMA is detectable in plasma after severe intestinal injury and maybe a clinically useful maker of intestinal muscle damage.
BACKGROUND: Despite emergence of markers of intestinal mucosal damage such as intestinal fatty-acid binding protein (i-FABP), there are no specific markers of damage extending into the muscle layers. We hypothesized that smooth muscle actin (SMA) released from the intestinal muscularis would be detectable in plasma after severe intestinal injury. MATERIALS AND METHODS: Serial blood samples were collected from rats (n = 10) undergoing intestinal ischemia-reperfusion injury (IRI) and controls (n = 5). Additionally, admission and/or preoperative plasma samples were collected from twelve neonates with necrotizing enterocolitis (NEC), and five age- and weight-matched controls. Plasma ileal fatty-acid binding protein (rat) or i-FABP (human) were measured by enzyme-linked immunosorbent assay, and plasma SMA was detected by western blotting. RESULTS: Plasma ileal fatty-acid binding protein was low in both the control group and IRI at baseline, but became rapidly elevated in the IRI group even during ischemia. SMA was detected in reperfusion plasma samples of all IRI rats, but in none of the control samples. Plasma i-FABP was higher in infants with NEC than age- and weight-matched controls. Although i-FABP was higher in infants with severe surgical disease compared with focal disease, there was no difference between the operative and nonoperative groups. SMA was detected in the plasma of all four neonates with severe surgical NEC, but not in those with focal disease or those who were successfully conservatively managed. CONCLUSIONS: SMA is detectable in plasma after severe intestinal injury and maybe a clinically useful maker of intestinal muscle damage.