ObjectiveTo study the changes of levels of α subunits of stimulatory (Gsα) and inhibitory guanine nucleotide binding protein (Giα) in newborn guinea pig (0 2 days old) myocardium undergoing global ischemic reperfusion, and influences on the changes by St.Thomas Ⅱ and cold blood cardioplegic solution.MethodsThirty newborn guinea pigs were randomly assigned to three groups. GroupⅠ ( n = 10): the newborn hearts suffered by hypothermic global ischemia; group Ⅱ( n =10): the newborn hearts arrested by St. Thomas Ⅱ , and group Ⅲ ( n = 10): the newborn hearts arrested by cold blood cardioplegic solution. Levels of Gsα and Giα were investigated with Western blot analysis.ResultsNo differences of levels of Gsα and Giα were found in three groups before ischemia ( P gt;0.05). The level of Gsα after ischemia was significantly decreased than before ischemia in groupⅠand group Ⅱ ( P lt; 0 01), whereas no pronounced changes in group Ⅲ ( P gt;0.05) were noted after ischemia. The level of Gsα in group Ⅲ was not significantly changed after reperfusion compared with before ischemia( P gt;0 05), and it was much higher than those in groupⅠand group Ⅱ ( P lt; 0 01). Level of Giα was found not markedly changed in group Ⅲ after reperfusion compared with that before ischemia, but was notable higher in groupⅠand group Ⅱ( P lt;0.01). ConclusionsSignificant decrease of level of Gsα, whereas marked increase of level of Giα are found in myocardium of newborn guinea pig undergoing hypothermic (20℃) ischemic reperfusion. No impact of St. Thomas Ⅱ on these changes is verified, but recovery to the level of Gsα and Giα before ischemia is achieved by cold blood cardioplegic solution after ischemia and reperfusion. Unbalance between Gsα and Giα is the one of the mechanisms of ischemic reperfusion injury for immature myocardium.
rough the ultramicroscopic observation on muscle and microcirculation, Group A,where a largeamount of DXM combined with heporin was given svstematically and locally into the femoral artery of the severed limb before replantation, and in Group B only heporin was given, and Group C and D ascontrol.The results showed that if the hormone and heparin were administred in large dosage, it wasadvantageous to reduce the tissues from reperfusion injury during delayed replantation.
目的 探讨异氟醚通过抑制细胞间黏附分子（ICAM-1）表达参与减轻肝脏缺血-再灌注（IR）损伤的可能调节机制。 方法 32只雌性SD大鼠分为4组。A组大鼠行腹腔注射1%戊巴比妥钠40 mg/kg麻醉，进行手术但不阻断入肝血流；B组1%戊巴比妥钠麻醉后行部分肝脏IR；C组大鼠仅接受1.0 MAC异氟醚吸入麻醉，不阻断血流；D组采用1.0 MAC异氟醚麻醉，建立肝脏IR模型。肝脏缺血60 min，再灌注3 h后取肝组织和血液标本，检测血清丙氨酸转氨酶（ALT）和天冬门氨酸转氨酶（AST）、肝组织ICAM-1和肝组织还原型谷胱甘肽（GSH）、脂质过氧化物丙二醛（MDA）和超氧化物歧化酶（SOD）含量。 结果 与戊巴比妥钠麻醉比较，采用异氟醚处理后明显降低血清ALT和AST的水平，再灌注肝组织内GSH、SOD含量明显高于而MDA含量降低，同时抑制肝组织ICAM-1的表达。 结论 异氟醚麻醉能够有效减轻肝脏IR损伤，抑制氧自由基的生成和释放，具体机制可能与抑制ICAM-1表达致使细胞内GSH含量增加密切相关。
