Protective effect of L-arginine preconditioning on ischemia and reperfusion injury associated with rat small bowel transplantation

AIM: To investigate the protective effect and possible mechanism of L-arginine preconditioning on ischemia and reperfusion injury associated with small bowel transplantation (SBT).METHODS: Male inbred Wistar rats weighting between 180 and 250 g were used as donors and recipients in thestudy. Heterotopic rat SBT was performed according to the techniques of Li and Wu. During the experiment, intestinal grafts were preserved in 4 ℃ Ringer's solution for 8 h before being transplanted. Animals were divided into three groups. In group 1, donors received intravenous L-arginine (50 mg/kg, 1 mL) injection 90 min before graft harvesting. However, donors in control group were given normal saline (NS) instead. In group 3, six rats were used as sham-operated control. Specimens were taken from intestinal grafts 15 min after reperfusion. Histological grading, tissue malondialdehyde (MDA) and myeloperoxidase (MPO) levels were assessed. The graft survival of each group was monitored daily until 14 d after transplantation. RESULTS: Levels of MDA and MPO in intestine of shamoperated rats were 2.0±0.22 mmol/g and 0.66±0.105 U/g. Eight hours of cold preservation followed by 15 min of reperfusion resulted in significant increases in tissue MDA and MPO levels. Pretreatment with L-arginine before graft harvesting resulted in lower enhancement of tissue levels of MDA and MPO and the differences were significant (4.71±1.02 mmol/g vs8.02±3.49 mmol/g, 1.03±0.095 U/g vs 1.53±0.068 U/g, P＜0.05). Besides, animals in L-arginine pretreated group had better histological structures and higher 2-wk graft survival rates comparing with that in NS treated group (3.3±0.52 vs6±0.1, 0/6 vs6/6, P＜0.05or 0.01).CONCLUSION: L-arginine preconditioning attenuates ischemia and reperfusion injury in the rat SBT model,which was due to antioxidant activities partially.

Cellular preconditioning and mesenchymal stem cell ferroptosis

In this editorial,we comment on the article published in the recent issue of the World Journal of Stem Cells.They focus on stem cell preconditioning to prevent ferroptosis by modulating the cystathionineγ-lyase/hydrogen sulfide(H_(2)S)pathway as a novel approach to treat vascular disorders,particularly pulmonary hypertension.Preconditioned stem cells are gaining popularity in regenerative medicine due to their unique ability to survive by resisting the harsh,unfavorable microenvironment of the injured tissue.They also secrete various paracrine factors against apoptosis,necrosis,and ferroptosis to enhance cell survival.Ferroptosis,a regulated form of cell death characterized by iron accumulation and oxidative stress,has been implicated in various pathologies encompassing dege-nerative disorders to cancer.The lipid peroxidation cascade initiates and sustains ferroptosis,generating many reactive oxygen species that attack and damage multiple cellular structures.Understanding these intertwined mechanisms provi-des significant insights into developing therapeutic modalities for ferroptosis-related diseases.This editorial primarily discusses stem cell preconditioning in modulating ferroptosis,focusing on the cystathionase gamma/H_(2)S ferroptosis pathway.Ferroptosis presents a significant challenge in mesenchymal stem cell(MSC)-based therapies;hence,the emerging role of H_(2)S/cystathionase gamma/H_(2) S signaling in abrogating ferroptosis provides a novel option for therapeutic intervention.Further research into understanding the precise mechanisms of H_(2)S-mediated cytoprotection against ferroptosis is warranted to enhance the thera-peutic potential of MSCs in clinical settings,particularly vascular disorders.

