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Objective To investigate the expression of dopamine receptor in brain of rats with pancreatic encephalopathy and provide a theoretical basis to reveal pathogenesis of pancreatic encephalopathy. Methods A rat model of experimental pancreatic encephalopathy was induced by retrograde injection of 5％sodium taurocholate into the pancreatic duct. The pathological changes of pancreas and brain were detected. The water content in brain tissue was determined. The superoxide dismutase activity and malondialdehyde content in brain tissue homogenate were detected by the chemical colorimetry. Levels of TNF-α,IL-1β,tyrosine hydroxylase and dopamine receptor-2 were detected by immunohistochemistry(SP method). Results Cerebral sulcus was shallow,ventricle was small-er and the superficial veins were dilated and congested. The inflammatory cell infiltration and pancreatic acinar cell necrosis in the pancreas and neuron edema ,inflammatory cell infiltration ,microvessel adherent leukocytes in brain were observed by light microscope in model groups at 3,6,12 hours. Compared with the control group. The activities of superoxide dismutase in brain tissue in model groups at 3,6,12 hours were significantly decreased (P < 0.01). The level of malondialdehyde and the water content of brain tissue were significantly increased (P <0.01 ,respectively). Compared with the control group ,levels of brain TNF-α,IL-1β,tyrosine hydroxylase and dopamine receptor-2 in model groups at 3,6,12 hours were significantly increased(P < 0.01,respectively).Conclusions The incidence of pancreatic encephalopathy may be related to the influx of oxygen free radical and inflammatory factors,invading nerve center by blood-brain barrier and inducing the increased production of dopa-mine and the upregulation of dopamine receptor in brain.
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Objective To investigate the expression of dopamine receptor in brain of rats with pancreatic encephalopathy and provide a theoretical basis to reveal pathogenesis of pancreatic encephalopathy. Methods A rat model of experimental pancreatic encephalopathy was induced by retrograde injection of 5％sodium taurocholate into the pancreatic duct. The pathological changes of pancreas and brain were detected. The water content in brain tissue was determined. The superoxide dismutase activity and malondialdehyde content in brain tissue homogenate were detected by the chemical colorimetry. Levels of TNF-α,IL-1β,tyrosine hydroxylase and dopamine receptor-2 were detected by immunohistochemistry(SP method). Results Cerebral sulcus was shallow,ventricle was small-er and the superficial veins were dilated and congested. The inflammatory cell infiltration and pancreatic acinar cell necrosis in the pancreas and neuron edema ,inflammatory cell infiltration ,microvessel adherent leukocytes in brain were observed by light microscope in model groups at 3,6,12 hours. Compared with the control group. The activities of superoxide dismutase in brain tissue in model groups at 3,6,12 hours were significantly decreased (P < 0.01). The level of malondialdehyde and the water content of brain tissue were significantly increased (P <0.01 ,respectively). Compared with the control group ,levels of brain TNF-α,IL-1β,tyrosine hydroxylase and dopamine receptor-2 in model groups at 3,6,12 hours were significantly increased(P < 0.01,respectively).Conclusions The incidence of pancreatic encephalopathy may be related to the influx of oxygen free radical and inflammatory factors,invading nerve center by blood-brain barrier and inducing the increased production of dopa-mine and the upregulation of dopamine receptor in brain.
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Pancreatic encephalopathy (PE)is a serious complication of pancreatitis,with difficulties in early diagnosis and poor prognosis. This article introduces the possible pathogenesis of PE involving pancreatin activation,cytokines,infection,water and electrolyte imbalance, and vitamin deficiency,summarizes the clinical manifestations and laboratory features of PE,and points out that the clinical manifestations of PE lack specificity and there are no reliable biochemical indices or diagnostic criteria.This article also elaborates on the diagnosis and treat-ment strategies for PE and points out that the key to PE treatment is active and effective treatment of the primary disease.Most PE patients are improved with the control of pancreatitis.
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Pancreatic encephalopathy(PE)is one of the severe complications in acute pancreati-tis,which is characterized by a group of neurological signs and symptoms. Itˊs very difficult to have an early diagnosis,while the morality of PE is very high and the prognosis is very poor. Eliminating causes of pan-creatic encephalopathy,early diagnosis and combined therapy are the keys to achieve good curative effects. This paper reviewed the recent progress in the main mechanisms,clinical manifestations,diagnosis and therapy of PE.
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Pancreatic encephalopathy (PE)is one of the severe complications of severe acute pancreatitis (SAP).Early diagnosis mostly depends on the history of disease as well as clinical symptoms and signs.PE progresses rapidly and is often complicated by multiple organ dysfunction,and it may finally develop into multiple organ failure with a high fatality rate if not treated in time.It is currently known that de-myelination is one of the important pathological features of this disease,with fat -soluble demyelination of cerebral gray matter and white matter,as well as inflammatory changes such as hemorrhage and edema.The target antigen of demyelinating lesions,however,is myelin basic protein (MBP).This paper reviews the changes in MBP levels in the demyelinating lesions of the central nervous system among PE pa-tients,with the purpose of providing clues for the early diagnosis and prognostic study of demyelinating lesions in PE.
