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Query: UMLS:C0030305 (pancreatitis)
 16,014 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A canine model was devised to measure the oxygen consumption of the pancreas in experimentally induced pancreatitis. Over the 120 minute investigation period the oxygen consumption fell by 63% in the presence of a diminishing pancreatic blood flow and constant arteriovenous percentage saturation across the pancreas. Dextran 40 has been previously shown to maintain the pancreatic circulation. Accordingly a second group of dogs was treated with Dextran 40 (1.5 ml/kg) 60 minutes after induction of the pancreatitis. This produced a significant increase in the pancreatic oxygen consumption and widening of the arteriovenous difference. Dextran 40 appears to reverse the hypoxia of the pancreas noted in acute experimental pancreatitis.
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PMID:Experimental acute pancreatitis: the changes in pancreatic oxygen consumption and the effect of Dextran 40. 51 73

In spite of extensive investigations, many aspects of the hemodynamic changes occurring in acute pancreatitis are understood poorly. A dog model was established in which continuous measurements of pancreatic arterial blood flow, cardiac output, and mean arterial blood pressure were made using electromagnetic flow probes and a pressure transducer, respectively. Pancreatitis was induced and the animals were monitored for 3 hours. In addition, control animals (group I) without pancreatitis also were done. All animals 50 ml of saline in the first hours. Three methods of therapy then were instituted in the dogs with pancreatitis and their effects were recorded. group I 6 dogs control animals no pancreatitis saline 50 ml/hr group II 10 dogs saline 50 ml/hr group III 6 dogs plasma 15 ml/kg over 45 min then saline 50 ml/hr group IV 10 dogs saline 50 ml and 1.5 ml/kg of dextran 40/hr These results confirm the observations made previously using a transillumination technique--that the pancreatic circulation rapidly reduces in acute pancreatitis. Administration of plasma produced a significant (P less than 0.05) but transient increase in the cardiac output and pancreatic blood flow; however, the blood pressure remained low. Dextran 40 minimally increased cardiac output, but it significantly improved the blood pressure and maintained the pancreatic blood flow. Low-dose, low-molecular weight dextran 40 appears to help to maintain pancreatic blood flow in acute pancreatitis. The possible mechanisms concerning the made of action of dextran 40 will be discussed.
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PMID:Experimental pancreatitis: Effect of plasma and dextran on pancreatic blood flow. 68 23

In vivo microscopy was performed to assess the effect of dextran 40, gabexate mesilate and somatostatin on the microcirculation in sodium taurocholate-induced pancreatitis in rats. Intraductal infusion of 0.4 ml of a 4% solution of sodium taurocholate decreased capillary blood flow, induced capillary stasis and increased vascular permeability in the head of the pancreas. Dextran 40, gabexate mesilate and somatostatin improved capillary blood flow in the initial phase of acute pancreatitis significantly and prevented stasis in 5 of 9, 3 of 8 and 7 of 10 (p < 0.05) cases. Only dextran 40 reduced the increase of vascular permeability. Decrease of capillary blood flow, capillary stasis and vascular permeability changes are important factors contributing to the pathogenesis of sodium taurocholate-induced pancreatitis. Dextran 40, gabexate mesilate and somatostatin exert a beneficial effect on the microcirculatory changes in this model of acute pancreatitis.
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PMID:The effect of somatostatin, gabexate mesilate and dextran 40 on the microcirculation in sodium taurocholate-induced pancreatitis. 128 68

Dextran of different molecular weight (Dx 40, Dx 60/70) has often been evaluated as adjunct treatment of experimental acute pancreatitis. A beneficial effect has been documented by a decrease in its lethality. However, the mechanism of action is poorly understood. A specific effect on the pancreatic microcirculation generally has not been documented and differentiation from unspecific improvement of pancreatic blood flow due to volume expansion has been difficult. This investigation was designed to quantify the effect of dextran on the impairment of pancreatic microcirculation during acute biliary pancreatitis by means of intravital microscopy. Dextran 60 (Dx 60, molecular weight 60,000) was chosen in light of the increase in vascular permeability in the early stage of pancreatitis as demonstrated previously in the same model. Isovolemic hemodilution, i.e., exchange of whole blood for Dx 60 was used as a mode of administration to achieve instantaneous onset of therapy without changes in intravascular volume. In the control group a progressive reduction of pancreatic capillary perfusion commenced 30 minutes after induction of acute pancreatitis, resulting in cessation of nutritive tissue perfusion after 3 hours. In the animals subjected to hemodilution, stabilization of the pancreatic microcirculation was accomplished throughout the observation period of 6 hours. Because volume-related effects could be excluded by the protocol and by monitoring central venous pressure and hematocrit, a specific effect of hemodilution with DX 60 on the pancreatic microcirculation is indicated by our results.
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PMID:Therapeutic effect of isovolemic hemodilution with dextran 60 on the impairment of pancreatic microcirculation in acute biliary pancreatitis. 168 93