RBC aggregation,deformation and adhesion to endothelium:Role of nitric oxide derived from L-Arginine and sodium nitroprusside

Red blood cells(RBCs)are the most abundant human blood cells.RBC aggregation and deformation strongly determine blood viscosity which impacts hemorheology and microcirculation.In turn,RBC properties depend on di®erent endogenous and exogenous factors.One such factor is nitric oxide(NO),which is mainly produced by endothelial cells(EC)from L-arginine amino acid in the circulatory system.Since the mechanisms of the RBC-endothelium interplay are not clear up to date and considering its possible clinical importance,the aims of this study are to investigate in vitro:(1)The effect of L-arginine induced NO on RBC aggregation and adhesion to endothelium;(2)the NO e®ect on RBC aggregation and deformation induced by L-arginine and sodium nitroprusside without the presence of endothelium in the samples.The RBC aggregation and adhesion to a monolayer of EC were studied using optical tweezers(OT).The RBC deformability and aggregation without endothelium in the samples were studied using the flow chamber method and Myrenne aggregometer.We confirmed that NO increases deformability and decreases aggregation of RBCs.We showed that the soluble guanylate cyclase pathway appears to be the only NO signaling pathway involved.In the samples with the endothelium,the "bell-shaped"dependence of RBC aggregation force on L-arginine concentration was observed,which improves our knowledge about the process of NO production by endothelium.Additionally,data related to L-arginine accumulation by endothelium were obtained:Necessity of the presence of extracellular L-arginine stated by other authors was put under question.In our study,NO decreased the RBC-endothelium adhesion,however,the tendency appeared to be weak and was not confirmed in another set of experiments.To our knowledge,this is the first attempt to measure the forces of RBC adhesion to endothelium monolayer with OT.

Small extracellular vesicles from hypoxia-preconditioned bone marrow mesenchymal stem cells attenuate spinal cord injury via miR-146a-5p-mediated regulation of macrophage polarization

Spinal cord injury is a disabling condition with limited treatment options.Multiple studies have provided evidence suggesting that small extracellular vesicles(SEVs)secreted by bone marrow mesenchymal stem cells(MSCs)help mediate the beneficial effects conferred by MSC transplantation following spinal cord injury.Strikingly,hypoxia-preconditioned bone marrow mesenchymal stem cell-derived SEVs(HSEVs)exhibit increased therapeutic potency.We thus explored the role of HSEVs in macrophage immune regulation after spinal cord injury in rats and their significance in spinal cord repair.SEVs or HSEVs were isolated from bone marrow MSC supernatants by density gradient ultracentrifugation.HSEV administration to rats via tail vein injection after spinal cord injury reduced the lesion area and attenuated spinal cord inflammation.HSEVs regulate macrophage polarization towards the M2 phenotype in vivo and in vitro.Micro RNA sequencing and bioinformatics analyses of SEVs and HSEVs revealed that mi R-146a-5p is a potent mediator of macrophage polarization that targets interleukin-1 receptor-associated kinase 1.Reducing mi R-146a-5p expression in HSEVs partially attenuated macrophage polarization.Our data suggest that HSEVs attenuate spinal cord inflammation and injury in rats by transporting mi R-146a-5p,which alters macrophage polarization.This study provides new insights into the application of HSEVs as a therapeutic tool for spinal cord injury.

Searching for the optimal precondition procedure for mesenchymal stem/stromal cell treatment:Facts and perspectives

Mesenchymal stem/stromal cells are potential optimal cell sources for stem cell therapies,and pretreatment has proven to enhance cell vitality and function.In a recent publication,Li et al explored a new combination of pretreatment condi-tions.Here,we present an editorial to comment on their work and provide our view on mesenchymal stem/stromal cell precondition.