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Objective The aim of this study is to demonstrate the diagnostic effect of brainstem evoked potential for pancreatic encephalopathy in rats with severe acute pancreatitis. Methods Sixty male Sprague-Dawley (SD) rats were randomly divided into two equal groups: a sham-operated (SO) group and a severe acute pancreatitis (SAP) group. Each group was evaluated at 3, 6, and 12 h during the experiment. To detect the brain stem evoked potential change at different time points. The ultrastructure of brain tissue was observed by transmission electron microscope (TEM). The expressions of the apoptosis-related proteins Bcl-2, Bax and caspase-3 were observed using immunohistochemical and Western Blot technique. Results In SAP group, congestion, edema, inflammatory cell infiltration, mitochondrial swelling and cell apoptosis were apparent. Compared with SO group, the brain stem evoked potential in severe acute pancreatitis group was obviously reduced in SAP group. Compared with SAP group, the expressions of Bcl-2 have increased, whereas the expressions of Bax and caspase-3 have decreased in SO group significantly ( <0.05) . Conclusion Brain stem evoked potential is a sensitive method in detection of rat brain damage. The results showed that the consistency and the damage degree of rats may be important clinical diagnostic index of pancreatic encephalopathy.
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Objective To study the expression of aquaporins-4 (AQP4) in the brain tissue of rats with pancreatic encephalopathy (PE) induced by phospholipase A2 and to explore the role of aquaporins-4 in PE.Methods Twenty five healthy Wistar rats were randomized into 3 groups:blank group ( n =5),PE group (n =10 ) and control group (n =10 ).The experimental model was established in rats by injecting phospholipase A2 into carotid artery (0.1 ml/100 g body weight).Same amount of normal saline was used in the control group and no treatment was used in the blank group.One day later,the rats were sacrificed,then the measurement of brain tissue wet/dry (W/D) weight ratio was performed,and brain tissue was routinely pathologically examined,immunohistochemistry and Western blotting were performed in each group to detect the expression of aquaporins-4.Results There was no obvious brain tissue pathological change in the control group and blank group.Neurons in the brain tissue of PE rats presented with significant edema and ballooning degeneration,infiltration of inflammatory cells,leukocyte aggregation around the microvessels.The water contents in the brain tissue in the blank group and control group,PE group were (61.44 ±0.36)％,(63.20±0.32)％ and (78.33 ±0.24)％,and it was significantly higher in PE group than that in the control and blank group (P＜0.05).The expressions of aquaporins-4 in the brain tissue were 0.41 ±0.27,0.49 ±0.13,0.98 ±0.21,respectively,and it was significantly increased in PE group than that in the control and blank group (P ＜ 0.05 ).Conclusions Aquaporins-4 may play important roles in the pathogenesis of pancreatic encephalopathy.
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Objective To explore the mechanism 、diagnosis of pancreatic encephalopathy(PE);To evaluate the therapy of PE.Methods To analyze the treatment and diagnosis of 23 PE patients.Results 12 PE patients were cured.11patients were dead,the mortality is 47.8%,5patients in operation group died,the mortality is 62.5%.6 patients in non-operation group were dead,the mortality is 40%,among them,5patients died for multiple organ system falure.one died for septic shock.Conclusions PE is relating to serum amylase inflammatory mediators and infection etc.The diagnosis of PE is based on AP and neurological and mental abnormality.The relative auxiliary diagnosis standard is uncertain.the conventional therapy of PE 、the remedy of MOSF and disorder in water and electroltes were basic therapy.the nerve preserving is necessary for PE's therapy.
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@#ObjectiveTo study the protective effects of tumor necrosis factor-α(TNF-α) antibody on pancreatic encephalopathy in rats. MethodsSixty SD rats were randomly divided into the normal control group, acute necrotizing pancreatitis induction group and TNF-α antibody treated group. Acute hemorrhage necrotizing pancreatitis model in rats were induced by retrograde injection of 5% sodium taurocholate into the pancreatobiliary duct. Serum TNF-α was detected and animals were killed 12 h after drug administration. The changes of brain water contents, leucocyte accumulation and adhesion were measured, and pathological studies of pancreas and brain were performed. ResultsIn group of TNF-α antibody treated, serum TNF-α level decreased, brain water contents and leucocytes accumulation and adhension decreased significantly than that of acute necrotizing pancreatitis induction group (P<0.05). The histopathological change of pancrea was alleviative. ConclusionTNF-α antibody can alleviate the brain damage in acute hemorrhage necrotizing pancreatitis.
