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.
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.
Abstract： Objective To investigate the protective effects of adenosine (ADO) on lung ischemia/reperfusion injury following heart-lung transplantation in canine. Methods Canine heart-lung transplantation was performed．Canines were divided into two groups: transplant control groupand ADO group. The changes of arterial partial pressure of oxygen(PaO2) after reperfusion in two groups at 30，60，90，120 min were observed．The tissue contents of nitric oxide (NO) were measured at 10 min before ischemia, 10 min and 120 min after ischemia; 10 min and 60 min after reperfusion．The lung tissue samples were obtained 1h after reperfusion．The tissue myeloperoxidase(MPO) activity,content of malondialdehyde(MDA), content of superoxide dismutase(SOD), wet/dry ratio of lung(W/D) were measured.Microscopic examination of lungs was also conducted. Results (1)In ADO group，PaO2 were significantly higher than that in control group at 30，60，90 and 120 min after reperfusion (Plt;0.05)．(2) The tissue contents of NO at 120 min after ischemia, 10 min and 60 min after reperfusion were significantly lower than that at 10 min before ischemia(Plt;0.05). In ADO group，the tissue contents of NO at 120 min after ischemia, 10 min and 60 min after reperfusion were higher than that in control group respectively(Plt;0.05). (3)The tissue MPO activity, content of MDA, W/D in ADO group were significantly lower than those in corresponding control group. The content of SOD in ADO group were higher than that in control group(Plt;0. 05)．(4)The microscopic examination showed that there were severe leukocyte infiltration and edema formation in the alveolar space in control group, but the changes were less severe in ADO group. Conclusion Administration of ADO in canine heart-lung transplantation can protect the donor lung against ischemia／reperfusion injury．
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 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.
Objective To make clear the effect of gastrointestinal tract ischemia on multiple organ dysfunction syndrome (MODS). Methods The literature in the recent years was reviewed.Results The low-flow states of gastrointestinal tract and decrease of gastrointestinal intramucosal pH, which occured following a variety of insults (sever trauma, hemorrhagic shock, et al), as well as overgrowth of enterobacteria, may result in a significant increase of permeability of bowel and lead to endotoxemia and bacterial translocation. Ischemia also resulted in release of TNF, IL-6 into the systemic circulation, dysfunction of gastrointestinal tract motility, and activation of neutrophile which was integral in local and distant organ damage. Conclusion These data suggest that the management of correct ischemia of gastrointestinal tract, which include fluid infusion to replacement of blood volume, early enteral nutrition, improvement of gastrointestinal movement, could contribute to improve the intestinal barrier function, and prevent the development of MODS.
【Abstract】 Objective The present study employed both static and dynamic imaging modal ities to study bothintra- and extravascular events attributing to steroid-associated osteonecrosis (ON) using an experimental protocol with a single low-dose l i ppolysaccharide (LPS) injection and subsequently three injections of high-dose methylprednisolone (MPS). Methods Fourteen 28-week-old male New Zealand white rabbits received one intravenous injection of LPS (10 μg/ kg). After 24 hours, three injections of 20 mg/kg of MPS were given intramuscularly at a time interval of 24 hours. Additional 6 rabbits were used as controls. Dynamic MRI was performed on bilateral femora for local intraosseous perfusion before and after LPS injection. Blood samples were collected for haematological examinations before and after LPS injection. Bilateral femora were dissected and decalcified for microCT-based microangiography. ON lesion, intravascular thrombus and extravascular marrow fat cell size were examined histopathologically. Results Intravascular thrombus was observed in all ON rabbits. Extravascular marrow fat cell size was significantly increased in ON rabbits than that of the controls (P lt; 0.05). Compared to basel ine, a significant decrease in ratio of tissue-type-plasminogen-activator/plasminogen-activator inhibitor 1,activated-partial- thromboplatin-time, and a significant increase in ratio of low-density-l ipoprotein/high-density-l ipoprotein were only found in ON rabbits (P lt; 0.05). Dynamic MRI showed a significant decrease in the perfusion index ‘maximum enhancement’ in the ON rabbits (P lt; 0.05) and microCT-based microangiography showed blocked stem vessels in ON samples.Overall, 93% of the rabbits (13/14) developed ON and no rabbits died throughout the experiment period. Conclusion Bothintra- and extravascular events were found attributing to the steroid- associated ON based on our experimental protocol with a single low-dose LPS injection and subsequent three injections of high-dose MPS. Both high ON incidence and no mortal ity in rabbits treated with this inductive protocol suggested its effectiveness for future studies on evaluation of therapeutic efficacy of interventions developed for prevention of steroid-associated ON.