Hypoxia-preconditioned bone marrow-derived mesenchymal stem cells protect neurons from cardiac arrest-induced pyroptosis

Cardiac arrest can lead to severe neurological impairment as a result of inflammation,mitochondrial dysfunction,and post-cardiopulmonary resuscitation neurological damage.Hypoxic preconditioning has been shown to improve migration and survival of bone marrow–derived mesenchymal stem cells and reduce pyroptosis after cardiac arrest,but the specific mechanisms by which hypoxia-preconditioned bone marrow–derived mesenchymal stem cells protect against brain injury after cardiac arrest are unknown.To this end,we established an in vitro co-culture model of bone marrow–derived mesenchymal stem cells and oxygen–glucose deprived primary neurons and found that hypoxic preconditioning enhanced the protective effect of bone marrow stromal stem cells against neuronal pyroptosis,possibly through inhibition of the MAPK and nuclear factor κB pathways.Subsequently,we transplanted hypoxia-preconditioned bone marrow–derived mesenchymal stem cells into the lateral ventricle after the return of spontaneous circulation in an 8-minute cardiac arrest rat model induced by asphyxia.The results showed that hypoxia-preconditioned bone marrow–derived mesenchymal stem cells significantly reduced cardiac arrest–induced neuronal pyroptosis,oxidative stress,and mitochondrial damage,whereas knockdown of the liver isoform of phosphofructokinase in bone marrow–derived mesenchymal stem cells inhibited these effects.To conclude,hypoxia-preconditioned bone marrow–derived mesenchymal stem cells offer a promising therapeutic approach for neuronal injury following cardiac arrest,and their beneficial effects are potentially associated with increased expression of the liver isoform of phosphofructokinase following hypoxic preconditioning.

L-Arginine Supplementation Mitigates Dichlorvos-Induced Haematocardiotoxicity, and Oxidative Stress in Male Wistar Rats

Due to its toxicity, dichlorvos—a common organophosphate pesticide—poses significant risks to human health. This study utilized male Wistar rats to explore the potential protective effects of L-arginine supplementation against dichlorvos-induced toxicity, focusing on cardiotoxicity, haematotoxicity and oxidative stress. The rats were divided into four groups: Control, L-arginine (L), Dichlorvos (D), and L-arginine + Dichlorvos (L + D). Dichlorvos was administered to the D group, L-arginine (100 mg/kg) to the L group, and both L-arginine and dichlorvos to the L + D group. The study evaluated various parameters, including cardiovascular, oxidative stress markers, and haematological indices. Significant changes in haematological parameters such as haemoglobin (Hb), haematocrit (HCT), and red blood cell count (RBC) indicated haematotoxicity after dichlorvos administration. Additionally, elevated cardiac markers, including lactate dehydrogenase (LDH) and creatine kinase-MB (CK-MB), suggested cardiotoxic effects. Exposure to dichlorvos also resulted in decreased antioxidant enzyme levels and increased oxidative stress indicators like malondialdehyde (MDA). Remarkably, L-arginine supplementation mitigated the damage caused by dichlorvos. It normalized the altered haematological parameters, demonstrating its protective effect against haematotoxicity. The rise in cardiac markers was reduced with L-arginine supplementation, indicating protection against cardiotoxicity. Moreover, L-arginine significantly decreased oxidative stress, as evidenced by lower MDA levels and restored antioxidant enzyme activity. In conclusion, L-arginine supplementation in male Wistar rats showed promising protective effects against dichlorvos-induced cardiotoxicity, haematotoxicity and oxidative stress. This suggests that L-arginine may offer a beneficial intervention to mitigate the adverse effects of dichlorvos on blood and heart health, paving the way for potential treatments for pesticide poisoning.

Hypoxia and inflammatory factor preconditioning enhances the immunosuppressive properties of human umbilical cord mesenchymal stem cells