目的研究依达拉奉影响肝脏缺血再灌注过程中TNF-α的表达情况，探讨依达拉奉对肝脏缺血再灌注损伤的逆转作用。 方法将80只Wistar大鼠编号，根据计算机产生随机数字，前40为一组，后40为一组，分为实验组和对照组2组，建立常温下部分肝缺血再灌注损伤动物模型。 在肝脏缺血再灌注损伤开始前1 h和开始时对实验组大鼠给予依达拉奉注射液10 ml，对照组则给予同等容量的生理盐水。分别于再灌注后0、1、2及4 h测定肝脏脂质过氧化物酶（LPO）和肝脏谷草转氨酶(AST) 浓度； 应用RT-PCR法检测肝组织TNF-α mRNA含量，并测定肝组织和血清中TNF-α水平； 应用TUNEL染色法检测缺血肝组织的细胞凋亡情况。结果再灌注后1、2及4 h，实验组大鼠肝脏LPO及AST浓度均明显低于对照组（Plt;0.001）； 实验组再灌注后1 h时肝组织TNF-α mRNA表达量、肝组织和血清TNF-α含量均明显升高且达峰值，但均明显低于对照组（Plt;0.05）； 再灌注后各时相实验组肝细胞凋亡率明显升高，但均明显低于对照组（Plt;0.05）。 结论依达拉奉能抑制氧化应激反应，从而降低肝缺血再灌注损伤； 并显著减少炎性细胞因子TNF-α的产生，抑制炎性反应的发生，减少肝细胞的凋亡。
Objective To review the treatment methods and techniques of ischemia-reperfusion injury of flap. Methods Recent basic research l iterature concerning ischemia-reperfusion injury of flap was reviewed and analyzed in terms of treatment techniques. Results Ischemia-reperfusion injury is one of the leading causes of flap necrosis postoperatively. Interventions against any l ink of the ischemia-reperfusion injury progress could effectively reduce the damageand improve the survival rate of flaps. Conclusion Including production of reactive oxygen species, neutrophil infiltrationetc are thought to be the main mechanisms of ischemia-reperfusion injury. Treatment including medicine administration and physical intervention against any specific l ink of ischemia-reperfusion injury can interfere or block the whole progress, which reduce the damage of ischemia-reperfusion injury and improve the survival rate of animal flap models eventually.
Augmenter of liver regeneration (ALR) is a newly discovered cytokine that can promote liver regeneration and proliferation of damaged liver cells. In the renal tissue, ALR is mainly expressed in the cytoplasm of the medullary loops, collecting ducts and distal convoluted tubules in the renal medulla, and is low in the glomerular and cortical tubules. Various stimulation, such as ischemiacal, hypoxia, poisoning and inflammatory stimulation, can induce the expression of ALR in the epithelial cells of proximal tubule regeneration and the damaged areas of cortex, and participate in the repair process. Current studies have found that in acute kidney injury (AKI), exogenous ALR can protect renal tubular epithelial cells by inhibiting apoptosis of renal tubular epithelial cells, promoting proliferation of renal tubular epithelial cells, inhibiting the activities of inflammatory cells, and promoting the reduction of renal injury. This paper intends to review the basic characteristics of ALR and the pathogenesis of AKI, summarize the characteristics of the mechanism of ALR in AKI by combing the relevant literature on ALR and AKI in recent years, and provide knowledge reserve and direction reference for the in-depth study of ALR in kidney in the future.
