内皮素、一氧化氮与阻塞性黄疸肾功能障碍关系的实验研究

目的 研究内皮素(Endothelin ET)、一氧化氮(Nitric Oxide NO)与阻塞性黄疸(Obstructive Jaundice OJ)肾功能障碍的关系。方法 雄性SD大鼠胆总管结扎后随机分成5天、10天、15天三组，同时建立对应的假手术对照组。观察肾功能的变化，同时测定血和肾组织ET、NO水平及一氧化氮合酶(Nitric Oxide Synthetase NOS)活性，并用图像分析检测ET—1mRNA和NOS—mRNA表达的部位和量的变化。结果 随胆总管梗阻时间的延长，血和肾组织ET升高，NO下降，ET／NO比值与内生肌酐清除率(Creatinine clearance rate Ccr)、肾皮质血流(Renal cortex blood flow RCBF)呈负相关。肾组织ET—1mRNA和iNOS mRNA表达增加，血和肾组织NOS活性降低。结论 血和肾组织ET升高，NO下降，ET／NO比值升高是导致OJ时肾功能损伤的原因之一。     

内毒素引起阻塞性黄疸大鼠肾功能障碍的机制

目的 探讨阻塞性黄疸(obstructive jaundice,OJ)时内毒素引起肾功能障碍的机制.方法 SD大鼠60只,胆总管结扎后,分5 d(B1),10 d(B2),15 d(B3)三组,每组各10只,同时建立相应对照组(A1,A2,A3),另30只胆总管结扎后分3组(SHUD,LAC,NS),每组各10只,分别用2 ml舒胆合剂、乳果糖液、生理盐水灌胃,连用9 d.观察内毒素、血和肾组织中内皮素(endothelin,ET)、一氧化氮(nitric oxide,NO)的含量、一氧化氮合酶(nitric oxide synthase,NOS)活性及肝、肾功能的变化.结果 血内毒素与血、肾组织ET含量,ET/NO比值呈显著正相关(P＜0.05,r=0.630,0.438,0.496,0.453),与肌肝清除率(creatinine clearance,Ccr)和肾皮质血流量(renal cortical blood flow,BCBF)呈显著负相关(P＜0.05,r=-0.600,-0.410).血、肾组织ET/NO比值与Ccr,RCBF呈显著负相关(P＜0.05,r=-0.449,-0.558,-0.626,-0.731).血和肾组织内NO水平与内毒素水平呈负相关(P＜0.05,r=-0.518,-0.441),与Ccr、RCBF呈正相关(P＜0.05,r=0.422,0.496,0.400,0.659).SHUD组与LAC血内毒素、ET水平组明显降低,血和肾组织NO,NOS活性以及Ccr,RCBF较NS组明显升高.结论 OJ时内毒素可通过刺激ET的释放,提高ET/NO比值,使肾内缩血管因子与扩血管因子比例失调而损伤肾功能.     

肿瘤坏死因子、内皮素和一氧化氮在肝硬化大鼠门静脉高压高动力循环综合征中作用的研究

目的 了解肿瘤坏死因子（TNF）、内皮素（ET）和一氧化氮（NO）在门静脉高压高动力循环综合征（HCS）中的作用和地位以及门静脉血中含量的高低对HCS的影响。方法 四氯化碳诱导肝硬化大鼠在用抗TNF抗体，一氧化氮合成酶（NOS）抑制剂N^G－甲基－L－精氨酸处理前后测定门脉血TNF，ET和NO含量及肝组织NOS活性，同时监测血流动力学。结果 肝硬化大鼠门脉血中TNF，NO水平显著增高，ET也有轻度上升，肝组织NOS活性显著增高。在注射抗TNF抗体后，门脉血中TNF含量显著下降至对照水平，ET水平无变化，肝组织NOS活性较处理前下降15％－30％，同时HCS部分缓解。在注射N^G-甲基－L－精氨酸后，门脉血NO含量及肝组织NOS活性显著降低至对照水平，HCS明显缓解，门脉压力降至正常范围。结论 NO在HCS形成中起关键作用，TNF可能通过激活NOS使NO升高而发挥作用，ET与HCS形成无直接因素关系。     

