Okutan Huseyin, Kiris Ilker, Adiloglu Ali K, Savas Cagri, Kapucuoğlu Nilgün, Altuntas Irfan, Akturk Onur
Department of Cardiovascular Surgery, Suleyman Demirel University Medical School, Isparta, Turkey.
Surg Today. 2008;38(1):30-7. doi: 10.1007/s00595-007-3575-8. Epub 2007 Dec 24.
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).
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.
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).
Our results indicate that L-arginine aggravates the lung injury induced by aortic IR, while L-NAME attenuates it.
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。
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。
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)。
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。