Objective To investigate the maximum tolerance limit of rats to hepatic inflow occlusion with portal vein blood bypss (PBB) in normothermia. Methods First. A new animal model was established, the animal survival rate were calculated following 7 days of reperfusion after hepatic inflow occlusion of 30, 60, 90, 100, 110, 120 min or portal triad clamping (PTC) of 30 min. And then, the hepatic energy metabolism (RCR, P/O, ATP, AKBR) was studied following 30, 90, 120 min of ischemia or 1, 6, and 24 hours of reperfusion after the ischemia. According to the reversibility of the hepatic motochondrial function injury and maximum as long as a period of liver warm ischemia of all animal postoperative 7 days survial, the safe limit of rat to hepatic inflow occlusion was evaluated. Results The survival rate on postoperative 7 days was one hundred percent subjected to 30, 60 and 90 min of hepatic inflow occlusion, and 50, 30, 20 percent in 100, 110, 120 min, respectively, the survival rate in rats with 30 min of portal triad champing was about 40 percent. The parameters of hepatic motochondrial function reflecting the degree of liver damage to ischemia showed significantly different as compared to sham group. The functional lesion was exacerbated during inital reperfusion, then was restored progressively in PBB-30 min and PBB-90 min groups, but was maintained low level in PBB-120 min and PTC-30 min groups.Conclusion The 90 minutes is the maximum limit of rats to hepatic inflow occlusion in normothermia.
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.
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 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 analyze the protective effects of heat-shock response on the retinae of the rats after retinal ischemic reperfusion injury.Method Twenty Wistar rats (20 eyes) were divided into 4 groups: intracameral perfusion group (group P), intracameral perfusion after quercetin injection group (group P+Q), intracameral perfusion after heat shock group (group P+H), and in tracameral perfusion after quercetin injection and heat shock group (group P+Q+H ). According to the standard program established by International Society for Clinical Visual Electrophysiology, we recorded the results of the dark-adapted electroretinogram (D-ERG ),oscillatory potentials (OPs),and light-adapted ERG (L-ERG) of the rats with intraocular hypertension after induced by heat shock response. The expressions of HSP 70 of the rats in all groups were observed by Western blotting.Results The expression of HSP 70 of the rats in group P+H was the highest in all groups, but the expressions of HSP70 in group P+Q and P+Q+H were inhibited significantly. The amplitudes of a and b wave of ERG and O2 wave of OPs decreased, and the delitescence of them were delayed significantly in rats after intracameral perfusion. The amplitude of b wave of D-ERG and O2 wave of OPs in group P+H were higher than which in group P. Zero hour after perfusion, the amplitudes of all waves in group P+H increased significantly (Plt;0.05). Twenty-four hours after perfusion, the retinal functional resumption of the rats in group P+H was better than which in group P. In group P+Q and P+Q+H, the delitescences of all waves of ERG and O2 wave of OPs were the longest and the amplitudes were the lowest, and some waves even disappeared.Conclusions The heat-shock response may improve the recovery ability of the retinal cells after injury of ischemic reperfusion.(Chin J Ocul Fundus Dis，2003，19：117-120)
Objective To investigate the pathological changes in the neuromuscular junction during ischemiareperfusion(IR) in the skeletal muscle. Methods Forty-eight healthy adult Wistar rats (24 male, 24 female) were equally randomised into the following 6 groups: Group A (control group): no ischemiareperfusion; Group B: ischemia by clamping the blood vessels of the right hindlimb for 3 hours; Group C: ischemia by clamping for 4.5 hours;Group D: ischemia by the clamping for 4.5 hours followed by reperfusion for 1.5hours; Group E: ischemia for 4.5 hours followed by reperfusion for 24 hours; and Group F: ischemia for 4.5 hours followed by reperfusion for 2 weeks. Then, the medial head of the gastrocnemius muscle flap model was applied to the right hindlimb of each rat. The medial head of the gastrocnemius muscle was isolated completely,leaving only the major vascular pedicle, nerve and tendons intact.The proximal and distal ends (tendons) were ligated while the vessel pedicle was clamped. And then, Parameters of the muscle (performance,contraction index,colour,edema,bleeding) were observed. The muscle harvested was stained with gold chloride(AuCl3) and the enzymhistochemistry assay (succinate dehydrogenase combined with acetylcholine esterase) was performed. Morphology and configuration of the neuromuscular junction were observed during the ischemiareperfusion injury by means of the AuCl-3 staining. The result of the enzymhistochemical reactions was quantitatively analyzed with the computer imageanalysis system. And then, additional 5 rats were prepared for 3 different models identical with those in Groups A, C and E separately. The specimens were harvested from each rat and were stained with HE and AuCl-3, and they were examined under the light microscope. Results During the period of ischemia, the skeletal muscle of Group B showed the colour of purple and edema.The colour and edema became worse in Group ,while dysfunction of elasticity and contraction appeared obviously with plenty of dark red hemorrhagic effusion at the same time.After reperfusion,the color and edema of muscle in Group D became improved while the elasticity and function of contraction was not improved. Hemorrhagic effusion of Group D turned clearer and less than Group C.Group E was similar to Group D in these aspects of muscle except for much less hemorrhagic effusion. Skeletal muscle in Group F showed colour of red alternating with white, adhesion,contracture of muscle, exposure of necrotic yellow tissue and almost lost all its functions. The AuCl3 staining showed that during IR, necrosis of the myocytes was followed by degeneration of their neuromuscular junctions, and finally the nerve fibers attached to these neuromuscular junctions were disrupted like the withering of leaves. The enzymhistochemistry assay showed thatthere was no significant difference in the level of acetylcholine esterase between the ischemic group (Groups B and C) and the control group (Group A) (Pgt;0.05). However, the level of acetylcholine esterase in all the reperfused groups (Groups D, E and F) decreased significantly when compared with the control group（Group A）and the ischemic groups (Groups B and C) (Plt;0.01). Conclusion The distribution of the nerve fibers and the neuromuscular junctions in the mass of the muscles is almost like the shape of a tree. The neuromuscular junction seems to be more tolerant for ischemia than the myocyte. Survival ofthe neuromuscular junction depends on its myocytes alive. Therefore, an ischemiareperfusion injury will not be controlled unless an extensive debridement of the necrotic muscle is performed.
