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Excerpt
Background: All three selectin family members (P.E and L) have been implicated as mediators of neutrophil migration through the endothelium during I/R injury. We hypothesized that PSGL-1, a homodimeric mucin which can bind all three selectins, would ameliorate intestinal mucosal and pulmonary capillary hyperpermeability in a rat model of superior mesenteric artery (SMA) occlusion and reperfusion.
Methods: To investigate the role of selectins in intestinal I/R injury. PSGL-1 (0.4 mg/kg, i.v bolus) or vehicle (n=6/group) were administered 5 min prior to 60-min ischemia and 1 min prior to 60-min reperfusion. Five segments of small intestine were isolated at baseline (BL). 30- and 60-min ischemia (130 and 160, respectively), and 30- and 60-min reperfusion (R30 and R60, respectively). Intestinal permeability was assessed using an everted gut sac technique by measuring the mucosal-to-serosal clearance (nl/min/cm2) of fluorescently labelled dextran (MW=4 kDa. FD4). Serosal and mucosal blood flow (SBF and MBF, respectively) were monitored by Doppler Laser flowmetry. To evaluate remote lung injury. FD4 (5 mg/kg. i.v. bolus) was given 30 min prior to SMA occlusion (n=6/group). Bronchoalveolar lavage (BAL) of right lung was obtained at the end of the R60 period for determination of BAL/plasma ratio (%BPR), white blood cell count (wbc: x104 cells/ml), and protein concentration ([micro sign]g/ml). Percent total water content (TW) of the left lung was also determined.
Results: SBF and MBF were not significantly different between the two groups. (Table 1)
Conclusion: These data support the idea that selectins play a role in the pathogenesis of I/R-induced gut mucosal hyperpermeability, but also suggest that other factors, not blocked by PSGL-1, are important as well.