一氧化氮与阻塞性黄疸肾功能障碍关系的实验研究

目的: 研究一氧化氮(N0)与阻塞性黄疸(OJ)肾功能障碍的关系. 方法: 雄性SD大鼠胆总管结扎后随机分成5 d、10 d及15 d三组(B1组、B2组、B3组),同时建立对应的假手术对照组.观察肾功能的变化,同时测定血和肾组织N0水平及一氧化氮合酶(NOS)活性,并用图像分析检测NOS-mRNA于肾脏表达的部位和量的变化. 结果: B1、B2及B3各组的血及肾组织NO含量分别是(43.72±10.61)μm01/L,(0.515±0.082)μmol/g@pro;(34.44±9.63)μmol/L,(0.375±0.096)μmoL/g@pro;(27.34±8.88)μmol/L,(0.251±0.086)μmol/g@pro.血及肾组织NO与内生肌酐清除率(Ccr)、肾皮质血流(RCBF)呈正相关.肾组织iNOSmRNA表达增加,血和肾组织NOS活性降低. 结论: 血和肾组织NO水平下降,是导致OJ时肾功能损伤的原因之一,体内NO水平的持续下降是由于NOS活性降低而非NOS基因表达减少.     

舒胆合剂防治阻塞性黄疸肾功能障碍的作用机制

目的 探讨在阻塞性黄疸(OJ)时舒胆合剂的抗内毒素及对肾功能的保护作用。方法 SD大鼠胆总管结扎后分3组，每组10只，分别用2mL舒胆合剂、乳果糖液(每100mL含乳果糖67g)、生理盐水灌胃，连用9d。假手术组10只，用2mL生理盐水灌胃。观察内毒素、血和肾组织中内皮素(ET)、一氧化氮(NO)的含量、一氧化氮合酶(NOS)活性及肾功能的变化。结果 舒胆合剂组与乳果糖组血内毒素、血和肾组织ET水平较生理盐水组明显降低，血和肾组织N0、NOS活性、内生肌酐清除率、肾皮质血流量较生理盐水组明显升高。结论 在OJ时，中药舒胆合剂有抗内毒素作用，并通过减少体内内毒素水平来降低体内ET水平，升高N0水平起到保护肾功能的作用。     

一氧化氮在梗阻性黄疸大鼠肝、肾、肠组织中含量变化及意义

目的 了解一氧化氮（NO）在梗阻性黄疸大鼠肝，肾，肠组织中含量变化及意义。方法 大鼠胆总管结扎后，分别于第一周内和第三周内变化Aminoguanidine(AG)抑制NO合成，同时应用生理盐水（NS）作对照，检测不同时段抑制NO合成后大鼠肝，肾，肠组织中NO和丙二醛（MDA）含量，肌酐清除率（Ccr)，血清总胆红素（T－BIL）和丙氨酸氨基转移酶（ALT）含量及肠系膜淋巴结细菌移位（BT）率的变化。结果 胆总管结扎后，大鼠肝，肾，肠组织中NO含量明显升高，在胆总管结扎第一周抑制NO合成后，肝，肾肠组织中NO含量明显下降，MDA含量明显升高，血ALT明显升高，Ccr明显下降，肠系膜淋巴结BT率明显升高；而在胆总管结扎第三周抑制NO合成后，肝，肾，肠组织中NO和MDA含量明显下降，血ALT明显下降，Ccr明显升高，肠系膜淋巴结BT率明显下降。结论 NO在胆道梗阻引起的肝，肾，肠粘膜屏蔽功能障碍的发生机制中具有重要作用，既有保护作用，又有损害作用。梗阻早期表现为对组织的保护作用，后期表现为对组织的损害作用。     

一氧化氮在梗阻性黄疸大鼠肝、肾、肠组织中含量变化及意义

目的 了解一氧化氮（NO）在梗阻性黄疸大鼠肝、肾、肠组织中含量变化及意义。方法 大鼠胆总管结扎后,分别于第一周内和第三周内应用Aminoguanidine（AG）抑制NO合成,同时应用生理盐水（NS）作对照,检测不同时段抑制NO合成后大鼠肝、肾、肠组织中NO和丙二醛（MDA）含量、肌酐清除率（Ccr）血清总胆红素（T-BIL）和丙氨酸氨基转移酶（ALT）含量及肠系膜淋巴结细菌移位（BT）率的变化。结果 胆总管结扎后,大鼠肝、肾、肠组织中NO含量明显升高,在胆总管结扎第一周抑制NO合成后,肝、肾、肠组织中NO含量明显下降,MDA含量明显升高,血ALT明显升高、Ccr明显下降、肠系膜淋巴结BT率明显升高;而在胆总管结扎第三周抑制NO合成后,肝、肾、肠组织中NO和MDA含量明显下降,血ALT明显下降、Ccr明显升高。肠系膜淋巴结BT率明显下降。结论NO在胆道梗阻引起的肝、肾、肠粘膜屏障功能障碍的发生机制中具有重要作用,既有保护作用,又有损害作用。梗阻早期表现为对组织的保护作用,后期表现为对组织的损害作用。     

