Alican I, Yegen C, Olcay A, Kurtel H, Yegen B
Department of Physiology, Marmara University, School of Medicine, Haydarpaşa, Istanbul, Turkey.
Digestion. 1998 Jul-Aug;59(4):343-8. doi: 10.1159/000007513.
BACKGROUND/AIMS: To evaluate the involvement of ET-1 in ischemia-reperfusion (I/R) injury.
Superior artery occlusion was performed in Wistar albino rats for 30 min followed by 2-hour (early reperfusion; ER) or 24-hour (late reperfusion; LR) reperfusion periods.
Intestinal transit was found to be reduced in the ER and LR groups (19.0 +/- 2.5%; p < 0.001 and 72.7 +/- 6.0%; p < 0.05, respectively) compared to the control group (85. 8 +/- 2.5%), while treatment with the ET receptor antagonist bosentan (BOS; 10 mg/kg i.v.) abolished this delay in LR. Myeloperoxidase activity showed a significant increase in ER (7.07 +/- 85.70 U/g; p < 0.001) compared to control (281.16 +/- 43.23 U/g), but BOS had no effect on this increase. The protein oxidation level was found to be higher in LR (5.92 +/- 0.77 nmol/mg protein; p < 0. 05) compared to the control (3.77 +/- 0.45 nmol/mg protein), and was reversed by BOS treatment.
The results of the present study imply that I/R delays intestinal transit involving an endothelin-dependent mechanism.
背景/目的：评估内皮素-1（ET-1）在缺血再灌注（I/R）损伤中的作用。
对Wistar白化大鼠进行肠系膜上动脉阻断30分钟，随后分别进行2小时（早期再灌注；ER）或24小时（晚期再灌注；LR）的再灌注。
与对照组（85.8±2.5%）相比，ER组和LR组的肠道运输均减少（分别为19.0±2.5%；p<0.001和72.7±6.0%；p<0.05），而用ET受体拮抗剂波生坦（BOS；10mg/kg静脉注射）治疗可消除LR组的这种延迟。与对照组（281.16±43.23U/g）相比，ER组髓过氧化物酶活性显著增加（7.07±85.70U/g；p<0.001），但BOS对这种增加无影响。与对照组（3.77±0.45nmol/mg蛋白）相比，LR组蛋白氧化水平更高（5.92±0.77nmol/mg蛋白；p<0.05），BOS治疗可使其逆转。
本研究结果表明，I/R通过内皮素依赖性机制延迟肠道运输。
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