Nitric oxide and endothelin relationship in intestinal ischemia/reperfusion injury

Gastrointestinal mucosal blood flow is dependent on a balanced release of v asoactive substances from endothelium. Nitric oxide (NO) may increase the f low by vasodilatation and/or antiaggregation whereas endothelin (ET) may de crease it by vasoconstriction and aggregation. NO and ET may have counterba lancing effects on each other in tissue damage. in order to test this hypot hesis, in this study on rats, L-arginine to increase NO levels and NG-nitro -L-arginine methyl esther (L-NAME) to decrease NO levels have been used in an intestinal ischemia/reperfusion (I/R) injury model and portal vein Ei re sponse was evaluated. Lipid peroxidation product measurements and chemilumi nescence (CL) studies were also carried out in ileal tissue samples. Intest inal I/R injury caused an increase in portal venous ET levels with levels o f 9.4+/-0.5 fmol/ml in sham operation and 14.8+/-1.6 fmol/ml in I/R group. ET level of L-NAME-sh group was lower than that of sham-operated group and also ET level of L-NAME-I/R group was lower than that of I/R group. This yi elded the conclusion that inhibition of NO synthesis decreases portal venou s ET levels in this model. increased NO production by L-arginine caused inc reased ET levels in sham operated groups but this effect was not observed i n I/R injury state. This study also showed that inhibition of NO synthesis has a protective role by reducing the reperfusion damage in this model. It is likely that NO and ET have a feedback effect on each other both under ph ysiologic conditions and I/R injury.