L-精氨酸对阻塞性黄疸大鼠单核吞噬细胞系统功能的影响

目的：探讨L－精氨酸（L－Arg)对阻塞性黄疸大鼠单核吞噬细胞系统（MPS）吞噬功能的影响。方法：将SD雄性大鼠54只随机分为3组：假手术对照组（SO）;胆总管结扎组（BDL）;胆总管结扎＋L－精氨酸组（BDL＋L－Arg),每组术后又分设7,14,21d3个时间点检测MPS和枯否细胞（KC）的吞噬功能,并测定肝组织丙二醛（MDA）和NO2^-/NO3^-含量。结果：与SO组比较,BDL组各时间点MPS吞噬功能（P＜0．01）和KC吞噬功能（P＜0．05）明显减弱。BDL＋L－Arg组在胆管结扎7,14d时MPS和KC吞噬功能明显强于BDL组（P＜0．05）,21d时两组MPS和KC吞噬功能差异无显著性（P＞0．05）,但与SO组相比,BDL＋L－Arg组各时间点MPS吞噬功能仍明显降低（P＜0．05）。BDL L-Arg组在胆管结扎7,14d时血清转氨酶和肝组织MDA含量显著低于BDL组（P＜0．05）,而NO2^-/NO3^-含量显著高于BDL组（P＜0．01）。结论：L－精氨酸有减轻阻塞性黄疸时肝脏损伤和增强MPS,KC吞噬功能的作用,但存在一定时效关系。     

门静脉部分结扎大鼠门脉血中一氧化氮水平与高动力循环综合征的关系

目的：了解一氧化氮（NO）在高动力循环综合征（HCS）形成中的作用以及NO水平升高或降低时对HCS的影响。方法：结扎大鼠部分门静脉使之形成稳定的HCS模型后，应用一氧化氮合成酶（NOS）抑制剂NG-甲基-L-精氨酸（L-NMMA）处理前、后检测其门静脉血中NO含量及肝组织NOS活性，同时检测左心室功能及血流动力学指标。结果：门静脉部分结扎后大鼠门静脉血中NO含量及肝组织中NOS活性二者呈平行变化，与HCS的形成关系密切；在注射L-NMMA后门静脉血中NO含量及肝组织中NOS活性均明显降低并接近对照水平，HCS明显缓解。结论：NO在HCS形成中起关键作用。降低或消除NO的作用则能明显缓解或阻断HCS，使门静脉压力明显降低直至恢复到正常范围。     

梗阻性黄疸患者并发肾功能损害时血清一氧化氮的保护作用

目的 探讨梗阻性黄疸患者并发肾功能损害时血清一氧化氮（NO）的变化及其意义。方法 检测梗阻性黄疸并发肾功能损害患者25例，并选取26例健康人作对照。分别测定血清NO，一氧化氮合成酶（NOS）活性，血尿素氮（BUN），肌酐（Cr）值。结果 梗阻性黄疸组BUN和Cr均高于健康对照组（P＜0．01），NO和NOS则低于健康对照组（P＜0．01）。相关分析显示NO与BUN，Cr呈负相关（P均＜0．01）。结论 梗阻性黄疸患者并发肾功能损害时血清NO和NOS下降，提示NO在梗阻性黄疸时对肾功能有一定的保护作用。     

