A Supraceliac Aortic Cross Clamping Model to Explore Remote Lung Injury and the Endothelial Glycocalyx.

BACKGROUND:We hypothesized that supraceliac aortic cross clamping could induce lung injury mediated by an inflammatory ischemia-reperfusion (IR) trigger. We aimed to characterize glycocalyx (GCX), a component of endothelial membrane, participating to remote lung injury. METHODS:Rats underwent supraceliac aortic cross clamping for 40 min and were sacrificed at 0, 3, 6, and 24 hr of reperfusion (n = 10/group). Each group was compared to sham (n = 6/group). GCX products (syndecan-1 [Sdc-1] and heparan sulfate [HS]), tumor necrosis factor-alpha (TNF-α), and interleukin-1β (IL-1β) were measured in plasma (enzyme-linked immunosorbent assay[ELISA]). Lungs were harvested for measurements of TNF-α, IL-1β (polymerase chain reaction) and Sdc-1 (western blotting [WB]). Histologic lung injury scoring and pulmonary gravimetry were analyzed in a blinded manner. RESULTS:Plasmatic Sdc-1, HS, TNF-α, and IL-1β reached peak levels at 3 hr. Levels were significantly higher in clamping groups than sham at 6 hr for Sdc-1, at 0 and 3 hr for HS, at 3 and 6 hr for TNF-α, and at 3 hr for IL-1β. Lung TNF-α and Interleukin-1β reached peak levels at 6 hr. Levels were significantly higher than sham at 6 and 24 hr for TNF-α and at 6 hr for IL-1β. Lung Sdc-1 was lowest at 3 hr. Sdc-1 was not significantly different compared to sham at the different reperfusion times. At 3 hr, it was 0.27 ± 0.03 vs. 0.33 ± 0.02 (sham) (P = 0.09). Histopathologic scores at 6 and 24 hr were higher in clamping groups than sham. At 6 and 24 hr, it was higher for hemorrhage, polynuclear neutrophil (PNN) infiltration and intravascular leukocytes. Pulmonary edema was higher by gravimetry at 0 and 6 hr. CONCLUSIONS:Supra celiac aortic clamping causes early lung injury in relation with a systemic inflammatory response associated with altered GCX structure.