Effects of penehyclidine hydrochloride in small intestinal damage caused by limb ischemia-reperfusion

AIM：To investigate the protective effect of penehyclidine hydrochloride post-conditioning in the damage to the barrier function of the small intestinal mucosa caused by limb ischemia-reperfusion（LIR） injury. METHODS：Male Wistar rats were randomly divided into three groups（36 rats each） ：the sham-operation group（group S） ,lower limb ischemia-reperfusion group（group LIR） ,and penehyclidine hydrochloride postconditioning group（group PHC） .Each group was divided into subgroups（n=6 in each group） according to ischemic-reperfusion time,i.e.immediately 0 h（T1） ,1 h（T2） ,3 h（T3） ,6 h（T4） ,12 h（T5） ,and 24 h（T6） .Bilateral hind-limb ischemia was induced by rubber band application proximal to the level of the greater trochanter for 3 h.In group PHC,0.15 mg/kg of penehyclidine hydrochloride was injected into the tail vein immediately after 3 h of bilateral hind-limb ischemia.The designated rats were sacrificed at different time-points of reperfusion;diamine oxidase（DAO） ,superoxide dismutase（SOD） activity,myeloperoxidase（MPO） of small intestinal tissue,plasma endotoxin,DAO,tumor necrosis factor-α（TNF-α） ,and interleukin（IL） -10 in serum were detected in the rats. RESULTS：The pathological changes in the small intestine were observed under light microscope.The levels of MPO,endotoxin,serum DAO,and IL-10 at T1-T6,and TNF-αlevel at T1-T4 increased in groups LIR and PHC（P0.05） compared with those in group S,but tissue DAO and SOD activity at T1-T6 decreased（P0.05） .In group PHC,the tissue DAO and SOD activity at T2-T6,and IL-10 at T2-T5 increased to higher levels than those in group LIR（P0.05） ;however,the levels of MPO,endotoxin,and DAO in the blood at T2-T6,and TNF-αat T2 and T4 decreased（P0.05） . CONCLUSION：Penehyclidine hydrochloride post-conditioning may reduce the permeability of the small intestines after LIR.Its protection mechanisms may be related to inhibiting oxygen free radicals and inflammatory cytokines for organ damage.