Clonidine pre-treatment prevents hemorrhagic shock-induced endotoxemia and oxidative stress in the gut, liver, and lungs of the rat.

To study the effect of clonidine pre-treatment on hemorrhagic shock (H/S)-induced endotoxemia and oxidative stress (OS) in three vital organs of the rat. The study protocol consisted of two arms: one for the measurement of organic hydroperoxide (LOOH) and superoxide radical (O(2)(-·)) production in the gut, liver, and lungs (n = 32 rats) and one for the measurement of endotoxin in portal and systemic circulation (n = 32 rats). Four animal groups (sham, clonidine, H/S, and clonidine-H/S group) were used in each arm. Three hours after H/S and concominant blood resuscitation, tissues were collected for LOOHs and O(2)(-·) measurement and blood samples were obtained for endotoxin determination. Clonidine pre-treatment prior to H/S resulted in a significant reduction of LOOHs and O(2)(-·) production in all vital organs (P < 0.05-0.001), while additionally, clonidine reduced H/S-induced endotoxemia in portal (P < 0.05) and systemic circulation as well (P < 0.01). Clonidine pre-treatment prevents endotoxemia and OS in the gut, liver, and lungs of rats subjected to severe H/S. The improved intestinal barrier function probably stems from the antioxidant effect of clonidine on the intestinal epithelium, whereas the reduced endotoxemia may contribute to a decreased OS observed in the liver and lungs.