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首页> 外文期刊>Journal of Surgical Research: Clinical and Laboratory Investigation >Pentoxifylline reduces venular leukocyte adherence ('reflow paradox') but not microvascular 'no reflow' in hepatic ischemia/reperfusion.
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Pentoxifylline reduces venular leukocyte adherence ('reflow paradox') but not microvascular 'no reflow' in hepatic ischemia/reperfusion.

机译：己酮可可碱可减少肝缺血/再灌注中静脉白细胞的粘附（“回流悖论”），但不降低微血管“无回流”。

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摘要

Postischemic reperfusion injury is caused by microcirculatory disturbances, including both nutritive perfusion failure (no reflow) and leukocyte activation (reflow paradox). Recent studies brought evidence that pentoxifylline (PTX) reduces tissue injury, decreases enzyme release, and improves survival after normothermic liver ischemia/reperfusion. The mechanisms of action, however, by which PTX protects postischemic tissue from injury have not been elucidated yet. With the use of fluorescence microscopy in a rat hepatic ischemia/reperfusion model, we studied in vivo the action of PTX on the manifestation of postischemic sinusoidal perfusion failure and microvascular leukocyte adherence. Microvascular reperfusion after 20 min portal triad cross-clamping was characterized by the cessation of blood flow within individual sinusoids (no reflow) and accumulation of leukocytes within the hepatic microvasculature, with stasis in sinusoids and rolling and firm adherence in postsinusoidal venules. PTX (20 mg/kg x hr i.v.) significantly (P < 0.05) attenuated microvascular leukocyte accumulation (44,600 +/- 1833 mm(-3) vs 67,684 +/- 2620 mm(-3) in saline-treated controls) and firm adherence of leukocytes in postsinusoidal venules (316.9 +/- 40.9 mm(-2) vs 522.9 +/- 95.0 mm(-2)); however, PTX did not influence manifestation of individual sinusoidal perfusion failure. Since reperfusion-induced parenchymal cell damage was found reduced in treated animals, we conclude that PTX attenuates postischemic injury in rat liver by reduction of leukocytic/inflammatory response but not by prevention of nutritive perfusion failure.
机译：缺血后再灌注损伤是由微循环障碍引起的，包括营养性灌注衰竭（无回流）和白细胞活化（回流悖论）。最近的研究提供了证据表明己酮可可碱（PTX）减少了组织正常的肝脏缺血/再灌注后的组织损伤，减少了酶的释放并提高了存活率。然而，尚未阐明PTX通过其保护缺血后组织免受损伤的作用机理。通过在大鼠肝缺血/再灌注模型中使用荧光显微镜，我们在体内研究了PTX对缺血后正弦曲线灌注衰竭和微血管白细胞粘附表现的作用。门脉三联征交叉钳夹20分钟后的微血管再灌注的特征是单个窦内的血流停止（无回流）和肝微脉管系统内白细胞的积聚，窦内淤滞和窦房后小静脉的滚动和牢固粘附。 PTX（20 mg / kg x hr iv）显着（P <0.05）减弱了微血管白细胞积累（在盐水处理的对照组中为44,600 +/- 1833 mm（-3）对67,684 +/- 2620 mm（-3））和牢固窦后小静脉中白细胞的粘附性（316.9 +/- 40.9 mm（-2）对522.9 +/- 95.0 mm（-2））;但是，PTX不会影响个体正弦灌注失败的表现。由于发现在治疗的动物中再灌注诱导的实质细胞损伤减少，我们得出结论，PTX通过减少白细胞/炎症反应而不是通过预防营养性灌注衰竭来减轻大鼠肝脏缺血后损伤。

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