内皮素对阻塞性黄疸肾功能影响的实验研究

目的：研究内皮素与阻塞性黄疸肾功能障碍的关系,方法：大鼠胆总管结扎后分为5天,10天、15天3组,同时建立相应的对照组,观察血和肾组织内皮素与肝肾功能的变化,并用原位杂交观察肾组织ET－1mRNA的表达。结果：随着胆管梗阻时间的延长,血和肾组织内皮素持续升高,与内生肌酐清除率,肾皮质血流量呈明显负相关,肾小球,肾小管,集合管,肾内小血管ET－1 mRNA的表达持续增加,排钠分数梗阻5天时升,15 时低于对照组,结论：内皮素是引起阻塞性黄疸肾功能障碍的原因之一,肾组织内ET水平升高是由于肾小管,集合管,肾内小血管ET－1mRNA表达升高的缘故,在阻黄早期ET可促进利尿排钠,后期则可抑制水钠排泄。     

L-精氨酸对内毒素诱导大鼠肺组织线粒体损伤的影响

目的 评价L精氨酸(L-Arg)对内毒素(LPS)诱导大鼠肺组织线粒体损伤的影响,探讨其减轻内毒素性急性肺损伤的作用机制.方法 雄性SD大鼠24只,随机分为3组(n=8):假手术组(S组)、LPS组和L-Arg组.LPS组和L-Arg组静脉注射LPS 5 mg/kg(用生理盐水稀释至1 ml/kg),S组给予生理盐水1 ml/kg,3 h后L-Arg组腹腔注射L-Arg 500 mg/kg(用生理盐水稀释至1 ml/kg),S组和Au组给予生理盐水1 ml/kg.注射L-Arg或生理盐水后3 h.取肺组织.提取线粒体,测定超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)、ATPase、丙二醛(MDA)、一氧化氮合酶(NOS)、诱生型一氧化氮合酶(iNOS)、结构型一氧化氮合酶(cNOS)、一氧化氮(NO)的水平、线粒体膜肿胀度、线粒体活力和线粒体膜流动性;电镜观察肺组织超微结构.结果 与S组比较,LPS组SOD、GSH-Px、ATPase、线粒体活力和线粒体膜流动性降低,MDA、NOS、iNOS、NO及线粒体膜肿胀度升高(P<0.01);与LPs组比较,L-Arg组SOD、GSH.Px、ATPase、线粒体活力和线粒体膜流动性升高,MDA含量和线粒体膜肿胀度降低(P<0.05).L-Ars组细胞肿胀、线粒体肿胀和空泡化的程度轻于LPS组.结论 L-Arg可减轻LPS诱导大鼠肺组织线粒体损伤,其机制与增强抗过氧化能力有关.     

L-arginine deficiency and supplementation in experimental acute renal failure and in human kidney transplantation

BACKGROUND: The "L-arginine paradox" refers to situations where L-arginine (L-Arg) supplementation stimulates nitric oxide (NO) synthesis, despite saturating intracellular concentrations. This paradox is frequently observed in acute renal failure (ARF). First, the effects of L-Arg on renal function of rats with ARF were studied. Based on the promising results from these initial studies, the second part of our study searched for a form of ARF in humans that could be studied easily under conditions with little variance and yet was linked with endothelial dysfunction. Thus, we investigated the effects of L-Arg supplementation immediately after kidney transplantation in 54 patients. METHODS: In uranyl nitrate-induced ARF in rats the effects of L-Arg and L-NNA (inhibitor of nitric oxide synthase; NOS) on glomerular filtration rate (GFR), renal plasma flow (RPF), blood pressure (BP) and NOx (NO2- +NO3-) excretion were examined. Tissue L-Arg levels, NOS activities, immunodetection of NOS and superoxide dismutase (SOD), activities of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase and xanthine oxidase, and nitrotyrosine immunoreactive protein (NT-IR) were determined and compared to sham operated animals. Secondly, in a randomized, double-blind study, the effects of L-Arg on GFR and RPF were investigated in 54 kidney transplant recipients, receiving IV L-Arg for three days. GFR and RPF were measured on days 1, 3, 5 and 10 by scintigraphy. RESULTS: In experimental ARF, decreased RPF and GFR were associated with reduced tissue L-Arg levels, endothelial NOS-III expression, NO formation and NOx excretion. Reduction in GFR, RPF and NOx excretion were reversed upon administration of exogenous L-Arg. There also was a loss of Cu,Zn-SOD, a key enzyme against oxidative stress, and an elevation of NT-IR, an indicator of nitrosative stress and suggested marker for pathological actions of NO. However, NT-IR was not dependent on de novo NO synthesis and not related to the functional effects of l-Arg administration. In kidney transplant recipients receiving organs with a short cold ischemia time (CIT) and from young donors, that is, those with a higher likelihood of a functional endothelium, early administration of L-Arg improved renal function. CONCLUSION: Both experimental and clinical data show that \L-Arg deficiency and endothelial dysfunction are pathomechanistically relevant in ARF. The data suggest a therapeutic potential for the administration of L-Arg in ARF and kidney transplantation, at least in patients receiving kidneys with shorter CIT and from younger donors.     

