Altavilla D, Squadrito F, Canale P, Ioculano M, Campo G M, Squadrito G, Ammendolia L, Caputi A P
Institute of Pharmacology, School of Medicine, Messina, Italy.
Eur J Pharmacol. 1995 Jan 16;272(2-3):223-9. doi: 10.1016/0014-2999(94)00658-t.
We investigated the involvement of E-selectin in the pathogenesis of splanchnic artery occlusion shock. Splanchnic artery occlusion shock was induced in anaesthetized rats by clamping splanchnic arteries for 45 min. Sham-operated animals were used as controls. Survival time, serum tumor necrosis factor-alpha, while blood cell count, mean arterial blood pressure and myeloperoxidase activity were determined. Splanchnic artery occlusion-shocked rats had a decreased survival time (85 +/- 8 min, while sham-shocked rats survived more than 4 h), reduced mean arterial blood pressure, increased serum levels of tumor necrosis factor-alpha (186 +/- 9 U/ml) and myeloperoxidase activity in the ileum (0.10 +/- 0.04 U x 10(-3)/g tissue) and in the lung (1.5 +/- 0.06 U x 10(-3)/g tissue). Shocked rats showed histological alterations in the ileum and in the lung. Administration of a hyperimmune serum containing specific antibodies raised against E-selectin significantly increased survival time (225 +/- 10 min), reduced leukopenia and myeloperoxidase activity both in the ileum (0.035 +/- 0.001 U x 10(-3)/g tissue) and in the lung (0.3 +/- 0.005 U x 10(-3)/g tissue), improved the cardiovascular changes and reduced the histological alterations in the ileum and lung. Our data are consistent with an involvement of E-selectin in the pathogenesis of splanchnic artery occlusion shock.
我们研究了E-选择素在内脏动脉闭塞性休克发病机制中的作用。通过夹闭内脏动脉45分钟,在麻醉大鼠中诱导产生内脏动脉闭塞性休克。假手术动物用作对照。测定存活时间、血清肿瘤坏死因子-α,同时测定血细胞计数、平均动脉血压和髓过氧化物酶活性。内脏动脉闭塞性休克大鼠的存活时间缩短(85±8分钟,而假手术休克大鼠存活超过4小时),平均动脉血压降低,血清肿瘤坏死因子-α水平升高(186±9 U/ml),回肠(0.10±0.04 U×10⁻³/g组织)和肺(1.5±0.06 U×10⁻³/g组织)中的髓过氧化物酶活性增加。休克大鼠的回肠和肺出现组织学改变。给予含有针对E-选择素的特异性抗体的超免疫血清可显著延长存活时间(225±10分钟),减少回肠(0.035±0.001 U×10⁻³/g组织)和肺(0.3±0.005 U×10⁻³/g组织)中的白细胞减少和髓过氧化物酶活性,改善心血管变化,并减少回肠和肺中的组织学改变。我们的数据表明E-选择素参与了内脏动脉闭塞性休克的发病机制。