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
Objective To establish a new model on isolated human cadaver testes with ischemiareperfusion (I/R). MethodsThirteen isolated cadaver testes contributed by 13 persons were preserved under 0℃-4℃ hypothermia and then reperfused under 37℃. Histological and histochemical changes were observed. Results4℃ cold ischemia in 12 hours induced only trivial swelling and vascular degeneration of endothelial cells (ECs), obvious pathologic changes occurred after 24 hours, including detachment of ECs, separation between basement membrane and seminiferous epithelium, degeneration and detachment of spermatogenous cell and edema of mesenchyme. Injury was worse along with the prolongation of cold preservation time. Changes of LDH and SDH activities were found by histochemical staining. Reperfusion following 6 hours ischemia induced tissue injury and unusual enzyme activity. All changes were more obvious after reperfusion following 12,18,24 or 36 hours cold ischemia.Conclusion This new model on isolated cadaver testes with ischemiareperfusion is successful, it can substitute other solid organs of human beings for I/R injury study.
【摘要】 目的 通过建立活体大鼠心肌缺血再灌注模型，模拟人类冠心病，研究聚合血红蛋白（PolyHb）在心肌缺血再灌注中的保护作用，探究PolyHb在冠心病领域中的保护和治疗作用。 方法 将45只Sprague-Dawley（SD）大鼠随机分成3组:实验组（15只）、对照组（15只）、假手术组（15只），建立大鼠心肌缺血模型。实验组建立动物模型后，结扎冠状动脉35 min，并于结扎后5 min，通过SD大鼠尾静脉按1 mL/min的速度注射1 mL（100 g/L）的PolyHb溶液。缺血完成后开放灌注120 min。对照组建立动物模型，结扎冠状动脉35 min，并于结扎后5 min，通过SD大鼠尾静脉按1 mL/min的速度注射1 mL生理盐水。缺血完成后开放灌注120 min。假手术组仅建立动物模型，但不结扎冠状动脉，也不再灌注。比较3组SD大鼠的血流动力学参数左室内压最大上升和下降速率、心肌酶（血清肌酸激酶、乳酸脱氢酶）及病理学检查（梗死心肌占总心肌面积的百分比），来衡量PolyHb的作用。 结果 与对照组比较，用PolyHb处理的实验组可增强再灌注时左室内压最大上升和下降速率（Plt;0.05），减少血液中血清肌酸激酶和乳酸脱氢酶的含量（Plt;0.05），并明显减少心肌梗死面积百分比（Plt;0.05）。 结论 在心肌缺血的SD大鼠中，PolyHb可以有效的降低缺血再灌注损伤，从而达到心肌保护作用。【Abstract】 Objective To investigate the protective effect of polymerized hemoglobin (PolyHb) for myocardial ischemia-reperfusion and explore the field of polymerized hemoglobin in the protection and treatment of human coronary heart disease, by simulating human coronary heart disease and establishing myocardial ischemia-reperfusion model in living rats. Methods Forty-five Sprague-Dawley (SD) rats were randomly divided into 3 groups: experimental group (n=15), control group (n=15), and sham operation (SHAM) group (n=15). Rat models of myocardial ischemia-reperfusion were established. For the rats in the experimental group, we ligated their left coronary artery for 35 minutes, and injected 1 mL (100 g/L) PolyHb solution into their body at a speed of 1 mL/min 5 minutes later. After ischemia was completed, reperfusion was performed for 120 minutes. The procedures carried out for the rats in the control group were exactly the same except that the PolyHB solution was replaced by 1 mL saline solution. Ligation of the artery and reperfusion were not performed on the rats in the SHAM group. Hemodynamic parameters (maximal rising and falling rates of left ventricular pressure), enzymes (serum creatine kinase, lactate dehydrogenase) and results of histopathologic examinations (percentage of myocardial infarction area over the total myocardial area) were measured and compared among the three groups to evaluate the function of PolyHb. Results Compared with the control group, the experimental group treated with PolyHb had higher maximum rising and falling rates of left ventricular pressure (Plt;0.05), lower blood levels of creatine kinase and lactate dehydrogenase (Plt;0.05), and lower percentage of myocardial infarction area over the total myocardial area (Plt;0.05). Conclusion Polymerized hemoglobin can effectively reduce the ischemia-reperfusion injury and achieve myocardial protection in SD rats with myocardial ischemia.
OBJECTIVE: To observe the changes of heme oxygenase-1 (HO-1) expression in the skeletal muscle after ischemia-reperfusion of hind limb in rats. METHODS: A model of hind limb ischemia was made by clamping femoral artery with a microvascular clip. Soleus muscle was obtained from the animals received sham operation, 4 h ischemia without reperfusion and 2 h, 4 h, 8 h, 16 h, 24 h reperfusion after 4 h ischemia. Soleus histology and malondialdehyde (MDA) content were measured. The levels of HO-1 mRNA and protein were measured in different time by Northern blotting, Western blotting and immunohistochemistry technique. RESULTS: After ischemia-reperfusion of limb, HO-1 mRNA increased at the 2nd hour, reached a peak at the 8th hour, and returned toward baseline at the 24th hour. The change of protein level was essentially in agreement with that of mRNA. Immunohistochemical results showed that HO-1 expressed primarily in skeletal muscle cytoplasma. There were no positive signals of mRNA and protein in sham group and in ischemia group. After limb reperfusion, MDA contents in the soleus muscle increased significantly when compared with that in the sham group (P lt; 0.05). MDA content of the 8th after reperfusion decreased significantly when compared with that of the 4 h after reperfusion (P lt; 0.05). CONCLUSION: Ischemia-reperfusion can induce HO-1 expression in skeletal muscle in rats, which may provide protection for injured tissue.
