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 investigate the effects of ischemic postconditioning （IPO） on inflammatory response inischemia-reperfusion （IR） injury of rat lungs in vivo. Methods Forty SD rats were randomly divided into 5 groups inclu-ding a sham surgery group （S group），a 30-minute IR group （I/R-30 group），a 120-minute IR group（IR-120 group），a 30-minute IPO group （IPO-30 group），and a 120-minute IPO group （IPO-120 group）. There were 8 rats in each group. All therats received left thoracotomy after anesthesia. In the sham surgery group，a line was only placed around the left hilum butnot fastened. In the I/R-30 group and I/R-120 group，a line was fastened to block the blood flow of the left lung for 1 hour，then loosened for reperfusion for 30 minutes and 120 minutes respectively. In the IPO-30 group and IPO-120 group，afterblocking the blood flow of the left lung for 1 hour，the left hilum was fastened for 10 seconds and loosened for 10 seconds（repeating 3 times for 1 minute），then the line was loosened for 30 minutes and 120 minutes respectively. The levels of interleukin-10 （IL-10） in lung tissues and soluble intercellular adhesion molecule-1 （sICAM-1） in plasma were measured. Histopathological changes of lung tissues were observed and diffuse alveolar damage （DAD） scores was calculated.Results The levels of plasma sICAM-1 in the I/R-30 group and I/R-120 group were significantly higher than that of S group ［（2.140±0.250）μg/L vs. （0.944±0.188）μg/L，P=0.003；（2.191±0.230）μg/L vs. （0.944±0.188）μg/L，P=0.003］. IL-10levels in lung tissues in the I/R-30group and I/R-120 group were also significantly higher than that of S group［（15.922±0.606）pg/mg pro vs. （7.261±0.877）pg/mg pro，P=0.037；（17.421±1.232）pg/mg pro vs. （7.261±0.877）pg/mg pro，P=0.042］. Pathologic lesions of lung tissues in the I/R-30 group and I/R-120 group were more severe than that of S group. After IPO, plasma sICAM-1 levels in the IPO-30 group and IPO-120 group were significantly lower than those in the I/R-30group and I/R-120 group respectively ［（1.501±0.188）μg/L vs.（2.140±0.250）μg/L，P=0.038；（1.350±0.295）μg/L vs.（2.191±0.230）μg/L，P=0.005］. IL-10 levels in lung tissues in the IPO-30 group and IPO-120 group were significantly higherthan those in the I/R-30 group and I/R-120 group respectively ［（20.950±1.673）pg/mg pro vs.（15.922±0.606）pg/mgpro，P=0.008；（25.334±1.173）pg/mg pro vs.（17.421±1.232）pg/mg pro，P=0.006］. DAD scores in the IPO-30 group andIPO-120 group were significantly lower than those in the I/R-30 group and I/R-120 group respectively ［6.8±1.4 vs. 11.5±1.9，P=0.007；7.5±1.6 vs. 13.2±1.7，P=0.005］. Pathological lesions of the lung tissues of IPO groups were less severe than those of I/R groups. Conclusion IPO can attenuate IR injury by inhibiting inflammatory response in rat lungs.
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.
Objective To study the effect of dexamethasone to protect flaps from an ischemia-reperfusion injury and elucidate its mechanism of regulating the death course of the neutrophils.Methods The rats were randomly divided into 3 groups.The vein of the rat was clamped for 8 h after the flap had formed. Group A: the normal flap; Group B: the saline control flap; Group C: the treatment flap with dexamethasone. The survival area of the flaps was measured at 7 days; the apoptotic and necrotic neutrophils,tumor necrosis factor α （TNF-α）, and interleukin 10 （IL-10） concentrations were measured. Results The flap survival areas in Groups A and C were larger than those in Group B. The apoptotic neutrophils in Group B were fewer than those in Groups A and C on the 1st and 3rd days after operation; however, they were more in number in Group B than in groups A andC on the 6th day. The necrotic cells in Group B were more in number than those in Groups A and C. In Group B, the plasma TNF-α concentration reached the maximum level at 1 h,while the IL-10 level reached the lowest 3 h after the reperfusion. In Group C, the TNF-α concentration was lower than that in Group B and decreased dramatically at 6 h. The IL-10 concentration was the lowest at 1 h, and increased rapidly at 3 h. Thus, ischemia reperfusion could injure the flaps, probably through the abnormal action of the neutrophils, such as the disordered secretion of the cytokines and abnormal death course of the neutrophils. Conclusion Dexamethasone can protect the flap from an ischemia-reperfusion injury by its regulation for the neutrophil function.
