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Nω-硝基-L-精氨酸甲酯和L-精氨酸对腹主动脉阻断-再灌注诱导的肺损伤的影响。

The effect of Nomega-nitro-L-arginine methyl ester and L-arginine on lung injury induced by abdominal aortic occlusion-reperfusion.

作者信息

Okutan Huseyin, Kiris Ilker, Adiloglu Ali K, Savas Cagri, Kapucuoğlu Nilgün, Altuntas Irfan, Akturk Onur

机构信息

Department of Cardiovascular Surgery, Suleyman Demirel University Medical School, Isparta, Turkey.

出版信息

Surg Today. 2008;38(1):30-7. doi: 10.1007/s00595-007-3575-8. Epub 2007 Dec 24.

DOI:10.1007/s00595-007-3575-8
PMID:18085359
Abstract

PURPOSE

The aim of this study was to examine the effects of Nomega-nitro-L-arginine methyl ester (L-NAME) and L-arginine on lung injury after aortic ischemia-reperfusion (IR).

METHODS

Twenty-four Wistar-Albino rats were randomized into four groups (n = 6) as follows: Control (sham laparotomy), Aortic IR (30 min ischemia and 120 min reperfusion), L-Arginine (intraperitoneal 100 mg kg(-1) live weight)+aortic IR, and L: -NAME (intraperitoneal 10 mg kg(-1) live weight)+aortic IR. In the lung specimens, the tissue levels of malondialdehyde (MDA), vascular endothelial growth factor (VEGF), and nitric oxide (NO) were measured and a histological examination was done.

RESULTS

Aortic IR increased MDA, VEGF, and NO. L-Arginine further significantly increased MDA and NO, and decreased VEGF (P < 0.05 vs aortic IR). L-NAME significantly decreased MDA and NO (P < 0.05 vs L-arginine+aortic IR) and increased VEGF (P < 0.05 vs other groups). A histological examination showed the aortic IR to significantly increase (P < 0.05 vs control) while L-arginine also further increased (P > 0.05 vs aortic IR), whereas L-NAME caused a significant decrease in pulmonary leukocyte infiltration (P < 0.05 vs aortic IR).

CONCLUSIONS

Our results indicate that L-arginine aggravates the lung injury induced by aortic IR, while L-NAME attenuates it.

摘要

目的

本研究旨在探讨Nω-硝基-L-精氨酸甲酯(L-NAME)和L-精氨酸对主动脉缺血再灌注(IR)后肺损伤的影响。

方法

将24只Wistar白化大鼠随机分为四组(每组n = 6),如下:对照组(假手术)、主动脉IR组(30分钟缺血和120分钟再灌注)、L-精氨酸组(腹腔注射100 mg/kg体重)+主动脉IR组、L-NAME组(腹腔注射10 mg/kg体重)+主动脉IR组。检测肺组织标本中丙二醛(MDA)、血管内皮生长因子(VEGF)和一氧化氮(NO)的组织水平,并进行组织学检查。

结果

主动脉IR使MDA、VEGF和NO升高。L-精氨酸进一步显著升高MDA和NO,并降低VEGF(与主动脉IR组相比,P < 0.05)。L-NAME显著降低MDA和NO(与L-精氨酸+主动脉IR组相比,P < 0.05),并升高VEGF(与其他组相比,P < 0.05)。组织学检查显示,主动脉IR使肺组织显著增加(与对照组相比,P < 0.05),而L-精氨酸也进一步增加(与主动脉IR组相比,P > 0.05),而L-NAME使肺白细胞浸润显著减少(与主动脉IR组相比,P < 0.05)。

结论

我们的结果表明,L-精氨酸加重主动脉IR诱导的肺损伤,而L-NAME减轻这种损伤。

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