Objective To study the effects of heat shock proteins (HSPs) in the course of hepatic ischemia reperfusion injury (HIRI), and analyze its mechanism. Methods The relationship between HSPs and HIRI was studied by reviewing literatures. Results HSPs was a kind of stress protein induced after cell was sitmulated by the stress. It could improve body′s tolerance to tough situation. Though hepatic ischemia reperfusion usually results in serious hepatic injury, at the same time it could induce can increase the production of HSPs that can protect liver from and lessen ischemia reperfusion injury. Conclusion HSPs can improve the tolerance to HIRI and lessen injury. In addition, HSPs is thought to be markers of HIRI, and can be used as a efficient indicator to test the level of hepatic injury and assess prognosis.
To investigate the role of platelet-activating factor (PAF), neutrophils in ischemia-reperfusion-induced liver injury and their possible mechanism, PAF and the degree of neutrophil infiltration in liver tissue and the preventive effects of PAF antagonist kadsurenone were evaluated in this study by means of a partial liver ischemia model, in which it was induced by clamping only left and median lobes of the liver without causing intestinal congestion. The present study was undertaken to find out the mechanism of liver ischemia-reperfusion injury and preventive effect of kadsurenone. The results indicate that in early stage of reperfusion liver injury possibly caused by the generation of free radicals, declined of autioxidant defence and increased Ca２＋ influx, and in the later stage of reperfusion injury was mainly mediated by accumulation of PAF in the liver, which elicits the release of polymorphonuclear leukocytes induced toxical free radical, endothelial damage, microcirculatory collapse. The authors conclude that the effectiveness of antagonist kadsurenone in protecting against ischemiareperfusioninduced liver injury is due not only to their action in preventing the direct effects of PAF, but also to their ability to inhibit both PAF priming and PAF dependent feedback processes, thus preventing escalation of auto generated inflammatory damage.
OBJECTIVE: To investigate the injury on isolated testes induced by ischemia/reperfusion(I/R), and the protective effect of Yisheng injection on the injury. METHODS: Twenty-six isolated cadaver testes contributed by 13 persons were preserved with 4 degrees C 250 ml hypertonic citrate alloxuric (HCA) solution and then reperfused with 37 degrees C 500 ml HCA. Solution of experimental group contained 500 micrograms/ml Yisheng injection. In simple cold preservation test, involving in 8 experimental and 8 control testes, a series of time points (6, 12, 18, 24, 36, 48, 60, 72 hours) were set to harvest. 10 testes (1 testis respectively on 6, 12, 18, 24 and 36 hours in experimental and control groups) were reperfused with 37 degrees C HCA for 6 and 12 hours. Histological and histochemical changes were observed. RESULTS: In the experimental testes, 4 degrees C cold preservation in 24 hours could not induce obvious pathologic changes. After 24 hours, changes such as swelling, vacuolar degeneration or detachment of endothelial cells (ECs), separation between basement membrane and seminiferous epithelium, mal-alignment of spermatogenous cell and edema of mesenchyme could be observed. In the testes preserved for 12 hours, the activity of lactic dehydrogenase(LDH) and succinic dehydrogenase (SDH) increased, then fallen after 24 hours. The activity of Nitric oxide synthetase(NOS) decreased after 18 hours. All changes were more obvious after following 37 degrees C reperfusion. In the control testes, swelling and vacuolar degeneration of ECs occurred on 12 hours cold preservation, and injury was worse along with the prolongation of cold preservation time. Pathologic changes of ECs, seminiferous epithelium and mesenchyme were serious after 37 degrees C reperfusion. CONCLUSION: 4 degrees C cold preservation in 24 hours can only cause mild ECs’ injury, and obvious abnormal testes’ histological profile can be observed beyond 24 hours. 37 degrees C reperfusion will make injury worse. Yisheng injection can keep isolated testes histologic structure well in 24 hours cold preservation, and it has protective effect on I/R injury.
Objective To decrease the operative difficulty, with the purpose of looking for an orthotopic liver autotransplantation model which not only materializes the liver transplantation but also possesses higher survival rate. Methods This model was established via portal vein perfusion in thirty rats, and from which the result of the liver after perfusion, the operative time and the survival rate were observed. Liver tissues were researched at 24 h after operation under the light microscope. Results This model was easy to be perfused, the operative time was (48±3.0) min and the survival rate was 96.7% (29/30). The structure of hepatic tissue was basically normal with a little hydropic degeneration under the light microscope. Few erythrocytes residual occurred in the interlobular arteries under the light microscope. Conclusion The orthotopic liver autotransplantation model via portal vein perfusion has an exclusively blockage pattern which possesses a higher survival rate. It prevents the injury of immunological rejection and purely reflects the hepatic ischemia-reperfusion. But it is better to be applied in the non-hepatic artery anastomosis or the research nothing to do with the hepatic artery because the hepatic artery does not have sufficient perfusion.
Acute kidney injury (AKI) is characterized by a sudden and rapid decline of renal function and associated with high morbidity and mortality. AKI can be caused by various factors, and ischemia-reperfusion injury (IRI) is one of the most common causes of AKI. An increasing number of studies found out that exosomes of mesenchymal stem cells (MSCs) could alleviate IRI-AKI by the adjustment of the immune response, the suppression of oxidative stress, the reduction of cell apoptosis, and the promotion of tissue regeneration. This article summarizes the effect and mechanism of MSC-derived exosomes in the treatment of renal ischemia-reperfusion injury, in order to provide useful information for the researches on this field.