BACKGROUND Mesenchymal stem cells(MSCs)have great potential for the treatment of various immune diseases due to their unique immunomodulatory properties.However,MSCs exposed to the harsh inflammatory environment of damaged tissue after intravenous transplantation cannot exert their biological effects,and therefore,their therapeutic efficacy is reduced.In this challenging context,an in vitro preconditioning method is necessary for the development of MSC-based therapies with increased immunomodulatory capacity and transplantation efficacy.AIM To determine whether hypoxia and inflammatory factor preconditioning increases the immunosuppressive properties of MSCs without affecting their biological characteristics.METHODS Umbilical cord MSCs(UC-MSCs)were pretreated with hypoxia(2%O_(2))exposure and inflammatory factors(interleukin-1β,tumor necrosis factor-α,interferon-γ)for 24 h.Flow cytometry,polymerase chain reaction,enzyme-linked immunosorbent assay and other experimental methods were used to evaluate the biological characteristics of pretreated UC-MSCs and to determine whether pretreatment affected the immunosuppressive ability of UC-MSCs in coculture with immune cells.RESULTS Pretreatment with hypoxia and inflammatory factors caused UC-MSCs to be elongated but did not affect their viability,proliferation or size.In addition,pretreatment significantly decreased the expression of coagulationrelated tissue factors but did not affect the expression of other surface markers.Similarly,mitochondrial function and integrity were retained.Although pretreatment promoted UC-MSC apoptosis and senescence,it increased the expression of genes and proteins related to immune regulation.Pretreatment increased peripheral blood mononuclear cell and natural killer(NK)cell proliferation rates and inhibited NK cell-induced toxicity to varying degrees.CONCLUSION In summary,hypoxia and inflammatory factor preconditioning led to higher immunosuppressive effects of MSCs without damaging their biological characteristics.

Helmholtz Decomposition of Vector Fields Using an Optimal Preconditioned Conjugate Gradient Algorithm

In this article, we study numerically a Helmholtz decomposition methodology, based on a formulation of the mathematical model as a saddle-point problem. We use a preconditioned conjugate gradient algorithm, applied to an associated operator equation of elliptic type, to solve the problem. To solve the elliptic partial differential equations, we use a second order mixed finite element approximation for discretization. We show, using 2-D synthetic vector fields, that this approach, yields very accurate solutions at a low computational cost compared to traditional methods with the same order of approximation.

L-Arginine及衰老对大鼠阴茎组织中NO、ET-1的影响

目的 探讨喂养左旋精氨酸 (L Arginine)及衰老对大鼠阴茎组织中“NO cGMP通路”及ET 1的影响及意义。方法 将不同月龄 ( 2、8、16、2 4月 )大鼠随机分为对照组与实验组 (喂养L Arginine) ,进行了以下研究 :①阴茎组织中一氧化氮(nitricoxide ,NO)、环磷酸鸟苷 (cGMP)含量测定 ;②阴茎组织一氧化氮合酶 (nitricoxidesynthase ,NOS)活性变化 ;③阴茎组织中ET 1(endothelin 1)含量测定。结果 ①阴茎组织中NO含量先升高后降低 ,8月龄最高 ,2 4月龄最低 ,NOS活性变化与其一致 ,各月龄组间差别均非常显著 (P <0 0 1) ;cGMP含量表现为显著降低 (P <0 0 1) ;ET 1含量呈升高趋势 ,ET 1/NO比值也显著升高 (P <0 0 1) ;②L Arginine长时间喂养大鼠后 ,阴茎组织中NOS活性及NO、cGMP含量均显著增加 (P <0 0 1) ,ET 1含量无明显改变。结论 阴茎组织中cGMP含量及ET 1/NO比值可能决定着平滑肌细胞舒缩状态 ;L Arginine对增强NOS活性、增加NO、cGMP含量有明显作用 ,表明L Arginine有用于治疗勃功能障碍 (erectiledysfunction ,ED)

Blind Deconvolution Method Based on Precondition Conjugate Gradients

In seismic data processing, blind deconvolution is a key technology. Introduced in this paper is a flow of one kind of blind deconvolution. The optimal precondition conjugate gradients (PCG) in Kyrlov subspace is also used to improve the stability of the algorithm. The computation amount is greatly decreased.

