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Query: UMLS:C0001339 (acute pancreatitis)
 10,593 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

An ischemia-reperfusion injury on the pancreas is involved in the pathophysiology of acute pancreatitis or tissue injuries after pancreas transplantation. On the other hand, recent studies have demonstrated that ischemia-reperfusion induces apoptosis in several organs such as kidney, heart, and brain. In the present study, we sought to characterize a pattern of injury during ischemia-reperfusion on the pancreas and determined whether ischemia-reperfusion on the pancreas causes the apoptotic process. Ischemia-reperfusion was induced by blocking the inferior splenic artery and removing the clamp in pentobarbital-anesthetized rats. Rats were sacrificed at 0-72 hr following a 60-min ischemia. Evans blue extravasation showed 3.5-fold increase at 2 hr after reperfusion, indicating a rapid increase of vascular permeability. Tissue myeloperoxidase activity, an index of neutrophil accumulation, significantly increased in a time-dependent manner until 48 hr after reperfusion. Histological analysis revealed the existences of interstitial cell infiltration and edema. DNA breaks of acinar cells were detected by gel electrophoresis and in situ nick end-labeling, and the numbers strikingly increased at 48 hr after reperfusion. Furthermore, Bax protein, an effector of apoptotic cell death, was expressed in acinar cells. The results indicate that an ischemia-reperfusion injury on the pancreas in rats resembles many features of acute pancreatitis. Apoptosis in acinar cells may be one of the specific features of the ischemia-reperfusion injury on the pancreas.
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PMID:Ischemia-reperfusion injury on the pancreas in rats: identification of acinar cell apoptosis. 929 80

We studied the pancreatic high-energy phosphates in two models of acute pancreatitis using 31P nuclear magnetic resonance (NMR) in rats for the first time in vivo. Alcoholic pancreatitis was induced by acute ethanol intoxication and an obstruction-hyperstimulation mechanism. Taurocholate pancreatitis was generated by intraparenchymal administration of 1 ml of 1-10% taurocholate-Na+. In addition to the obligate control groups, a simple ischemia experiment was performed. The high-energy phosphates were monitored by 31P NMR spectroscopy at 2.0 T. Additionally, by means of a scoring system, the quality and quantity of pathomorphologic parameters were quantified after 24 h. 31P spectra acquired after injection of taurocholate showed an increase in inorganic phosphate with a concomitant decrease in ATP levels, similar to pancreatic ischemia. This irreversible decrease was accompanied histologically by severe pancreatic hemorrhage. After induction of alcoholic acute pancreatitis a reversible decrease in ATP was occasionally seen. Even when alcoholic pancreatitis had been fully established at 24 h, the 31P NMR spectrum was normal in all animals. In conclusion, depletion of high-energy phosphates seems to occur as a result of pancreatic cell death rather than being a cause of pancreatic necrosis. For the first time we applied in vivo NMR in the rat pancreas to study the time course in acute pancreatitis.
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PMID:Different changes in high-energy phosphates in alcoholic acute pancreatitis and taurocholate acute pancreatitis in rats using NMR spectroscopy at 2.0 T. 936 Oct 88

Despite numerous experimental and clinical investigations there is no consensus on the evolution of chronic pancreatitis (CP). In the 1970s and 1980s, Sarles persistently emphasised the de novo evolution of CP due to pancreatolithiasis. In recent years, however, clinical and morphological studies have provided strong evidence for the initial proposal of acute pancreatitis progressing to chronic pancreatitis. The so-called necrosis-fibrosis-sequence theory is supported by immunohistochemical work suggesting that inflammatory mediators primarily contribute to tissue destruction and that infiltration of pancreatic nerves by immune cells is a pathogenetic factor for the generation of pain in CP. While Sarles postulates that acinar hypersecretion and an imbalance of pancreatic stone promoting and inhibiting factors trigger the evaluation of CP, the necrosis-fibrosis-sequence theory also involves other pathomechanisms (e.g. changes in ductal permeability, ischemia, oxidative stress) which have been shown to cause (acute) pancreatic injury. Despite this unifying template, which also lessens the need to identify independent mechanisms for the pathogenesis of acute and chronic alcoholic pancreatitis, there are still open questions, e.g. on genetic factors that (like in hereditary CP) may explain the different susceptibility of the pancreas to injury and the individual immunological response.
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PMID:[New aspects in the pathophysiology of chronic pancreatitis]. 941 Jun 72

