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首页> 外文期刊>The Open Physiology Journal >Polymerized Bovine Hemoglobin Infusion Does Not Induce Lung Damage in a Rat Model
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Polymerized Bovine Hemoglobin Infusion Does Not Induce Lung Damage in a Rat Model

机译：聚合牛血红蛋白输注不会在大鼠模型中引起肺损伤

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Establishing a hemoglobin-based oxygen carrier (HBOC) has potential to improve transfusion medicine andprovide a novel intervention to minimize tissue damage during hypoxic or ischemic insults. However, in vitro studiessuggest that HBOCs have toxic effects on endothelial cell barrier function. The purpose of this study was to determine ifthe HBOC polymerized bovine hemoglobin (PBvHb) alters pulmonary endothelial barrier function in rats duringnormoxia or hypoxia. Conscious male Sprague-Dawley rats were treated with lactated Ringer’s (LR) or PBvHb (3 ml of1.3 mg PBvHb/ml in lactated Ringer’s) and exposed to 4hr of normoxia (FiO2=21%) or hypoxia (FiO2=10%). Evans bluedye (EBD) extravasation (estimate of pulmonary vascular leak), pulmonary artery (Pa) pressure, inflammatory mediators,vascular endothelial growth factor (VEGF), fms-like tyrosine kinase-1 (sFlt-1), and hypoxia inducible factor-1 (HIF-1α)were measured in the lung and/or plasma. As expected with hypoxia, Pa pressure increased (p<0.05). PBvHb also resultedin a significant increase in Pa pressure independent of hypoxia. While a significant main effect of PBvHb on EBDextravasation was observed, no differences in inflammatory cytokines or pulmonary white blood cells existed amonggroups. No pulmonary edema was present upon assessment of wet:dry lung weights or histological examination. Hypoxiadid not influence plasma VEGF, but resulted in a small but significant increase in sFlt-1. Irrespective of hypoxia, PBvHbwas associated with increased unbound VEGF and its soluble receptor sFlt-1. However, no differences in lung VEGF orHIF-1 were observed. We conclude that in this model, acute administration of PBvHb does not have severe overalleffects on pulmonary endothelial barrier function or inflammation.
机译：建立基于血红蛋白的氧气载体（HBOC）可能会改善输血医学，并提供一种新的干预措施，以最大程度地减少缺氧或缺血性损伤期间的组织损伤。然而，体外研究表明HBOCs对内皮细胞屏障功能具有毒性作用。这项研究的目的是确定HBOC聚合的牛血红蛋白（PBvHb）在常氧或低氧期间是否会改变大鼠的肺内皮屏障功能。意识清醒的雄性Sprague-Dawley大鼠用乳酸林格氏（LR）或PBvHb（3 ml乳酸林格氏液中的1.3 mg PBvHb / ml）处理，并暴露于4小时的常氧（FiO2 = 21％）或低氧（FiO2 = 10％） 。 Evans bluedye（EBD）外渗（估计肺血管渗漏），肺动脉（Pa）压力，炎症介质，血管内皮生长因子（VEGF），fms样酪氨酸激酶1（sFlt-1）和缺氧诱导因子-在肺和/或血浆中测量了1（HIF-1α）。如缺氧所预期，Pa压力增加（p <0.05）。 PBvHb也导致Pa压力显着增加，而与缺氧无关。虽然观察到PBvHb对EBD外渗具有显着的主要作用，但各组之间在炎症细胞因子或肺白细胞方面没有差异。评估干湿肺重或组织学检查时无肺水肿。低氧血症不会影响血浆VEGF，但会导致sFlt-1出现小幅但显着的增加。与缺氧无关，PBvHb与未结合的VEGF及其可溶性受体sFlt-1升高有关。然而，未观察到肺VEGF或HIF-1的差异。我们得出结论，在该模型中，PBvHb的急性给药对肺血管内皮屏障功能或炎症没有严重的总体影响。

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