Ischemic preconditioning induces chaperone hsp70 expression and inhibits protein aggregation in the CA1 neurons of rats

Objective To investigate the effect of ischemic preconditioning on chaperone hsp70 expression and protein aggregation in the CA1 neurons of rats, and to further explore its potential neuroprotective mechanism. Methods Two-vesseloccluded transient global ischemia rat model was used. The rats were divided into sublethal 3-min ischemia group, lethal 10- min ischemia group and ischemic preconditioning group. Neuronal death in the CA1 region was observed by hematoxylineosin staining, and number of live neurons was assessed by cell counting under a light microscope. Immunochemistry and laser scanning confocal microscopy were used to observe the distribution of chaperone hsp70 in the CA1 neurons. Differential centrifuge was used to isolate cytosol, nucleus and protein aggregates fractions. Western blot was used to analyze the quantitative alterations of protein aggregates and inducible chaperone hsp70 in cellular fractions and in protein aggregates under different ischemic conditions. Results Histological examination showed that ischemic preconditioning significantly reduced delayed neuronal death in the hippocampus CA1 region （P 〈 0.01 vs 10-min ischemia group）. Sublethal ischemic preconditioning induced chaperone hsp70 expression in the CA1 neurons after 24 h reperfusion following 10-min ischemia. Induced-hsp70 combined with the abnormal proteins produced during the secondary lethal 10-min ischemia and inhibited the formation of cytotoxic protein aggregates（P〈0.01 vs 10-min ischemia group）.Conelusion Ischemic preconditioning induced chaperone hsp70 expression and inhibited protein aggregates formation in the CA1 neurons when suffered secondary lethal ischemia, which may protect neurons from death.

一氧化氮外源性供体L-arginine对破骨细胞骨吸收功能的影响

目的:一氧化氮在维持机体多个系统的生理功能中起重要作用,许多慢性疾病可造成一氧化氮产生减少,此时一氧化氮供体是一种必要的补充。观察一氧化氮外源性供体L-arginine对体外培养破骨细胞增殖及骨吸收功能的影响。方法:实验于2005-06/2006-05在四川大学华西医院生物治疗国家重点实验室干细胞与组织工程研究室完成。选择出生1d的清洁级SD大鼠乳鼠,采用骨髓诱导法体外培养破骨细胞,培养液内分别加入0.3,0.6,1.0g/L不同浓度的L-arginine,并以等体积三蒸水作为对照。培养7d后,以抗酒石酸酸性磷酸酶染色观察破骨细胞数目、形态,MIAS-2000图像分析仪检测骨片上骨吸收陷窝的数目和面积,并用扫描电镜观察不同浓度L-arginine对骨吸收陷窝的影响。结果:①破骨细胞的一般形态:破骨细胞较其他细胞大,形态不规则,呈油煎蛋形、长条形、腊肠形或漏斗形等,细胞内可见几个至几十个核不等。抗酒石酸酸性磷酸酶染色酶活性部分酒红色,颗粒状。②抗酒石酸酸性磷酸酶阳性细胞数:各组破骨细胞数目随着L-arginine浓度增加而减少(P<0.05)。③骨吸收陷窝的面积和数目:骨片培养7d,吸收陷窝计数的结果显示,0.3g/L以上浓度L-arginine对破骨细胞吸收功能均有明显抑制作用,并呈剂量相关性。0.3g/LL-arginine组陷窝面积为对照组的91%(P<0.05),0.6g/LL-arginine组为对照组的80%(P<0.05),1.0g/LL-arginine组为对照组的69%(P<0.01)。结论:采用骨髓诱导法培养的破骨细胞数量多、纯度高,且具有明显的骨吸收功能。L-arginine抑制破骨细胞增殖,抑制破骨细胞骨吸收功能,并呈剂量相关性。

