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.
Objective To investigate the effect of mesenteric lymphatic duct liagtion and glutamine enteral nutrition on intestine and distant organs in intestinal ischemia/reperfusion injury. Methods Forty male SD rats undergoing gastrostomy were randomly assigned into 5 groups (n=8): sham operation group, normal enteral nutrition group, normal enteral nutrition+lymphatic duct ligation group, glutamine group and glutamine+lymphatic duct ligation group. Sham operation group only received laparotomy after 7 days of full diet, the other four groups were subjected to 60 min of intestinal ischemia after 7 days of enteral nutrition, and the two lymphatic duct ligation groups were plus mesenteric lymphatic duct ligation. The original nutrition continued 3 days after reperfusion. Intestinal permeability was detected on day 1 before reperfusion, day 1 and 3 after reperfusion. Intestinal morphology was observed, endotoxin, D-lactate and diamine oxidase levels in serum, and apoptotic index in lung tissue were detected on day 3 after reperfusion. Results The intestinal permeability in each group was significantly increased on day 1 after reperfusion (Plt;0.05), and which in normal enteral nutrition+lymphatic duct ligation group and glutamine+lymphatic duct ligation group were significantly decreased on day 3 after reperfusion (Plt;0.05). The mucosal thickness and villus height of ileum and mucosal thickness of jejunium in glutamine+lymphatic duct ligation group were significantly higher than those in other groups (Plt;0.05), and villus height of ileum in glutamine group was higher than that in normal enteral nutrition group (Plt;0.05); those morphology indexes in normal enteral nutrition+lymphatic duct ligation group were higher than those in normal enteral nutrition group, but there was no statistical signification (Pgt;0.05). Apoptosis index of lung tissue in lymphatic duct ligation groups was significant lower than that in no-ligation groups (Plt;0.05). Levels of endotoxin, D-lactate, and diamine oxidase in lymphatic duct ligation groups had downward trends compared with no-ligation groups, but there was no statistical signification (Pgt;0.05). Conclusions Intestinal ischemia/reperfusion injury of rats can cause intestinal permeability increase, bacterial endotoxin translocation and systemic inflammatory response. Mesenteric lymphatic duct ligation and glutamine enteral nutrition intervention can weak lung tissue damage, increase thickness of intestinal mucosa, maintain intestinal barrier function, reduce endotoxin translocation and attenuate systemic inflammatory response. Enteral nutrition with glutamine was better than normal enteral nutrition.
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.
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
【Abstract】 Objective To study the effects of ischemic preconditioning (IP) on the activity of nuclear factor-κB （NF-κB） and the expressions of TNF-α and intercellular adhesion molecule-1 (ICAM-1) during early reperfusion following liver transplantation in rats. Methods The models of rat orthotopic liver transplantation were established. The donor livers were stored for 2 hours in Ringers solution at 4 ℃ before transplantation. All rats were randomly divided into sham operation group （SO group）， control group and IP group. IP group was achieved by clamping the portal vein and hepatic artery of donor liver for 10 minutes followed by reperfusion for 10 minutes before harvesting. The activity of NF-κB and expressions of TNF-α and ICAM-1 at 1 h, 2 h, 4 h and 6 h after reperfusion were measured. Serum ALT, LDH were also determined. Results The liver function of recipients with IP were significantly improved. Compared with SO group， the graft NF-κB activity increased after transplantation in control group and IP group (P＜0.05), while compared with control group that was significantly attenuated at 1 h and 2 h in IP group. Similarly, hepatic levels of TNF-α and ICAM-1 were significantly elevated in control group and were reduced in IP group. Conclusion IP might down-regulated TNF-α and ICAM-1 expression in the grafts after orthotopic liver transplantation through depressed NF-κB activation， and attenuate neutrophil infiltration in the grafts after reperfusion.
【Abstract】 Objective To investigate the effect of verapamil on apoptosis, calcium and expressions of bcl-2 and c-myc of pancreatic cells in ischemia-reperfusion rat model. Methods Wistar rats were randomly divided into three groups: control group （n=10）; ischemia-reperfusion group （n=10）; verapamil treatment group （n=10）. The anterior mesenteric artery and the celiac artery of rats in both ischemia-reperfusion group and verapamil treatment group were occluded for 15 min followed by 12-hour reperfusion. Verapamil （1 mg／kg） was injected via caudal vein to the rats in verapamil treatment group 15 min before occlusion and 1 hour after the initiation of reperfusion, respectively; and ischemia-reperfusion group was given the same volume of salient twice intravenously. Pancreatic tissues were collected from the dead rats after twelve hours since the reperfusion. The pathologic characters of pancreatic tissue were observed under light microscope; The level of calcium in the tissue was measured by atomic absorption spectrometer; TUNEL was used to detect apoptosis of pancreatic cells; and the expressions of c-myc and bcl-2 in the cells were also analyzed by immunohistochemistry technique and flow cytometry. Results The pathologic change in verapamil treatment group was less conspicuous than that of ischemia-reperfusion group. Both the calcium level and the number of apoptotic cells in verapamil treatment group were less than those of ischemia-reperfusion group 〔（411.1±55.8） μg/g dry weight vs （470.9±31.9） μg/g dry weight, P＜0.05 and （9.5±2.9）% vs （18.4±3.1）% 〕, P＜0.05. After taking verapamil, the number of apoptotic cells decreased, whereas the expressions of bcl-2 and c-myc increased. The fluorescent indexes of bcl-2 and c-myc in verapamil treatment group were significantly higher than those of ischemia-reperfusion group (1.72±0.11 vs 1.41±0.07, P＜0.05; 1.76±0.19 vs 1.55±0.13, P＜0.05. Conclusion Ischemia-reperfusion injury can induce apoptosis of pancreatic cells. Verapamil could protect the injured pancreatic tissue by reducing the level of calcium, stimulating the expressions of bcl-2 and c-myc and inhibiting apoptosis of pancreatic cells.