This experimental study was undertaken to clarify the role of pancreatic enzymes and endotoxin in the pathogenesis of pulmonary edema in acute pancreatitis, paying special attention to the effects of two different intravenous infusions: lactated Ringer's solution (LR) and Dextran 40 (D40). After acute pancreatitis was induced in dogs by injecting autologous gallbladder bile into the main pancreatic duct, plasma endotoxin levels increased markedly in both the LR and D40 groups, and PaO2 decreased more significantly in the D40 group. Extravascular lung water (EVLW) increased more significantly in the D40 group than in the LR group, in spite of the fact that colloid-hydrostatic pressure gradient (CHPG) had been maintained more efficiently in the D40 group. Significant correlation between EVLW and plasma endotoxin level was delineated in both groups, but the slope of the regression line in the D40 group was much greater than that of the LR group. Infusion of trypsin and elastase into the pulmonary artery in normal dogs caused moderate elevation of EVLW in the D40 group, but there was no significant alteration in the LR group. The changes of PaO2, EVLW, and CHPG after infusion of endotoxin were similar to those in the animals with experimental acute pancreatitis. In conclusion, endotoxin appears to play an important role in the pathogenesis of pancreatitis-induced pulmonary edema by causing an increase in pulmonary vascular permeability, and under these circumstances the infusion of large amount of colloid solution promotes the development of pulmonary edema.
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PMID:[An experimental study on the pathogenesis of pulmonary edema in acute pancreatitis, with special interest to the effects of colloid infusion and the role of endotoxin]. 172 52

An experimental model of edematous pancreatitis in pigs was established and measurement of pancreatic macro- and microcirculatory parameters and determinations of pancreatic enzymes (lipase, phospholipase A) and vasoactive mediators (prostanoids, kallikrein, kininogen) were performed. During general anesthesia the pancreas was isolated in situ. Pancreatic microcirculatory parameters were measured using videofluorescence microscopy after iv administration of FITC-Dextran. In hourly collected samples lipase and phospholipase A activities were determined enzymatically, concentrations of kallikrein, kininogen, and selected prostanoids were measured by radioimmunoassay. Two experimental groups were studied: (1) control (n = 9); (2) edematous pancreatitis induced by injection of oleic acid into the pancreatic artery (free fatty acid, ffa; n = 10). The animals were followed up for 6 hr. Systemic hemodynamic parameters remained constant in both groups. In the pancreatitis group pancreatic blood flow and O2-consumption decreased significantly (-55 and -49%), while pancreatic vascular resistance increased significantly (+50%). During baseline conditions 41% of all capillaries were perfused. In the pancreatitis group there were both areas with persistent stasis as well as areas with continuous perfusion. However, in the latter areas the portion of perfused capillaries decreased significantly to 27%. In the control group the portion of perfused capillaries remained constant. Liberation of lipase and phospholipase A especially into lymph and ascites fluid was measured during pancreatitis. Furthermore, considerable releases of kallikrein into lymph (+50%) and ascites (+800%) and a marked consumption of kininogen in lymph (+90%) and in ascites fluid (+80%) were measured. Activation of the arachidonic acid cascade and a significant release of prostacyclin and thromboxane A2 into pancreatic venous blood and lymph was observed.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Oleic acid induced pancreatitis in pigs. 199 Feb 28

A dog model was used to measure the hemodynamic changes occurring during acute pancreatitis induced by intraductal injection of fresh trypsin-bile-blood mixture. Continuous measurements of pancreatic blood flow, cardiac output, mean arterial blood pressure and pancreatic oxygen consumption were made under normal conditions and during acute pancreatitis. All animals received 100 ml of saline/h during the time of observation. Three methods of therapy then were instituted in the dogs starting 30 min after induction of pancreatitis. 10 dogs served as controls (saline 100 ml/h); in 6 dogs additionally 15 ml/kg plasma was infused over 45 min and 6 dogs received 1.5 ml/kg Dextran 40/h continuously. Hemorrhagic pancreatitis was characterized by a fall in cardiac output and mean arterial pressure and the development of severe impairment of the pancreatic microcirculation with early reduction of pancreatic blood flow followed by a fall in pancreatic oxygen consumption. Administration of plasma produced a significant increase in cardiac output; however, blood pressure and pancreatic blood flow remained low. Low-molecular weight Dextran has no influence on cardiac output, but significantly improved the blood pressure and leads to a normalization in pancreatic blood flow and oxygen consumption. These results suggest that low-molecular weight Dextran appears to reverse the impairment of microcirculation and hypoxia of the pancreas and limits the progression from edematous to hemorrhagic pancreatitis and irreversible pancreatic damage.
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PMID:[Hemorrhagic pancreatitis: effect of dextran 40 and plasma on microcirculation disorders of the pancreas]. 241 Jul 52

This study examines and compares the prophylactic role of aprotinin and Dextran 40 in acute pancreatitis. Experimental acute pancreatitis was induced in 70 male Wistar rats using the closed-duodenal-loop technique. The rats were randomly divided into four groups; sham operation, untreated acute pancreatitis, and therapy with aprotinin or Dextran 40. Samples of blood and urine were collected at the beginning and at the end of the 24-hr period for measurement of amylase and creatinine which allowed calculation of the amylase-creatinine clearance ratio (ACCR). Mortality in the aprotinin group was the same as the untreated rats (20%). Dextran 40 therapy was associated with a lower mortality rate (6.7%). Light microscopic examination confirmed that the histologic changes of acute pancreatitis were less severe in both the aprotinin- and Dextran 40-treated rats. The ACCR was elevated after Dextran 40 therapy, which was due mainly to high urinary amylase levels. These results suggest that Dextran 40 may have a prophylactic role in acute experimental pancreatitis but again emphasizes the high false-positive rate of the ACCR determination.
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PMID:Effect of Dextran 40 and aprotinin on experimental acute pancreatitis. 619 89

This paper reports the results of treatment of acute haemorrhagic pancreatitis produced experimentally in the dog, the agents used being isotonic saline, Dextran, "Trasylol" and antibiotics. Avenues of future inquiry are suggested in the light of these experiments and those of other workers in this field.
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PMID:The Treatment of Experimentally Induced Acute Pancreatitis1. 2926 29