BQ123与L-arginine在肝脏缺血再灌注损伤中的作用研究

目的 探讨肝脏缺血再灌注损伤的机制及 BQ12 3或 (和 ) L -arginine能否有效改善肝脏缺血再灌注损伤。方法 在大鼠肝脏缺血再灌注损伤模型基础上 ,对组织形态学、肝脏酶学、透明质酸、血浆内皮素及免疫组织化学染色情况进行观测。结果 肝脏缺血再灌注损伤时 ,血肝酶、透明质酶、血浆内皮素水平均显著增高 ,再灌注前使用 BQ12 3或 (和 ) L-arginine的肝脏 ,其组织结构及功能损伤均显著减轻。结论 肝脏缺血再灌注损伤与肝脏微循环改善有关 ,若能在肝脏再灌注前使用BQ12 3或 (和 ) L -arginine,可有效改善肝脏微循环 。

Capability matchmaking of semantic web services with preconditions and effects

In order to solve the problem that the current matchmaking methods for semantic web service mainly focus on the matchmaking of IO （inputs, outputs） descriptions which may result in one-sidedness, a description-logic-based IOPE （inputs, outputs, preconditions, effects） description and matchmaking method is proposed for semantic web service. The description logic concept is used to annotate service IO and the description logic assertion is employed to describe service PE（preconditions, effects）. TBox subsumption checking is used to measure the subsumption relationship between IO descriptions of service request and advertising; ABox consistency checking is used for checking the logical implication between PE descriptions of service request and advertising. Based upon the logical implication, four kinds of PE matching degrees are proposed to measure and compare the pros and cons of the results of matchmaking. They are the exact, perfect, side-effect and common match. Experiments show that the method has a higher precision rate under the same recall rate compared with the existing method.

Desferoxamine preconditioning protects against cerebral ischemia in rats by inducing expressions of hypoxia inducible factor 1α and erythropoietin

Objective To investigate whether desferoxamine （DFO） preconditioning can induce tolerance against cerebral ischemia and its effect on the expression of hypoxia inducible factor 1 α （HIF- 1α） and erythropoietin （EPO） in vivo and in vitro. Methods Rat model of cerebral ischemia was established by middle cerebral artery occlusion with or without DFO administration. Infarct size was examined by TTC staining, and the neurological severity score was evaluated according to published method. Cortical neurons were cultured under ischemia stress which was mimicked by oxygen-glucose deprivation （OGD）, and the neuron damage was assessed by MTT assay. Immunofluorescent staining was employed to detect the expressions of HIF-1 and EPO. Results The protective effect induced by DFO （decreasing the infarction volume and ameliorating the neurological function） appeared at 2 d after administration ofDFO （post-DFO）, lasted until 7 d and disappeared at 14 d （P 〈 0.05）; the most effective action was observed at 3 d post-DFO. DFO induced tolerance of cultured neurons against OGD： neuronal viability was increased 23%, 34%, 40%, 48% and 56% at 8 h, 12 h, 24 h, 36 h, and 48 h, respectively, post-DFO （P 〈 0.05）. Immunofluorescent staining found that HIF-1 α and EPO were upregulated in the neurons of rat brain at 3 d and 7 d post-DFO; increase of HIF-1 α and EPO appeared in cultured cortex neurons at 36 h and 48 h post-DFO. Conclusion DFO induced tolerance against focal cerebral ischemia in rats, and exerted protective effect on OGD cultured cortical neurons. DFO significant induced the expression of HIF- 1 α and EPO both in vivo and in vitro. DFO preconditioning can protect against cerebral ischemia, which may be associated with the synthesis of HIF- 1 α and EPO.

LOW MACH NUMBER FLOW COMPUTATION USING PRECONDITIONING METHODS AND COMPRESSIBLE NAVIER-STOKES EQUATIONS

The preconditioning method is used to solve the low Mach number flow. The space discritisation scheme is the Roe scheme and the DES turbulence model is used. Then, the low Mach number turbulence flow around the NACA0012 airfoil is used to verify the efficiency of the proposed method. Two cases of the low Mach number flows around the multi-element airfoil and the circular cylinder are also used to test the proposed method. Numerical results show that the methods combined the preconditioning method and compressible Navier-Stokes equations are efficient to solve low Mach number flows.

