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输血可改善脓毒症诱导的大鼠急性肾损伤中的肾氧合及肾功能。

Blood transfusion improves renal oxygenation and renal function in sepsis-induced acute kidney injury in rats.

作者信息

Zafrani Lara, Ergin Bulent, Kapucu Aysegul, Ince Can

机构信息

Department of Translational Physiology, Academic Medical Center, Amsterdam, The Netherlands.

Department of Intensive Care, Erasmus MC, University of Medical Center, Rotterdam, The Netherlands.

出版信息

Crit Care. 2016 Dec 20;20(1):406. doi: 10.1186/s13054-016-1581-1.

DOI:10.1186/s13054-016-1581-1
PMID:27993148
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5168817/
Abstract

BACKGROUND

The effects of blood transfusion on renal microcirculation during sepsis are unknown. This study aimed to investigate the effect of blood transfusion on renal microvascular oxygenation and renal function during sepsis-induced acute kidney injury.

METHODS

Twenty-seven Wistar albino rats were randomized into four groups: a sham group (n = 6), a lipopolysaccharide (LPS) group (n = 7), a LPS group that received fluid resuscitation (n = 7), and a LPS group that received blood transfusion (n = 7). The mean arterial blood pressure, renal blood flow, and renal microvascular oxygenation within the kidney cortex were recorded. Acute kidney injury was assessed using the serum creatinine levels, metabolic cost, and histopathological lesions. Nitrosative stress (expression of endothelial (eNOS) and inducible nitric oxide synthase (iNOS)) within the kidney was assessed by immunohistochemistry. Hemoglobin levels, pH, serum lactate levels, and liver enzymes were measured.

RESULTS

Fluid resuscitation and blood transfusion both significantly improved the mean arterial pressure and renal blood flow after LPS infusion. Renal microvascular oxygenation, serum creatinine levels, and tubular damage significantly improved in the LPS group that received blood transfusion compared to the group that received fluids. Moreover, the renal expression of eNOS was markedly suppressed under endotoxin challenge. Blood transfusion, but not fluid resuscitation, was able to restore the renal expression of eNOS. However, there were no significant differences in lactic acidosis or liver function between the two groups.

CONCLUSIONS

Blood transfusion significantly improved renal function in endotoxemic rats. The specific beneficial effect of blood transfusion on the kidney could have been mediated in part by the improvements in renal microvascular oxygenation and sepsis-induced endothelial dysfunction via the restoration of eNOS expression within the kidney.

摘要

背景

输血对脓毒症期间肾微循环的影响尚不清楚。本研究旨在探讨输血对脓毒症诱导的急性肾损伤期间肾微血管氧合及肾功能的影响。

方法

将27只Wistar白化大鼠随机分为四组:假手术组(n = 6)、脂多糖(LPS)组(n = 7)、接受液体复苏的LPS组(n = 7)和接受输血的LPS组(n = 7)。记录平均动脉血压、肾血流量及肾皮质内的肾微血管氧合情况。采用血清肌酐水平、代谢成本及组织病理学损伤评估急性肾损伤。通过免疫组织化学评估肾内的氧化应激(内皮型一氧化氮合酶(eNOS)和诱导型一氧化氮合酶(iNOS)的表达)。检测血红蛋白水平、pH值、血清乳酸水平及肝酶。

结果

液体复苏和输血均能显著改善LPS输注后的平均动脉压和肾血流量。与接受液体治疗的组相比,接受输血的LPS组肾微血管氧合、血清肌酐水平及肾小管损伤均显著改善。此外,在内毒素刺激下,肾内eNOS的表达明显受到抑制。输血而非液体复苏能够恢复肾内eNOS的表达。然而,两组之间在乳酸酸中毒或肝功能方面无显著差异。

结论

输血显著改善了内毒素血症大鼠的肾功能。输血对肾脏的特定有益作用可能部分是通过改善肾微血管氧合及通过恢复肾内eNOS表达来改善脓毒症诱导的内皮功能障碍介导的。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ae58/5168817/715f5df10130/13054_2016_1581_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ae58/5168817/f2a22008e20b/13054_2016_1581_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ae58/5168817/f7c4b1ab950c/13054_2016_1581_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ae58/5168817/c839f65dfb2b/13054_2016_1581_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ae58/5168817/ac02e78f56b3/13054_2016_1581_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ae58/5168817/715f5df10130/13054_2016_1581_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ae58/5168817/f2a22008e20b/13054_2016_1581_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ae58/5168817/f7c4b1ab950c/13054_2016_1581_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ae58/5168817/c839f65dfb2b/13054_2016_1581_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ae58/5168817/ac02e78f56b3/13054_2016_1581_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ae58/5168817/715f5df10130/13054_2016_1581_Fig5_HTML.jpg

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