【Abstract】ObjectiveOn the basis of traditional transplantation model, a successful model of pancreaticoduodenal transplantation (PDT) were established in rats, which is the foundation of basic and clinical transplantation research. Methods We improved the technique of microoperation on donor and harvested high-quality graft. The dual cuff technique was applied to end-to-end anastomose proximal part of abdominal aorta and portal vein with left renal aorta and vein of recipient, and distal part of abdominal aorta was connected with Y-tube. External secretion was performed by duodenum stoma. The PDT model was finished without blocking systemic circulation and portal vein system. Random blood glucose levels and drainage were monitored postoperatively to evaluate the function of endocrine and ectocrine. Results Thirty operations were done. The total procedure of transplantation lasted 2 hours. Moreover the operation on recipient and the reconstruction of vessels took only (26±5) and (25±5) minutes, respectively. The success rate was elevated to 100%. The ectocrine function was restored within 2 hours after operation. Except for 3 cases of non-function graft because of thrombosis in cannula, the glucose level of the remaining recipients was reduced to normal level 6 h or 24 h after transplantation. The survival rate of graft function was 90% (27/30). Conclusion This model is finished without special equipment and can recover the endocrine function in advance. It is a simple and stable model, which might be used in research of the theoretical problems involved in clinical pancreas transplantation.
【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 review the recent research progress about the pathogenesis and prevention of reactive oxygen species (ROS) in the hepatic ischemia-reperfusion injury (HIRI).
MethodsSearched the related literatures in recent years from the databases such as CNKI, PubMed and so on, summarized the recent research progress about the generation mechanism of ROS, the damage mechanism of ROS, and the prevention method of ROS.
ResultsA mass of ROS originated from polymorphonuclear leukocytes, Kupffer cells, mitochondria, and the enzymes in hepatic tissue in HIRI. It mainly destroyed sugar molecules of oligosaccharide chains on the cell membrane, unsaturated fatty acid, protein molecules, mitochondrial, and genetic material. This mechanism lead to cell injuried or even death. The main method of prevention and cure to HIRI is eliminating ROS by using enzymes, vitamins, Chinese herbal medicines etc.
ConclusionsThe research about ROS in HIRI has advanced. Aiming at the damage resulted from ROS in the liver, Scholars have came up with a variety of control methods which is feasible. However, many issues need to be further investigated.
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.
To investigate the effect of intracellular glycogen on liver ischemia-reperfusion and its mechanism, histomorphological and enzymological changes, histic ATP contents, the activity of Ca2+-ATPase on cytoplasmic membrane and intracellular free Ca2+concentration were observed during the ischemia-reperfusion of three groups of rabbit livers with different glycogen content. We found that the more vigorous energy metabolism, the higher activity of Ca2+-ATPase, the lower concentration of intracellular free Ca2+ and the slighter injury of histic structure and function appeared in the liver with the more abundant glycogen. The results suggest that intracellular abundant glycogen may reduce liver ischemiareperfusion injury.
Objective To investigate the protective effects of liposome prostaglandin E1（Lipo-PGE1） on myocardial ischemia-reperfusion injury （MIRI） during cardiopulmonary bypass （CPB）. Methods Thirty-two patients with clearly diagnosed heart valve disease and congenital heart disease such as atria septal defect （ASD） and ventricular septal defect （VSD） were selected in our hospital. The patients were randomly divided into two groups （16 patients in each group）, Lipo-PGE1 group： Lipo-PGE1（2ng/kg·min） was continuously pumped before starting of CPB until 2 h after ascending aortic off-clamping; control group： using the same volume of normal saline, arterial blood samples were taken before CPB, at 1, 2, 6 and 24 h after the ascending aortic off-clamping. The value of cardiac troponin I （cTnI）, creatine kinase MBmass （CK-MB）, interleukin-6 （IL-6）, tumour necrosis factor-α （TNF-α）, intercellular adhesion molecule-l（sICAM-1） were measured. Results cTnI, CK-MB, IL-6, TNF-α and sICAM-1 showed no significant difference in the two groups before CPB （P〉0. 05）. At 1,2, 6 and 24h after ascending aortic off-clamping, those values rose significantly than before CPB（P〈0. 01）, but Lipo-PGE1 group＇s values were lower than those in the control group （P〈0. 05）. Conclusions Lipo-PGE1 （2ng/kg·min） continuously pumped from before CPB to 2h after ascending aortic off-clamping can inhibit effectively the production of IL-6, TNF-α, and reduce the expression of sICAM-1, attenuate the process of inflammation, lighten the injuries of myocardial cells, and effectively protect the MIRI during CPB open heart surgeries.