OBJECTIVE: To study the hemorheology of island flap after ischemia-reperfusion injury and modulation of dexamethasone. METHODS: Sixty Wister rats were made ischemia-reperfusion injury model, and divided into two groups randomly(Group I: intraperitoneal injection of normal saline 2 ml/kg as control group; Group II: intraperitoneal injection of dexamethasone 5 mg/kg as experimental group). Flap survived areas were measured and neutrophil necrosis numbers in flaps were counted. Erythrocytes and neutrophil hemorheology were observed. RESULTS: Area survived flap in group II was larger than that in group I. Neutrophil necrosis numbers were less in group II than in group I (P lt; 0.05). Whole blood hyposhear viscosity, erythrocyte aggregation, Casson yield stress and nerutrophil adhesion ability were higher in group I than in group II (P lt; 0.05); and the neutrophil deformability was lower in group I than in group II. CONCLUSION: Flap inchemia-reperfusion can increase erythrocyte aggregation index and neutrophil adhesion ability. Dexamethasone can improve these and decrease neutrophil necrosis numbers, so as to prevent flap from ischemia-reperfusion injury.
ObjectiveTo study the protective effects of ischemia preconditioning (IPC) on cryopreservation injury of rat liver.MethodsThe model of isolated nonrecirculated perfusion rat liver was established. The grafts were treated with IPC in different time (ischemia preconditioning time in IPC1 group was 5 min; the time in IPC2 group was 10 min; while the time in IPC3 group was 15 min). The cryopreservation injury of the grafts in each group was determined and compared. ResultsThe levels of aspartate transaminase (AST) and alanine transaminase (ALT) in the effluent solutions in IPC1 group were (40.1±6.3) U/L and （17.1±0.5） U/L respectively, and IPC2 group (53.6±3.7) U/L, （19.7±0.5） U/L, which were much lower than those of nonpreconditioning (NPC) group 〔(64.5±8.2) U/L, （23.8±3.9） U/L〕 (P＜0.05). Those in IPC1 group was much lower than those in IPC2 group and IPC3 group 〔(63.8±7.2) U/L,（22.8±2.5） U/L〕 (P＜0.05). The level of lactic acid dehydrogenase (LDH) in NPC group (104.3±20.6) U/L, IPC1 group (84.1±19.7) U/L, IPC2 group (90.5±21.1) U/L, and IPC3 group (103.1±18.5) U/L were of no significant difference (Pgt;0.05). The contents of bile product and the hepatocellular contents of ATP in IPC1 group were (53.5±10.2) μl and (6.15±0.65) μmol/g respectively, and IPC2 group (41.5±8.1) μl, (4.77±0.21) μmol/g, which were much higher than those NPC group 〔(22.8±9.7) μl, (2.62±0.34) μmol/g〕 (P＜0.05). Those in IPC1 group were much higher than those in IPC2 group and IPC3 group 〔(27.5±2.8) μl, (2.61±0.29) μmol/g〕 (P＜0.05). The contents of malondialdehyde (MDA) in liver tissue in IPC1 group was (4.36±0.26) nmol/gand IPC2 group (5.51±0.13)
Objective To observe the influences of depolarized arrest and hyperpolarized arrest on alternation of fluidity of myocardial cell membrane during cardiopulmonary bypass (CPB) and evaluate the protective effects on myocardium of hyperpolarized arrest. Methods Seventy-two felines were randomized into three groups, each group 24. Control group: 180 minutes of CPB was conducted without aortic and vena caval cross-clamping. Depolarized arrest group: hearts underwent 60 minutes of global ischemia after aortic cross-clamping (ACC) followed by 90 minutes of reperfusion. The cardioplegic solution consisted of St. Thomas solution (K+16mmol/L). Hyperpolarized arrest group: the protocol was the same as that in depolarized arrest group except that the cardioplegic solution consisted of St.Thomas solution with pinacidil (50 mmol/L,K+5mmol/L). Microviscosity, the reciprocal of fluidity of myocardial membrane was measured in all groups by using fluorescence polarization technique. (Results )Microvis cosity of myocardial cell in depolarized arrest group during ACC period was significantly higher than that before ACC and kept on rising during reperfusion period. Microviscosity of myocardial cell in hyperpolarized arrest group during ACC was trending up and reperfusion periods as well, but markedly lower compared to that in depolarized arrest group at corresponding time points(Plt;0.01). Conclusion Hyperpolarized arrest is more effective in protecting myocardial cells from ischemia-reperfusion injury than depolarized arrest during CPB by maintaining better fluidity of myocardial membrane.