L-arginine对高糖诱导的内皮细胞衰老的作用

目的观察不同浓度的L-arginine对高糖诱导的人脐静脉内皮细胞（HUVECs）衰老的作用。方法HUVECs分别培养在正常糖浓度组（5．5mmol／L）、高糖组（33mmol／L）及高糖＋不同浓度L-arginine（0．4、0．8、1．6、3．2mmol／L）组，SAβ-gal活性评定细胞衰老的程度，PCR-ELISA法检测端粒酶活性，流式细胞术测定ROS及细胞周期，ELISA检测NO水平。结果与正常糖浓度组比较，高糖组SAβ-gal活性增强（P〈0．01），G0／G1期细胞比率增加（P〈0．01），端粒酶活性减弱（P〈0．01），细胞内ROS增多（P〈0．01），而NO水平减少（P〈0．001）。高糖环境下0．4—1．6mmol／L的L—arginine均可抑制SAβ—gal活性（P〈0．01），减少GD0/G0期细胞比率（P〈0．01），增强端粒酶活性（P〈0．01），减少细胞内ROS的生成（P〈0．01），增加NO水平（P〈0．01）。结论高糖可以诱导HUVECs的衰老。L-arginine可以延缓高糖诱导的内皮细胞衰老进程，但并没有明显的剂量依赖性。L—arginine可通过增强端粒酶活性，减少氧化应激，增加NO水平发挥抗内皮细胞衰老的作用。

The Potential Pathway of L-arginine·L-aspartate for Inhibition of Platelet Function

Aim L-Arginine· L-aspartate, a double salt, has been recently reported toinhibit platelet aggregation and thrombosis, but its action mechanism is not clear yet. This studywas conducted to investigate its effect on FITC-PAC-1, an anti-glycoprotein IIb/IIIa monoclonalantibody binding to activated platelets, and on correlative autacoid levels in plasma or inplatelets in order to explore its potential pathway of inhibiting platelet aggregation andthrombosis. Methods Monoclonal antibody binding to activated platelets was assayed by flowcytometry; NO was assessed by colorimetric method. cAMP, TXB_2 or 6-keto-PGF_(1α) levels wereassessed by radioimmunoassay. Results Gavaged 30 mg·kg^(-1) of L-arginine·L-aspartate increasedboth concentration of NO in plasma and 6-keto-PGF_(1) in incubated supernatant of aortic segment ofrats ex vivo (P < 0.05), but it did not influence cAMP content in platelets and the level of TXB_2or 6-keto-PGF_(1) in plasma of rats, whereas ASA significantly lowered TXB_2 or 6-keto-PGF_(1α) inplasma. Both 100 μmol-L^(-1) of L-arginine ·L-aspartate and ASA inhibited FITC-PAC-1 binding toactivated platelets in vitro. Conclusion The increase in NO and PGI_2 release from endo-thelialcells and consequent inhibition of platelet activation may contribute to the inhibition of plateletaggregation and thrombosis by L-arginine· L-aspartate; whereas arachidonic acid or cAMP metabolicpathway is not closely correlative with the studied effect.

L-arginine在高原鼠肝脏缺血再灌注损伤时肠道细菌易位中的作用研究

目的:探讨肝脏缺血再灌注损伤时肠道细菌易位的机制及精氨酸能否有效改善肠道细菌易位。方法:在大鼠肝脏缺血再灌注损伤模型基础上,对门静脉血、回肠系膜淋巴结进行肠道细菌培养。结果:肝脏缺血再灌注损伤时,血液及淋巴结可能培养出大肠埃希氏菌。但精氨酸预处理组与相同阻断时间组之间无差异。结论:高原地区第一肝门阻断的时间对肠道细菌易位有显著影响,但精氨酸对肝缺血再灌注损伤的肠道细菌易位无明显的保护作用。