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.
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.
【Abstract】ObjectiveTo investigate whether heme oxygenase-1 can alleviate the ischemiareperfusion injury of the aged donor liver. MethodsThe activity of superoxide dismutase (SOD) and catalase (CAT), and the contents of tocopherol (Vit E), ascorbic acid (Vit C) and malondialdehyde (MDA) were measured in the livers of adult SD rats (n=5) and aged SD rats (n=5). The experimental aged donor group (n=30) received intraperitoneal injection of Hemin 24 hours before operation, the control aged donor group(n=30) received saline. The histologic changes and apoptosis in the donor liver were observed. ResultsThe activity of SOD and the contents of Vit E and Vit C decreased significantly in 5 aged rats（P＜0.05）, but the content of MDA increased（P＜0.05）. Before the harvesting of the grafts, the activity of SOD and the contents of Vit E and Vit C increased significantly in rats pretreated with Hemin （P＜0.05） and the content of MDA decreased（P＜0.05）. The apoptotic cells in the livers pretreated with Hemin also decreased significantly after reperfusion（P＜0.05）. ConclusionThe liver of aged rat presents oxidative stress and peroxidative state. Ischemia-reperfusion injury can be alleviated by the induction of HO-1.
ObjectiveTo summarize the research progress of severed limb preservation by perfusion and to analyze difference in effect of severed limb preservation by different perfusate. MethodsThe domestic and foreign related literature about severed limb preservation by perfusion was extensively reviewed and analyzed. ResultsCurrently the main perfusate includes organ perfusate,free radical scavengers,energy mixture,blood substitutes,and whole blood.They can reduce the skeletal muscle's ischemia-reperfusion injury in different degrees. ConclusionDifferent perfusate can reduce the skeletal muscle's ischemia-reperfusion injury in different degrees,but the best effect of perfusate and personalized preservation method need further study.
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.
【Abstract】ObjectiveTo investigate the effect of ischemia-reperfusion （I/R） injury on apoptosis of pancreatic cells in rats with acute pancreatitis(AP). MethodsFifty-four SD rats were randomized into 3 groups: pancreatitis group (n=24), I/R-injury group (n=24) and control group (n=6). The animal model of AP was induced by retrograde injection of 3% sodium taurocholate into biliopancreatic duct in rats. Pancreatic I/R was caused by blocking the inferior splenic artery and removing the clamp after AP induction. At 1 h, 3 h, 6 h and 12 h, groups of rats were sacrificed. A terminal deoxynucleotidyl transferase-mediated dUTP-biotion nick end labeling (TUNEL) was used to detect pancreatic apoptosis, and histological changes of the pancreas were observed. ResultsPancreatic hemorrhage, necrosis were respectively observed in the pancreatitis rats at 6 h and the I/R-injury rats at 1 h. Histological changes of the pancreatitis rats at 1 h and 3 h were only congestion and edema. Apoptoic acinar cells increased after AP induction, the peak respectively appeared at 6 h in the pancreatitis rats and at 3 h in the I/R-injury rats. Compared with the pancreatitis rats, apoptosis index (AI) of the I/Rinjury rats was significantly higher at 1 h and 3 h (P＜0.01, P＜0.05, respectively), but lower at 6 h and 12 h (P＜0.05, P＜0.01, respectively). ConclusionI/R injury can induce conversion of edematous pancreatitis to hemorrhagic necrotizing pancreatitis and apoptosis of acinar cells. Apoptosis may be a beneficial response to pancreatic injury in AP.
Objective To study the influence of ischemia-reperfusion on the expression of the hyperpolarization activated cycl icnucleotide gated cation channel 4 (HCN4) and to discuss the mechanism of functional disturbance of sinoatrial node tissue (SANT) after ischemia reperfusion injury (IRI). Methods Eighty five healthy adult rabbits, weighing 2-3 kg, were randomly divided into 3 groups: control group [a suture passed under the root section of right coronary artery (RCA) without l igation, n=5], experimental group A (occluding the root section of RCA for 30 minutes, then loosening the root 2,4, 8 and 16 hours, n=10), experimental group B (occluding the root section of RCA for 1 hour, then loosening the root 2, 4,8 and 16 hours, n=10). At the end of the reperfusion, the SANT was cut off to do histopathological, transmission electronmicroscopical and immunohistochemical examinations and semi-quantitative analysis. Results The result of HE stainingshowed that patho-injure of sinoatrial node cell (SANC) happened in experimental groups A and B after 2 hours of reperfusion, the longer the reperfusion time was, the more serious patho-injure of SANC was after 4 and 8 hours of reperfusion, SANC reached peak of damage after 8 to 16 hours of reperfusion; patho-injure of SANC was more serious in experimental group B than in experimental group A at the same reperfusion time. Immunohistochemical staining showed that the expression of HCN4 located in cellular membrane and cytoplasm in the central area of SANC and gradually decreased from the center to borderl ine. The integral absorbance values of HCN4 expression in the control group (397.40 ± 34.11) was significantly higher than those in the experimental group A (306.20 ± 35.77, 216.60 ± 18.59, 155.40 ± 19.11 and 135.00 ± 12.30) and in the experimental group B (253.70 ± 35.66, 138.70 ± 13.28, 79.10 ± 9.60 and 69.20 ± 8.42) after 2, 4, 8 and 16 hours of reperfusion (P lt; 0.05). With reperfusion time, the expression of HCN4 of SANC decreased, which was lowest after 8 hours of reperfusion; showing significant difference among 2, 4 and 8 hours after reperfusion (P lt; 0.05) and no significant difference between 8 and 16 hours after reperfusion (P gt; 0.05). At the same reperfusion time, the expression of HCN4 was higher in the experimental group A than in the experimental group B. The result of transmission electron microscope showed that ultramicrostructure of SANC was damaged after reperfusion in experimental groups A and B. The longer the reperfusion time was, the more serious ultramicrostructure damage of SANC was, and reached the peak of damage after 8 hours of reperfusion. Ultramicrostructure of SANC was not different between 8 and 16 hours of reperfusion. At the same reperfusion time, the ultramicrostructure damage of SANC was moreserious in experimental group B than in experimental group A. Conclusion IRI is harmful to the morphous and structure ofSANC, and effects the expression of HCN4 of SANC, which is concerned with functional disturbance and arrhythmia.