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Objective To study the effects of malondialdehyde (MDA), superoxide dismutase (SOD) and tumor necrosis factor-? (TNF-?) on brain tissue in rats with pancreatic encephalopathy (PE). MethodsThirty-six Wistar rats were randomly divided into control group (n=6) and PE model group (n=30). In control group, rats were injected with normal saline by internal carotid artery (0.1 ml/100 g) and were killed on the first day after the injection. In PE model group, rats were injected with phospholipases A2 (0.1 ml/100 g, 1 000 U/0.1 ml) by internal carotid artery, to establish animal model of PE in rat and 10 rats were killed on day 1, 3, 7 respectively after the injection. The changes of water content in the brain were measured. Leucocytes aggregation and margination in the microvessels, and the changes of cerebral cells and nerve fibers were observed. The levels of MDA, TNF-? and the activity of SOD were tested in the brain homogenate in rats. ResultsIn PE model group, water contents of brain increased; The phenomena of leucocytes accumulation and margination, cellular edema of neurons and demyelination of nerve fibers became more obvious; The levels of MDA and TNF-? increased significantly than those in the control group, while the activity of SOD reduced (P
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Objective To discuss the causes,agents and treatment of pancreatic encephalopathy in acute pancreatitis.Method We reviewed 26 cases of acute pancreatitis combined with pancreatic encephalopathy within recent 10 years.Results Pancreatic encephalopathy occurred always accompanied with such agents as hyperpyrexia, waterelectrolyte disturbance,hypoxemia, azotemia and bloodsugar disturbance etc.Conclusions The occurrence of the pancreatic encephalopathy is based on the harm that pancreatin does to the brain.The causes of pancreatic encephalopathy vary.To inhibit the releasing of pancreatin is the principle to prevent pancreatic encephalopathy, and to maintain normal physiological function,to control infection and nutritional support are the important links to prevent the pancreatic encephalopathy from happening.
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Objective To investigate the clinical characteristics and the treatment of pancreatic encephalopathy (PE) and Wernicke's encephalopathy (WE). Method A retrospective study was conducted on 596 cases of acute pancreatitis. Results There were 93 cases of severe acute pancreatitis (SAP),among them encephalopathy was discovered in 10 patients (1.7%). All 6 patients of PE developed in SAP (6.5%);3 patients died (3% of SAP,50% of PE). Four cases of WE developed in AP (0.7%);2 patients died (0.3% of AP,50% of WE). Two patients of WE were treated with parenteral thiamine (vitamin B_ 1 ),and they survived. Conclusions PE occurred in early stage of SAP or recrudescence,while WE usually occurred in convalescent stage of SAP/AP. Long fasting,repeated vomiting,and total parenteral nutrition (TPN) without VitB_ 1 were main causes of VitB_ 1 deficiency,which might be the main causative factor in WE.
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Objective: To discuss the treatment of pancreatic encephalopathy(PE).Methods: Recombinant human growth hormone (rhGH)(Saizen)were applied in patients of severe acute pancreatitis(SAP) with suspicious early PE that presented with mental disorders. rhGH was also used in combination with somatostatin as the therapeutic method for SAP and its complication.Dosage and administration: Saizen 4U was injected intramuscularly twice a day for 5～7 days.Results: In 7 patients of this group, all of them showed improvement in the aspect of mental dysfunction and the symptoms disappeared after 48～72 hours. In 13 SAP cases underwent combined application of rhGH and somatostatin, no PE was observed.Conclusion: Application of rhGH showed therapeutic effect on the early manifestations of PE. It also suggested that combined use of rhGH and somatostatin could decrease the occurance of PE.
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Objective To discuss the predisposing factors,prognosis and treatment of pancreatic encephalopathy(PE) in acute pancreatitis(AP). Methods Nineteen cases of AP complicated with PE were retrospectively studied. Results The occurrence rate of PE was 12.0%. PE often occurred in association with such factors as hyperpyrexia, water-electrolyte disturbance, and hypoxemia. Among the 19 patients,11 patients received surgical operation and 8 were treated conservatively.The total fatality rate reached 52.6%(10/19), significantly higher than other concurrently treated cases of severe acute pancreatits(SAP) (20.7%,P
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Objective To investigate low molecular weight heparin(LMWH) therapy for pancreatic encephalopathy in severe acute pancreatitis(SAP).Methods SD rats were randomly divided into 3 groups:(1) Sham operation(S) group,(2) SAP group and(3) LMWH treatment(LT) group:LMWH was administrated at 4 hours after construction of SAP model.The levels of serum amylase,myelin basic protein(MBP),tumor necrosis factor alpha(TNF-?),interleukin 6(IL-6),brain water contents and pathological changes of pancreas and brain were measured at 24 h after models were set up in SAP and in S group,and 24 h after LMWH was administrated in LT group.Results(1) The levels of serum amylase,TNF-?,IL-6 in SAP group were significantly higher than those in S group and LT group(all P 0.05).(2) The brain water content in SAP group was significantly higher than that in S group and LT group(P