Type and frequency of abdominal complications after open heart surgery are described. Out of 3,312 patients, 48 patients (1.4%) developed early postoperative abdominal complications with a mortality rate of 14.5%. Paralytic ileus, erosive gastritis and gastrointestinal hemorrhage were the most frequent complications, whilst intestinal ischemia, acute cholecystitis and acute pancreatitis were less frequently observed. The comparison of the frequency of abdominal complications in cardiac surgery patients with the same complications in other operated patients showed no significant difference (hi-square test), with the exception of COLD which was more frequent in the group with abdominal complications. No association was found between perioperative treatment with aprotinine and the development of abdominal complications.
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PMID:Abdominal complications following cardiac surgery. 947 97

We studied the effects of SMS201-995, a long-acting somatostatin analogue, on bile-induced acute pancreatitis in the dog. According to morphometrical study, parenchymal necrotic ratio, zymogen granules area and zymogen granules occupied ratio of acinus were significantly decreased in SMS-treated pancreatitis. These results suggests that SMS-treated pancreatitis showed less damage than non-treated ones and decreased secretion of pancreatic enzyme. On the other hand, pancreatic blood flow showed a stronger decrease in SMS-treated dogs than in non-treated ones, and a significant difference was observed at 15 minutes and 1 hour after induction of pancreatitis. Many clinical and experimental evidences suggest that pancreatic ischemia causes acute pancreatitis. Pancreatitis may be worsened by an early phase treatment with SMS201-995, because this substance reduces pancreatic tissue blood flow. The harmful effect of this substance on pancreatic tissue blood flow must be kept in mind when SMS201-995 is used for therapeutic purpose of acute pancreatitis.
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PMID:[Experimental study on the therapeutic effects of SMS201-995 on bile-induced acute pancreatitis in the dog]. 954 45

We have previously shown that the acute phase reaction of the pancreas is a powerful emergency mechanism which protects the organism against further pancreatic aggression. In an attempt to understand the mechanisms involved in this protective effect we tried to characterize at the molecular level the phenotypic changes of the pancreatic cell during acute stress. Using a systematic approach, we identified the PC3/TIS21/BTG2 mRNA as strongly overexpressed in pancreas during the acute phase of pancreatitis. PC3/TIS21/BTG2 mRNA is also overexpressed in liver and kidney during acute pancreatitis but not in the other tissues analyzed. In addition, PC3/TIS21/BTG2 mRNA is overexpressed in kidney after a 30-min ischemia. Since acute pancreatitis and kidney ischemia-reperfusion-induced injury were associated with apoptosis, and PC3/TIS21/BTG2 has an antiapoptotic activity, we speculate that this protein may play a role in the control of apoptosis progression in these tissues.
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PMID:Overexpression of the PC3/TIS21/BTG2 mRNA is part of the stress response induced by acute pancreatitis in rats. 971 37

Pancreatic ischemia is a very rare etiology of clinical acute pancreatitis, complicating cardiac surgery, hemorrhagic shock, and transplantation of the pancreas. In this article, we present two patients with acute ischemic necrotizing pancreatitis, complicating a generalized atheromatous disease with extensive lesions in the splanchnic circulation (patient 1) and repair of a descending thoracic aortic aneurysm (patient 2). Diagnostic approach and management of ischemic necrotizing pancreatitis are discussed.
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PMID:Ischemic necrotizing pancreatitis. Two case reports and review of the literature. 981 45

