To elucidate the mechanism of renal injury following intestinal ischemia/reperfusion, reactive oxygen metabolites in kidney and plasma were examined in 20 rats following intestinal ischemia/reperfusion by measurement of lipid proxidation (LP).The plasma lipid peroxide concentration after reperfusion was higher than that of the contol group (Ｐ＜0.01),the LP in kidney homogenate was also significantly higher (Ｐ＜0.01) following intestinal ischemia/reperfusion.Our study suggests that reactive oxygen metabolites after intestinal ischemia/reperfusion plays an important role in kidney injury.
This prospective animal study was designed to investigate the changes of plasma endothelin (ET) levels in acute necrotizing pancreatitis (ANP). Sprague-Dawley rats were randomly devided into 3 groups: acute necrotizing pancreatitis (ANP) group in which ANP was induced by infusion of 5% sodium taurocholate (STC) into biliopancreatic duct, sham operation (SO) group and platelet activating factor antagonist BN50739 (BN) group. Blood levels of ET and platelet activating factor (PAF) were detected. Pancreatic microcirculatory blood flow was measured and pancreatic histological scores were evaluated. Results showed that the pancreatic microcirculatory blood flow in ANP group was decreased to a great extent immediatly after induction of ANP and soon began to rise slowly for 3 hours and again decreased steadily after that. The blood levels of ET, PAF and histological scores in ANP group were significantly higher than those in SO group. In BN group, the blood flow was significantly improved and the levels of blood ET, PAF and histological scores were all significantly lower as compared to those in ANP group. It is concluded that ischemia/ reperfusion is present in the initiation of acute necrotizing pancreatitis induced by STC in the rat. This leads to injuries of endothelial cells and increase in the production of ET and PAF. I/R lesions,and interaction of ET and PAF lead to a vicious circle, thus augmenting the pathological changes in the pancreas.
Objective To investigate the effects and mechanism of doxorubicin preconditioning in providing ischemic tolerance for rats abdomen island flaps. Methods Twenty-four healthy adult Sprague Dawley rats, 12 males and 12 females, were randomly divided into 3 groups (n=8): control group (group A), ischemic preconditioning group (group B), and doxorubicin preconditioning group (group C). After the abdomen island flap (6 cm × 3 cm in size) based on the superficial inferior epigastric neurovascular bundle was prepared, group A had no further treatment; group B was given a 10-minute ischemia followed by a 10-minute reperfusion for 4 times; and group C was given pretreatment with doxorubicin (1 mg/kg) by injection of the inferior epigastric vein. After 24 hours, the inferior epigastric vessels were blocked by vascular clamp for 4 hours, followed by reperfusion 2 hours to prepare ischemia/reperfusion (I/R) injury model. The rat survival was observed after operation; at 0, 8, 12, 24, and 30 hours after I/R injury, the malonyldiadehyde (MDA) and superoxide dismutase (SOD) levels were measured. At 7 days after I/R injury, the survival rate of flap were calculated and the flaps were harvested for histological observation. Results During experiment, 5 rats died (1 rat in groups A and B respectively, 3 rats in group C) and were added. The survival rates of the flap in group A (10.10% ± 0.43%) was lower than those in group B (91.63% ± 1.76%) and in group C (92.75% ± 1.48%) at 7 days after I/R injury, showing significant differences (P lt; 0.05), and there was no significant difference between groups B and C (t=0.29, P=0.77). Significant difference was found in MDA level and SOD level between group A and groups B, C after 8 hours (P lt; 0.05), and there was no significant difference between groups B and C (P gt; 0.05). Histological observation showed that inflammatory cells infiltration was more obvious and hyperplasia of fibers was weaker in group A than in groups B and C. Conclusion Doxorubicin preconditioning can provide ischemic tolerance for rats abdomen island flaps and protect flaps from the I/R injury. The possible mechanism may be related to that doxorubicin can induce endogenous protections.