Beneficial and harmful effects of L-arginine on renal ischaemia.

BACKGROUND: The role of nitric oxide (NO) in acute renal failure (ARF) is not yet completely understood. L-Arginine (L-arg) is protective against different ARF models, while L-arg addition in isolated proximal tubules enhances hypoxia/reoxygenation (H/R) injury. The aim of this study was to evaluate the effects of L-arg on renal ischaemia. METHODS: In in vivo studies, Wistar rats were subjected to 60 min renal artery clamping, and renal function was evaluated 2 and 15 days after ischaemia. Four groups were studied: (1) control; (2) acute L-arg (50 mg/kg/bw i.v.); (3) L-nitro-arginine-methyl esther (L-NAME; 0.5 mg/kg/bw i.v.); and (4) chronic L-arg (L-arg 0.25% in drinking water/7 days). For the in vitro studies, proximal tubules (PTs), isolated by collagenase digestion and Percoll gradient, were studied from three groups: (1) untreated; (2) L-arg-treated (L-arg 0.25% in drinking water/7 days); and (3) L-NAME-treated rats (3 mg/kg in drinking water/7 days). PTs were kept oxygenated or subjected to 15 min hypoxia (H-15) and 35 min reoxygenation (R-35). In some experiments, additional doses of L-arg and L-NAME were administered. Cell injury was assessed by lactate dehydrogenase (LDH) release. NO production was evaluated by NO2-/NO3- measurement (Griess reaction) in both urine and isolation medium. RESULTS: After 2 days, L-arg infusion protected against ischaemia compared with control rats (0.4 vs 0.2 ml/min/100 g, P < 0.001), while neither L-NAME nor chronic L-arg supplementation ameliorated renal function. After 15 days, both acute and chronic L-arg groups showed a higher glomerular filtration rate (0.6 and 0.75 ml/min/100 g) compared with control rats (0.3 ml/min/100 g, P < 0.05) and L-NAME-treated rats (0.2 ml/min/100 g, P < 0.05). Despite similar recovery in both L-arg groups, the mortality rate was 25% in the chronic L-arg group. Tubular function was also better preserved in the acute L-arg group. PTs isolated from L-arg-treated rats were more sensitive to isolation injury. L-Arg addition enhanced H/R injury (44.9 vs 51.8%, P < 0.05), whereas L-NAME addition protected (44.9 vs 24%, P < 0.001) in untreated rats. In L-arg-treated rats, addition of L-arg did not enhance H/R injury (49.6 vs 53.5%, NS) and L-NAME was still protective (49.6 vs 32.3%, P < 0.001). In PTs from L-NAME-treated rats, L-arg addition also did not enhance H/R injury (50 vs 54%, NS) whereas L-NAME was protective (50 vs 27%, P < 0.001). NO2-/NO3- production paralleled L-arg and L-NAME supplementation. CONCLUSION: It was demonstrated that acute L-arg infusion was beneficial in in vivo renal ischaemia while it was harmful in isolated H/R tubules. In contrast, chronic L-arg supplementation was deleterious both in in vivo and in vitro renal ischaemia, suggesting that injurious effects had overcome the beneficial effects during excess NO exposure.     

Endotoxin-induced acute renal failure in rats: effects of L-arginine and nitric oxide synthase inhibition on renal function

