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首页> 美国卫生研究院文献>American Journal of Physiology - Gastrointestinal and Liver Physiology >Vascular stasis intestinal hemorrhage and heightened vascular permeability complicate acute portal hypertension in cd39-null mice
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Vascular stasis intestinal hemorrhage and heightened vascular permeability complicate acute portal hypertension in cd39-null mice

机译：cd39无效小鼠的血管淤滞肠道出血和血管通透性升高使急性门脉高压复杂化

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Vasoactive factors that regulate splanchnic hemodynamics include nitric oxide, catecholamines, and possibly extracellular nucleosidesucleotides (adenosine, ATP). CD39/ectonucleoside triphosphate diphosphohydrolase-1 (NTPDase1) is the major vascular ectonucleotidase that hydrolyzes extracellular nucleotides. CD39 activity may be modulated by vascular injury, inflammation, and altered oxygen tension. Altered Cd39 expression by the murine hepatosplanchnic vasculature may impact hemodynamics and portal hypertension (PHT) in vivo. We noted that basal portal pressures (PPs) were comparable in wild-type and Cd39-null mice (n = 9). ATP infusions resulted in increments in PP in wild-type mice, but, in contrast, this significantly decreased in Cd39-null mice (n = 9) post-ATP in a nitric oxide-dependent manner. We then studied Cd39/NTPDase1 deletion in the regulation of portal hemodynamics, vascular integrity, and intestinal permeability in a murine model of PHT. Partial portal vein ligation (PPVL) was performed in Cd39-null (n = 44) and wild-type (n = 23) mice. Sequential measurements obtained after PPVL were indicative of comparable levels of PHT (ranges 14–29 mmHg) in both groups. There was one death in the wild-type group and eight in the Cd39-null group from intestinal bleeding (P = 0.024). Circulatory stasis in the absence of overt portal vein thrombosis, portal congestion, intestinal hemorrhage, and increased permeability were evident in all surviving Cd39-null mice. Deletion of Cd39 results in deleterious outcomes post-PPVL that are associated with significant microcirculatory derangements and major intestinal congestion with hemorrhage mimicking acute mesenteric occlusion. Absent Cd39/NTPDase1 and decreased generation of adenosine in the splanchnic circulation cause heightened vascular permeability and gastrointestinal hemorrhage in PPVL.
机译：调节内脏血流动力学的血管活性因子包括一氧化氮，儿茶酚胺和可能的细胞外核苷/核苷酸（腺苷，ATP）。 CD39 /外核苷三磷酸二磷酸水解酶-1（NTPDase1）是主要的血管外切核苷酸酶，可水解细胞外核苷酸。 CD39的活性可能受到血管损伤，炎症和氧张力改变的调节。鼠肝内脏脉管系统改变的Cd39表达可能会影响体内的血流动力学和门脉高压（PHT）。我们注意到，在野生型和Cd39无小鼠（n = 9）中，基本的门静脉压力（PPs）是可比的。 ATP输注导致野生型小鼠的PP增加，但是相比之下，ATP释放后的Cd39无小鼠（n = 9）则以一氧化氮依赖性方式显着降低。然后，我们在PHT小鼠模型中研究了Cd39 / NTPDase1缺失在门脉血流动力学，血管完整性和肠通透性调节中的作用。在Cd39无（n = 44）和野生型（n = 23）小鼠中进行部分门静脉结扎（PPVL）。 PPVL后进行的顺序测量表明两组的PHT水平相当（14-29 mmHg）。在野生型组中有1例死于肠道出血，在Cd39无效组中有8例死于肠道出血（P = 0.024）。在所有存活的Cd39无效小鼠中，没有明显的门静脉血栓形成，门静脉充血，肠出血和通透性增加时的循环停滞明显。 Cd39的删除导致PPVL后的有害结局，这与严重的微循环紊乱和主要肠道充血以及模拟急性肠系膜闭塞的出血有关。 Cd39 / NTPDase1的缺乏和内脏循环中腺苷的生成减少会导致PPVL的血管通透性增加和胃肠道出血。

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