Microcirculation and molecular biology are the hottest topics in modern surgical research. In familial adenomatous polyposis the incidence of carcinoma can be assessed by the localisation of the PAC-gene mutation. Restorative proctocolectomy with ileoanal pouch represents the procedure of choice. The optimal age for the operation varies between 20 and 35 years according to the localisation of the mutation. RT-PCR directed to recently defined surface antigens allows for the sensitive detection of intraoperative tumor cell liberation. Due to tumor cell detection in the systemic circulation the perioperative administration of monoclonal antibodies must be advocated. A preciser definition of lymphogenic tumor spread underlines the importance of systematic lymphadenectomy in resection of the colon. The understanding of microcirculatory disorders has optimized surgical decision-making intra- and perioperatively: function of renal and hepatic microcirculation is a reliable parameter to predict graft quality already intraoperatively and to monitor therapeutic approaches to ischemia/reperfusion injury. Results in the therapy of acute pancreatitis could be improved by operating less and later. Analysis of pancreatic microcirculation resulted in an improvement of ICU-therapy in the early stages of the disease. Transplantation of the liver is limited to hepatocellular carcinoma when its localisation or the residual hepatic function after resection preclude curative excision. In addition liver transplantation should not be carried out in tumors larger than 5 cm or in patients with more than 3 tumor nodules. Liver resection for colorectal metastases is a standard procedure. A second resection of recurrent metastases is advocated since an identical median survival can be achieved compared to the primary resection (32 mo). The surgical treatment of non-colorectal liver metastases is under evaluation and should be restricted to oncological centers. Special aspects of backwashileitis in ulcerative colitis will be outlined concerning timing of colectomy, pouch construction, and follow-up.
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PMID:[State of the art: gastroenterologic surgery]. 1006 3

Acute respiratory distress syndrome (ARDS) and multiple organ failure (MOF) are the most common causes of death in surgical intensive care units. A variety of stimuli, such as major surgery, trauma, shock, thermal injury, acute pancreatitis, and ischemia-reperfusion injury, initiate a systemic inflammatory response that contributes to the development of these complications. Splanchnic hypoperfusion is a common clinical event in critically ill patients. Recently, measurement of the adequacy of gut circulation has been demonstrated as an excellent tool for prediction of outcome in these patients. The emphasis of this review is on events associated with intestinal ischemia-reperfusion and subsequent distant organ injury.
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PMID:[Splanchnic hypoperfusion and distant organ injury]. 1041 57

Using in vivo microscopy red blood cell (RBC) velocities, functional capillary density (FCD) and capillary diameters were estimated after inducing acute pancreatitis by intraductal infusion of sodium taurocholate (0.8 ml; 4%) or after topical superfusion of the pancreas with ET-1 (100 pmol). Sodium taurocholate mediated a significant decrease in RBC velocities between 50 and 70%, transient decrease in capillary diameters by 10%, and a sustained decrease in FCD between 60 and 70% paralleled by a dramatic heterogeneity in blood flow. Topical superfusion of the exteriorized pancreas with ET-1 caused a significant decrease in RBC velocities between 65 and 75%, a sustained decrease in capillary diameters by 10%, and a decrease in FCD by 45% accompanied by an increase in flow heterogeneity. Following sodium taurocholate infusion pancreas histology revealed a severe edema and sublobular acinar cell necrosis, while topical ET-1 application displayed a severe edema of the pancreas with focal acinar cell necrosis. Thus, ET-1 mediated a deterioration of the pancreatic microcirculation, which is similar to the microcirculatory failure found in sodium taurocholate-induced experimental pancreatitis and was associated with focal acinar cell necrosis. We are thus inclined to hypothesize that endothelin released by injured endothelial cells during acute biliary pancreatitis promotes microcirculatory failure and ischemia in acute pancreatitis, eventually leading to acinar cell necrosis.
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PMID:ET-1 induces pancreatitis-like microvascular deterioration and acinar cell injury. 1042 33


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