Objective To observe the effects of melatonin on lung injury and NDRG2 ( N-myc downstream-regulated gene 2) expression after intestinal ischemia-reperfusion ( I/R) .Methods 40 healthy SD rats were randomly assigned to a sham group, an I/R group, a high-dose melatonin group ( 10 mg/kg) , and a low-dose melatonin group ( l mg/kg) . The model of lung injury was established by superior mesenteric artery clamping/unclamping. 30 minutes before clamping, melatonin was administered intraperitoneally to the rats in two melatonin groups, and normal saline in same volume was administered to the rats in the I/R group and the shamgroup. Then superior mesenteric arteries of the rats in the I/R group and two melatonin groups were clamped for 60 minutes. 45 minutes after unclamping, right lung tissues were sampled for pathological examination and wet/dry ( W/D) ratio measurement. The rats in the sham group underwent sham operation without clamping. The expression of NDRG2 protein in the lung tissue was detected by immunohistochemistry and Western-blot. Results Compared with the sham group, hemorrhage and inflammation of lung tissues were observed. The W/D was obviously increased and the NDRG2 expression was significantly decreased in the I/R group. Compared with the I/R group, mild hemorrhage and inflammation changes of lung tissues were observed and the W/D was decreased while the NDRG2 protein expression was increased significantly in two melatonin groups. There was no significant difference between two melatonin groups. Conclusion Melatonin may relieve lung injury after intestinal ischemia-reperfusion through up-regulating NDRG2 expression.
【Abstract】Objective The injury induced by hepatic artery ischemia (HAI) in the liver transplantation procedure and the protective effects of using hepatic artery bridge-conduit (HABC) technique were studied. Methods Thirtytwo dogs were randomly divided into 4 groups: control, HAI 30 min, HAI 2 h and HABC groups. We observed the pathological changes of hepatocytes and biliary tract tissues and the microstructure of chondriosome, which were based on the model of auto-orthotopic liver transplantation in dogs. Biochemical and spectrophotometric methodswere used to evaluate the content of MDA and SOD, SDH activities in the graft liver tissue respectively. Results The pathologic and electrical microscopic changes of hepatocytes and epithelial cells of bile ducts were found in HAI 30 min and HAI 2 h groups,while the content of MDA increased to （1.652±0.222） nmol/mg prot and (2.379±0.526) nmol/mg prot, and SOD activity decreased to (11.15±3.9) U/mg prot and (9.47±3.4) U/mg prot. At the same time, SDH activity was also down-regulated to 0.362±0.019 and 0.281±0.029. Compared with control group, the differences were significant (Plt;0.05, Plt;0.01). But these changes of functional index caused by HAI injury were not significant in HABC group. Conclusion The HABC technique can not only avoid HAI injury during operation but also alleviate the occurrence of complication after transplantation, especially the biliary tract complication.
Adenosine triphophate (ATP), substantially liberated from the injured cells, activates the inflammatory cells to secrete various inflammatory factors, thus triggering uncontrolled systemic inflammatory response and thrombosis with aggravating the degree of damage. Metabolic pathway of adenosine consists of adenosine (Ado) synthase CD39-CD73, nucleoside transporters (NTs) and termination system of adenosine deaminase (ADA) and adenosine kinase (ADK). As a " switch” of the inflammatory response, the metabolic pathway converts ATP (the pro-inflammatory cytokines) to Ado (the anti-inflammatory mediators), maintaining the homeostasis between pro-inflammatory and anti-inflammatory as well as affecting the outcome of the injury. This review focused on the recent progress of adenosine metabolic pathway in cell injury.