Objective To investigate the clinical efficacy and safety of hyperthermic intraperitoneal perfusion chemotherapy (HIPC) in treatment of advanced colorectal cancer.Methods The Meta-analysis was applied to analyze 8 randomized controlled quantitative studies published at domestic and abroad. These patients treated by HIPC after radical operation with colorectal cancer were included for the treatment group, and those treated only by radical operation with colorectal cancer for the control group. Relative risk (RR) of outcome variable of 3-year and 5-year survival rate and safety between the two groups were compared. Results There were 8 selected literatures, including 1 501 cases, in which 765 cases for treatment group, and 736 cases for control group. RR of 5-year survival rate of the total patients was 2.39 (95% CI: 1.66-3.45). RR of 3-year survival rate of the total patients was 2.13 (95% CI: 1.45-3.13). The results demonstrated that HIPC could improve 5-year and 3-year survival rate, and sensitivity analysis confirmed the conclusions more reliable. The security was described in 5 literatures, the available information showed smaller potential security issue. Conclusions HIPC after radical operation of advanced colorectal cancer can increase 5-year and 3-year survival rate of patients, improve the prognosis of patients. Whether patients with increased incidence of postoperative complications related to the HIPC is no clear-cut conclusions for lack of related research.
Objective To investigate the effects of different reperfusion sequence on hepatic warm ischemia-reperfusion injury and its related mechanisms. Methods Ninety-six healthy male Sprague Dawley rats were randomly divided into 6 groups by using random digits method (n=16, each)： Sham operation group, only shammed operation for negative control; the other 5 groups were all experimental groups, which were divided according to different reperfusion sequences of portal vein and hepatic artery: reperfusion first through the portal vein for 1 min with subsequent full reperfusion group, reperfusion first through the portal vein for 2 min with subsequent full reperfusion group, reperfusion first through the hepatic artery for 1 min with subsequent full reperfusion group, reperfusion first through the hepatic artery for 2 min with subsequent full reperfusion group, simultaneous reperfusion through the portal vein and hepatic artery group. Each group was further randomly divided into two subgroups (n=8, each) for sample collection at 2, 4 hours after reperfusion respectively. Serum alanine aminotransferase (ALT), aspartate aminotransferase (AST) and malondialdehyde (MDA), superoxide dismutase (SOD) and glutathion (GSH) in hepatic tissue were detected respectively. HE staining of histopathologic slides was used to observe the morphological changes of hepatic tissue. TUNEL method was used to assess the apoptosis index (AI) of hepatocytes. Results The liver of rat was approximately normal in the sham operation group with lower levels of ALT, AST, MDA and AI, and higher levels of SOD and GSH as compared with all the experimental groups (P＜0.01). Less hepatic ischemia-reperfusion injury was found in reperfusion first through the portal vein for 1 min with subsequent full reperfusion group, whose ALT, AST, MDA and AI levels were significantly lower than those of the other experimental groups (P＜0.05 or P＜0.01), and its SOD and GSH levels were higher than those of the other experimental groups (P＜0.05 or P＜0.01). HE staining also showed milder hepatic injury in reperfusion first through the portal vein for 1 min with subsequent full reperfusion group as compared with the other experimental groups. Conclusion Hepatic reperfusion first through portal vein for short time with subsequent full reperfusion could depress the synthesis of free oxygen radicals and suppress apoptosis of hepatocytes, thus relieving hepatic ischemia-reperfusion injury.
Objective To investigate the expression of nuclear factor (NF)-κB and intercellular adhesion molecule (ICAM)-1 in rat′s retina injured by ischemia-reperfusion, and the effect of pyrrolidine dithiocarbamate (PDTC) on the expression of NF-κB and ICAM-1. Method The model of retinal ischemia-reperfusion was set up in 60 SD rats, which were divided into two groups with 30 rats in each: ischemia-reperfusion group and ischemia-reperfussion with injection of PDTC group. The left cephalic artery of each rat was ligated, and the right side was the control. Every group was subdivided into group 1 hour, 6, 12, 24, 48, and 72 hours after ischemia-reperfusion injury, and with 5 rats in each group. mRNA of NF-κB and ICAM-1 mRNA was measured by in situ hybridization (ISH) method in rat′s retina. Every rat underwent electroretinography (ERG) at the corresponding time before executed by neck breaking. Results In ischemia-reperfusion group, expression of NF-κB and ICAM-1 was detected at the 6th hour after ischemia-reperfusion, reached the highest level at the 24th hour, and weakened gradually later. In ischemia-reperfusion with injection of PDTC group, expression of NF-κB and ICAM-1 was detected at the 12th hour after ischemia-reperfusion, and reached the highest level at the 24th hour but lower than that in ischemia-reperfusion group. No expression of NF-κB and ICAM-1 was found in the control group. The relative recovery rate of ERG a and b wave amplitude in ischemia-reperfusion groups was lower than that in ischemia-reperfusion with injection of PDTC group at every stage(P＜0.01 ). The lowest relative recovery rate of ERG a and b wave amplitude in different stages in both of the 2 groups was at the 24th hour(P＜0.01). Conclusions NF-κB and ICAM-1 may play an important role in retinal ischemia-reperfusion injury, as the inhibitor of NF-κB, PDTC may relieve the retinal ischemia-reperfusion injury. (Chin J Ocul Fundus Dis，2004，20：175-178)