To investigate the protective effect of propofol on ischemia/reperfusion induced spinal cord injury in rabbits and its influence on excitatory amino acid (EAA). Methods Sixty New Zealand white rabbits weighing 2.0-2.5 kg, half males and half females, were selected. The infrarenal circumaortic clamping model was used. And 6 mL/kg different fluids were continuously infused through a catheter into the aorta distal to the clamping site at a speed of 12 mL/(kg•h) during the 30 minutes ischemia period. According to the different infusing l iquids, the rabbits were randomized into 6 groups(n=10 per group): group A, normal sal ine; group B, 10% intral ipid; group C, propofol 30 mg/kg; group D, propofol 40 mg/kg; group E, propofol 50 mg/kg; group F, propofol 60 mg/kg. At 0, 6, 24, and 48 hours after reperfusion, neurologic outcomes were scored on a Tarlov scale system. At 48 hours after reperfusion, the number of normal neurons in the anterior spinal cord was counted, and concentration of EAA in the lumbar spinal cord was measured by high performance l iquid chromatography. Results The neuroethological score was better in groups C, D, E and F than that of groups A and B (P lt; 0.05), the score of group E was the highest (P lt; 0.05), and there was no significant difference between group A and group B (P gt; 0.05). The number of normal neurons in the anterior spinal cord of groups C, D, E and F was greater than that of groups A and B (P lt; 0.05), and group E was greater than groups C, D and F (P lt; 0.05). The concentration of EAA in groups A, B, C, D, E and F was greater than that of normal tissue, the group E was the lowest (P lt; 0.05), the groups A and B were the highest (P lt; 0.05), and there was no significant difference between group A and group B (P gt; 0.05). Concentrations of glutamate and aspartic acid were negatively correlated to normal neuron numbers in the anterior spinal cord and neuroethological scores 48 hours after reperfusion, and the corresponding correlation coefficient was — 0.613, — 0.536, — 0.874 and — 0.813, respectively (P lt; 0.01). Conclusion Propofol can significantly inhibit the accumulation of EAA in spinal cord and provide a protective effect against the ischemia/reperfusion injury induced spinal cord in rabbits.
Objective To investigate the effect of cold ischemia on the development of transplant arteriosclerosis (TA) in rat aortic isografts. Methods Aorta grafts from SD and Wister rats were stored in a cold perfusion solution for 0.5 hours and 4 hours respectively before being orthotopically transplanted to Wister recipients. After observation times ranging from 15 to 60 days, the grafts were examined by using histological and electron microscopy techniques. Regional changes in the lumen, intima and media layers were measured by using an image analysis system. Results Partial intima thickings were showed in control isografts at 60 day posttransplantation. Pronounced intima thickings were seen in experimental isografts and control allografts at the same time. The thicking neointimas consist mainly of monocyte/macrophage and smooth muscle cells (SMC). The broken interior elastic lamina (IEL) and necrosis SMC in media were detected in allogenic grafts. Conclusion The damage due to prolonged cold ischemia time is sufficient to cause pronouced graft arteriosclerosis.
ObjectiveTo investigate the effect of simulated in vivo physiological environment severed limb fostering system applying remote ischemic conditioning (RIC) perfusion on preserving severed limb. MethodEighteen adult Bama mini pigs (24-30 kg in weight) were randomly divided into 3 groups (n=6) . No ischemic treatment was given in group A as normal control group; the right lower limbs were completely amputated and preserved at room temperature for 3 hours to make ischemic models in groups B and C, and then the severed limbs were put into the simulated in vivo physiological environment severed limb fostering system. Continuous blood perfusion was performed in group B, and continuous blood perfusion was performed after RIC perfusion in group C. After 8 hours of perfusion, the skeletal muscle samples were harvested for the morphology observation by transmission electron microscopy. The protein levels of B-cell lymphoma-2(Bcl-2) and Caspase-3 were detected by Western blot. The content of cytochrome C in both mitochondria and cytoplasm was determined by ELISA. ResultsTransmission electron microscopy results illustrated that the muscle fibers arranged more orderly and the mitochondria swelling was slighter in group C than group B. Western blot analysis showed that the protein levels of Bcl-2 and Caspase-3 were significantly higher in groups B and C than group A (P<0.05) ; the protein level of Bcl-2 significantly increased and the protein level of Caspase-3 significantly decreased in group C when compared with those in group B (P<0.05) . ELISA detection implicated that mitochondrial cytochrome C significantly reduced and cytosolic cytochrome C significantly increased in group B when compared with those in groups A and C (P<0.05) , but no significant difference was found between group A and group C (P>0.05) . ConclusionsThe ischemia/reperfusion-induced injury to skeletal muscle could be considerably inhibited by RIC perfusion. The simulated in vivo physiological environment severed limb fostering system applying RIC perfusion can significantly prolong the severed limb preserving time.
From aortic declamping to weaning from cardiopulmonary bypass (CPB), myocardium needs recovery not only from surgical and ischemia/reperfusion injury, but also of its full performance of pumping function as quickly as possible. In the early period of resuming myocardial perfusion, coronary blood flow should be increased, but ventricular volume overload, large dosage of adrenaline and isoprenaline, and high-energy defibrillation should be avoided. Thenappropriate management according to cardiac function and ECG changes is needed for successful weaning from CPB.
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.