Objctive To explore the relationship between the expression of Fas/FasL and the apoptosis occurs in retinal ischemia/reperfusion injury of rats , as well as the therapeutic effects of bFGF on the ischemic retina.Methods Th emodels of retinal ischemia/reperfusion injury was made by transient elevating introcular pressure. A total of 28 rats were divided into normal and operation group.The latter were subdivided into 1 hour, 6, 12, 24, 48 and 72 hours after reperfusion group, in which the left eyes of the rats were in the ischemia/reper fusion groups and the right ones were in the treatment groups (bFGF intracameral injection). Apoptosis was assessed by the terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick-end labelling (TUNEL) method, and the expression of Fas and Fas ligand was studied by strept avidin-biotin complex （SABC）immunohistochemistry. Results No positive cells were observed in the normal rats′retinae, but there was a significant number of TUNEL positive cells in 6-24 hours after transient ischemia followed by a decrease at the 48th hour. The number of TUNEL positive cells reached a maximum at the 24th hour after ischemia. The expression of Fas gradually increased as early as when it was at the 6th hour, reached a peak at the 24th hour, and then decreased at the 48th hour. Similarly, the expression of Fas ligand was at peak in 24-48 hours in GCL and INL of retina. Conclusions Retinal ischemia-reperfusion after transient elevated IOP induced apoptosis of cells in the retina. Fas/FasL may play an important role in the early events of the apoptotic pathways. bFGF can rescue RGCs from retinal ischemia/reperfusion injury through downregulation of the expression of Fas/FasL and may represent an important mechanism for therapeutic neuroprotection. (Chin J Ocul Fundus Dis，2003，19：160-163)
Objective To summarize the function of Kupffer cell for the ischemia reperfusion injury after liver’s transplatation. Methods The literatures which about the function of Kupffer cell for the ischemia reperfusion injury after liver’s transplatation were reviewed. Results Kupffer cells are the resident macrophages of the liver, which can be activated to generate a range of inflammatory mediators, including cytokines, reactive oxygen intermediates, chemokines, and other factors to startup the ischemia reperfusion injury （IRI）, and to cause the liver graft dysfunction. On the other hand, Kupffer cells can protect the ischemia reperfusion injury by release NO and HO-1. The CO, which is the byproduct of heme degradation by the heme oxygenases （HO-1），has the same function for IRI. Conclusions The Kupffer cells have bidirectional function for the ischemia reperfusion injury of liver’s transpatation. Thus, how to decrease the harmful factors and up-regulate the beneficial substances by Kupffer cells will be the key points in preventing IRI after liver transplantation in future.
Objective To observe the protective role of the ectogenesis zinc on the cells in rat flap with ischemia reperfusion injury and study the mechanisms. Methods A right low abdominal island flap was created in Wistar rats. Fortyeight rats were randomly divded into 3 groups (n=16):the control group, the ischemia reperfusion group and adding zinc ischemia reperfusion group.The content of malondialdehyde(MDA) and the activity of myeloperoxidase(MPO) were measured by thiobarbituric acid methods and colorimetry. The location of expression of MT was observed,and the image analysis was performed. The quantity of MT was represented by the integratial optical density. The ultrastructure changes of skin flap with ischemia reperfusion injury and the flap viability were observed. Results In the ischemia reperfusion injury flaps, the content of MDA and MPO show no statistically significant difference among the control group,IR group and the adding-zinc-IR group (P＞0.05). Compared with the control group at 1 h and 24 h of reperfusion, the level of MDA increased 62.2% and 136.4%(P＜0.01) in the IR group, which increased 11.3% and 33.2%(P＜0.01) in the adding-zinc-IR group. The activity of MPO increased 238.4% and 503.4%(P＜0.01)in the IR group when compared with the control group, and increased 17.9%and 24.1%(P＜0.05) when compared with the adding-zinc-IR group. In the ischemia reperfusion injury falps, the content of MT in the control group and the IR group is too minimal to measure. While the content ofMT in the adding-zinc-IR group is 45.30±7.60. At 1 h and 24 h of reperfusiion, the content of MT in the adding-zinc-IR group increased 41.5% and 44.9% (P＜0.01) compared with the IR group, and increased 119.9% and 234.6% (P＜0.01) compared with the control group. The flap viability is 100% in the control group, 19.65%±4.38% in the IR group, and 24.99%±5.12% in the adding-zinc-IR group, which increased 27.2% (P＜0.05) compared with IR group. Conclusion Many kinds of cells in skin flap with ischemiareperfusion injury can be protected by ectogenesis zinc and the flap viability increases significantly.
Objective To study the efect of IH764-3 on ischemia-reperfusion (I/R) injury in rat liver. Methods Rats were divided into 3 groups, the control group was not subjected to ischemia and no treatment was given. I/R injury group was subjected to 40 minutes ischemia followed by reperfusion for 120 minutes. The IH7643 group (40mg/kg) was administred at ischemia and reperfusion. Results In the IH764-3 group, sereum levels of ALT, AST, AKP and γ-GT were significantly lower than those in the I/R group. Energy charge level recovery was significantly higher with IH7643 (P＜0.05), hepatic ultrastructure was better preserved with IH764-3. Conclusion IH764-3 may be useful in the treatment of hepatic ischemia reperfusion injury