Objective To observe the protective effects of diazoxide-preconditioning on myocardial ischemiareperfusion injury of rats and discuss its possible mechanisms. Methods Fourteen healthy SD rats were randomly divided into two groups（7 each group）,In diazoxide-preconditioning group diazoxide was injected with the dosage of 12.5mg/kg through the vein,and in control group the media with the same amount was only given before ischemia. The left anterior descending branch was ligated for 2 hours. The heart was quickly excised after 2 hours reperfusion to be used for measurement of the quantity of malondialdehyde（MDA）, the activity of superoxide dismutase （SOD）, the size of myocardial infarct area, and the cell apoptosis and ultrastructure in ischemic area. Results Compared with the control group, the quantity of MDA,the percentage of the weight of myocardial infarct area/ischemic area, and the rate of cell apoptosis in the diazoxide-preconditioning group were greatly reduced （P〈0.05, 0. 01）. The damage of cell uhrastructure was obviously alleviated,Conclusion Diazoxide-preconditioning provides evident cardioprotective effect on the myocardial ischemia-reperfusion injury of rats.
ObjectiveTo introduce the relationship between the apoptosis hepatocyte and its genic mediation and the ischemia of portal vein. MethodsThe combination of related literatures and our research findings were made.ResultsPortal vein ischemia may induced hepatocyte apoptosis, p53 and bcl2 gene alternatively adjust hepatocyte apoptosis. Expression of p53 gene is enhanced in hepatic tissue when hepatocyte apoptosis is not obvious, but after 24-72 h of portal vein ischemia, when hepatocyte apoptosis is obvious, enhanced expression of p53 gene or reduced expression of bcl2 gene occur. There exists close relationship between portal vein ischemia and hepatocyte apoptosis. Conclusion Apoptosis hepatocyte is involved in organic atrophy after ischemia of portal vein, and p53 and bcl2 gene alternatively adjust hepatocyte apoptosis. At present, the mechanism of apoptosis of hepatocyte induced by ischemia of portal vein is not clear, which needs further study.
Objective To evaluate the phenomena of apoptosis and its relevant mechanism during ischemia-reperfusion period. Methods The published papers to explore the apoptotic phenomena and its mechanism in organs or tissues which experienced ischemia-reperfusion injury were reviewed. Results Apoptosis was common in ischemia-reperfusioned organ or tissue. The severity of apoptosis was influenced by many factors such as ischemia, hypoxia, oxygen free radials, intracellular free calcium ion overloading, various cytokines, et al; and also was regulated by bcl-2 family, caspase family and NF-κB，et al. Conclusion Apoptosis is a common phenomenum in ischemiareperfusioned organ or tissue which is affected and regulated by various factors.
Objective To determine whether the different durations and times of the ischemic preconditioning affect the effectiveness of the ischemic preconditioning. Methods Ninety male Wistar rats were randomly divided into the control group and the eight preconditioned groups of 10 rats each. A transverse rectus abdominis musculocutaneous flap (TRAM) was elevated in each rat. The flaps were preconditioned by clamping the pedicle and reperfusing for 5 or 10 minutes per cycle. This was repeated for one or two cycles. The controls were simply perfused for 30 minutes. Each flap was then subjected to 4 hours of the global ischemia. Three rats in each group were killed for anestimate of the water content in the muscle and for observation on the muscularstructure under microscope. The flap surface survival areas of the other rats were calculated on the 7th postoperative day by the computerized video planimetry. Results The water content in the muscle was evidently reduced. The mean survival area of the flap in every preconditioned group increased by2-3 times compared with that of the controls(P＜0.001). The different proceduresof the ischemic preconditioning produced different protective effects. Conclusion The ischemic preconditioning is an available means to alleviate an ischemiareperfusion injury to the transverse rectus abdominis musculocutaneous flap in rats. The effect of the ischemic preconditioning is affected by the duration and time of the ischemic preconditioning.