BACKGROUND: The regulation of renal hemodynamics is closely related to the L-arginine (L-Arg)/nitric oxide (NO) pathway. NO - metabolized from L-Arg - is capable of improving renal function in ischemic and toxic acute renal failure (ARF), while NO synthase (NOS) inhibition induces deterioration in renal function. The mortality rate in patients with septic shock is increased when treated with a non-selective NOS inhibitor, while the incidence of ARF requiring renal replacement therapy is unaffected. To date, there are no studies on the impact of NOS substrate (L-Arg) and inhibitor (L-NMMA) on renal function in early lipopolysaccharide (LPS)-induced ARF. METHODS: ARF was induced by intravenous (i.v.) LPS. Animals were treated with L-Arg, L-NMMA (NOS substrate and inhibitor), a combination of both or saline. Glomerular filtration rate (GFR), urine flow, fractional sodium excretion, excretion of NO metabolism stable end products and blood pressure (BP) were recorded at baseline, after ARF induction, during drug infusion and thereafter. RESULTS: L-Arg induced better GFR during infusion. Excretion of the NO metabolism end products was highest in the L-Arg group and lowest in the NOS inhibitor group. L-Arg administration had no influence on BP, while L-NMMA induced a slight elevation. CONCLUSIONS: We conclude that exogenous L-Arg exerts beneficial effects in early LPS-induced ARF in rats during drug infusion, while NOS inhibition has no influence on GFR. Subcellular compartmentalization of the L-Arg pool in cytoplasma and the rapid utilization of exogenous L-Arg in such a micro-environment could explain this effect, which has been observed in other ARF models and was called the "L-Arg paradox". In further studies the effects of early and prolonged administration of L-Arg in endotoxinemia should be investigated.     

内皮素受体拮抗剂PD142893对梗阻性黄疸大鼠并发肾功能损害的影响

目的：了解梗阻性黄疸（obstructive jaundice，OJ）大鼠模型血浆和肾组织内皮素（endothelin，ET）含量变化对肾功能的影响以及应用ET受体拮抗剂PD142893后的变化。方法：假手术组、OJ组及OJ＋药物组共32只Wistar大鼠分别于术后5、10、15和20d（每组n=8）采用放射免疫法测定血浆和肾匀浆的ET含量，同时测定血清TBIL、肌酐清除率，对肾脏行光镜下病理组织形态学观察。结果：在OJ组和OJ＋药物组中血清TBIL含量、血浆和肾组织匀浆中ET含量随梗阻时间延长而明显增加；OJ组在术后5d即表现为肌酐清除率下降，随梗阻时间延长而加重并伴有肾脏病理形态的进行性改变，而OJ＋药物组对比OJ组相应的改变出现的较晚；在非药物治疗组中，肌酐清除率与血浆和肾组织匀浆中ET含量呈负相关。结论：OJ时的高胆红素血症是导致肾功能损害的原因之一，胆色素对肾脏有直接的毒性作用；OJ引起血浆和肾组织中ET的病理性升高，由其介导的多种生物学效应是最终导致肾功能损害的重要原因；肽类非选择性ET受体拮抗剂PD142893对OJ大鼠的肾脏具有保护作用。     

外源性NO在大鼠小肠缺血再灌注损伤中作用的实验研究

目的：了解外源性L－Arg在肠缺血再灌注损伤中的作用及其机制。方法：30只雄性Wistar大鼠随机分为5组,每组6只,肠系膜上动脉分离结束前10min静脉注射生理盐水2.0ml(C组）,缺血前10min静脉注射生理盐水2.0ml( IR组）,缺血前10min静脉注射L－Arg 200mg/kg(AIR组）;再灌注前10min静脉注射L－Arg 200mg/kg(IAR组）;再灌注前10min同时静脉注射L－Arg 200mg/kg和N－硝基L－精氨酸40mg/kg(INAR组）。120min实验结束后,所有动物取距回盲瓣5.0cm以上回肠肠断15cm,均分为3段,分别测定各组肠粘膜PMN浸润数量,MDA含量和粘膜组织学Chiu分级,另取36只大鼠随机分为生理盐水对照组和L－Arg实验组（再灌注前10min静脉L-Arg200mg/kg),每组再随机分为3组,每组6只。两组分别与缺血前,缺血60min和再灌注60min取小肠中段肠管2.0cm,测定小肠组织线粒体内Ca^2 含量。结果：再灌注前给予适量的外源性L－Arg后,与C组相比,各组的肠粘膜PMN浸润数量,MDA含量,线粒体内Ca^2 含量和粘膜组织学均无明显差异（P＞0．05）;缺血前给予L－Arg后,与IR组相比,上述各项指标除Ca^2 含量外均明显减少（P＜0．05）,但仍高于C组（P＜0．05）。结论 ：再灌注前给予外源性L－Arg对大鼠小肠缺血再灌注损伤具有明显的保护作用,缺血前给予L－Arg对肠粘膜损伤也能起到一定程度的保护作用。