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严重脓毒症中L-精氨酸一氧化氮途径的激活

Activation of the L-arginine nitric oxide pathway in severe sepsis.

作者信息

Duke T, South M, Stewart A

机构信息

Paediatric Intensive Care Unit, Royal Children's Hospital, Melbourne, Australia.

出版信息

Arch Dis Child. 1997 Mar;76(3):203-9. doi: 10.1136/adc.76.3.203.

DOI:10.1136/adc.76.3.203
PMID:9135259
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1717120/
Abstract

AIMS

To determine in children with sepsis syndrome and septic shock the time course of nitric oxide metabolites: nitrate and nitrite (nitrogen oxides). To determine whether serum concentrations of nitrogen oxides distinguished those children who died from sepsis from those who survived; those who required prolonged inotropic support compared with those who did not; and whether there was any relationship of the levels of nitrogen oxides to markers of tissue perfusion.

METHODS

Nitrogen oxides were measured in 30 children with sepsis syndrome or septic shock at admission, 12, 24, and 48 hours. A non-septic control group had serum nitrogen oxides measured at admission. Markers of haemodynamics and tissue perfusion measured were mean arterial pressure, blood lactate, base deficit, gastric intramucosal pH, and deltaCO2 (DCO2: the difference between arterial and gastric intraluminal carbon dioxide tensions). Inotrope doses, number of organ systems failing at 48 hours, and outcome as survival were recorded.

RESULTS

Children with sepsis had increased nitrogen oxide concentrations at presentation compared with a group of non-septic controls. Children with organ failure at 48 hours had higher serum nitrogen oxide concentrations than those with sepsis uncomplicated by organ failure at 48 hours. There was no difference in nitrogen oxide when patients were subgrouped according to the receipt of inotropes at 48 hours, and no association with markers of tissue perfusion, or survival.

CONCLUSIONS

While this study shows that nitric oxide production is increased in sepsis in children, there was a limited relationship with clinically important markers of illness severity and no relationship to survival.

摘要

目的

确定脓毒症综合征和脓毒性休克患儿体内一氧化氮代谢产物(硝酸盐和亚硝酸盐,即氮氧化物)的时间变化过程。确定血清氮氧化物浓度能否区分脓毒症死亡患儿和存活患儿;能否区分需要长时间使用血管活性药物支持的患儿和不需要的患儿;以及氮氧化物水平与组织灌注标志物之间是否存在任何关系。

方法

对30例脓毒症综合征或脓毒性休克患儿在入院时、12小时、24小时和48小时测量氮氧化物。一个非脓毒症对照组在入院时测量血清氮氧化物。测量的血流动力学和组织灌注标志物包括平均动脉压、血乳酸、碱缺失、胃黏膜内pH值和△CO2(DCO2:动脉血与胃腔内二氧化碳分压之差)。记录血管活性药物剂量、48小时时衰竭的器官系统数量以及存活结局。

结果

与非脓毒症对照组相比,脓毒症患儿在就诊时氮氧化物浓度升高。48小时时出现器官衰竭的患儿血清氮氧化物浓度高于48小时时未并发器官衰竭的脓毒症患儿。根据48小时时是否接受血管活性药物将患者分组后,氮氧化物无差异,且与组织灌注标志物或存活无关。

结论

虽然本研究表明儿童脓毒症时一氧化氮生成增加,但与疾病严重程度的重要临床标志物关系有限,与存活无关。

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