Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030305 (pancreatitis)
 16,014 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Caerulein-induced acute pancreatitis was studied in rats. Consistent with this type of acute pancreatitis morphological (edema, leukocytic infiltration and acinar cell vaculization) and biochemical (increase in pancreatic protein content. PAF release and serum amylase) changes developed 5 hours after caerulein administration. In addition increase in pancreatic weight and decrease in pancreatic blood flow were noticed. PAF administration caused pancreatic damage similar in some parameters to caerulein-induced pancreatitis, along with reduction of pancreatic blood flow, increase in pancreatic protein content, and serum amylase. TCV-309, a selective PAF antagonist, administered prior to caerulein and/or PAF, reduced caerulein-induced pancreatitis and prevented PAF-induced pancreatitis. Results of our present studies indicate the crucial role of PAF in pathogenesis of experimental acute pancreatitis.
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PMID:Platelet activating factor (PAF) inhibitor (TCV-309) reduces caerulein- and PAF-induced pancreatitis. A morphologic and functional study in the rat. 129 65

PAF-acether (platelet-activating factor) is a vasoactive substance appearing in plasma under certain pathological circumstances. The aim of our study was to determine plasma, peritoneal exudate and tissular levels of PAF-acether in bile reflux acute necro-hemorrhagic pancreatitis (ANP) in the conscious rat 60 minutes after induction. As we have previously demonstrated, ANP causes overwhelming shock in conscious rats. PAF-acether levels increased in plasma and peritoneal exudate of rats with ANP. In contrast, tissular PAF levels were similar to basal values. In conclusion, these data suggest a role of PAF-acether in the hemodynamic impairment that follows induction of pancreatitis.
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PMID:[The physiopathology of acute pancreatitis: the role of platelet-activating factor (PAF)]. 154 30

The aim of this study was to investigate the effect of Nafamostat mesilate (FUT-175) on some blood platelet properties during the first hours of acute experimental pancreatitis (AEP) in dogs. A significant decrease in platelet count, hyperaggregability of platelets by ADP and PAF as well as an increased level of TXB2, were found in the early stage of AEP. No changes in platelet aggregation induced with AA were demonstrated. FUT-175 prevented a decrease in platelet number and inhibited platelet aggregation induced with ADP, PAF and AA when it was given immediately after induction of AEP. No evident changes in TXB2 levels in dogs treated with FUT-175 were found. Our results indicate that the positive effect of FUT-175 in AEP in part depends on its antiaggregatory action.
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PMID:Blood platelet function in canine acute pancreatitis with reference to treatment with Nafamostat mesilate (FUT-175). 157 98

The purpose of this study was to analyse the clinical course of 410 patients of severe surgical infections (primary 251, postoperative 159) during recent 5 years and to evaluate the important background factors which make these patients serious. As a result, the following patients such as, (1) who have refractory primary infections, for example malignant lymphoma, severe pancreatitis etc. (2) whose infectious foci were uncontrolled. (3) who had finally complicated a septic MOF or DIC, seemed to be especially critical even though recent advanced surgical therapy. To improve these severe conditions, we believe to need a renewed approach like so called "multi-disciplinary therapy", additionally with both conventional antibiotics administration and drainage for infectious foci. Several methods such as, (1) rational nutrition management using indirect calorimetry. (2) plasma exchange for removing toxic substances such as bacterial toxins, chemical mediators etc, from circulating blood. (3) pharmacological block of these toxic substances, were shown. In terms of the harmful chemical mediators, we supposed that both PAF (platelet activating factor) and oxygen free radical were extremely important in septic conditions from previous clinico-experimental studies. Therefore the effects of those pharmacological blockers such as PAF antagonists, SOD, protease inhibitor in experimental endotoxin shock were discussed in detail.
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PMID:[Clinico-experimental analysis of backgrounds of the severe surgical infections]. 194 10

The role of blood platelets in the disturbed haemostasis in acute pancreatitis is not fully elucidated. The aim of this study was to evaluate the blood platelet function during the first hours of acute experimental pancreatitis (AEP) in dogs. AEP was induced by the retrograde injection of bile and trypsin into the main pancreatic duct. Platelet count, platelet aggregation induced with ADP, PAF, AA as well as plasma Beta-TG and TXB2 levels were determined. At 30 min after induction of AEP a significant decrease of platelet count was noted; these changes were observed until 4 th hr. At 30 min as well as at 60 min of AEP increased sensitivity of platelet aggregation to ADP was found. After that time evident decrease of platelet aggregation to ADP was shown. Platelets sensitivity to PAF was higher at 30 min of AEP whereas 60 min, 2 and 4 hrs after AEP normalization of platelet aggregation by PAF was observed. The significant increase of plasma Beta-TG and TXB2 concentrations corresponded well to changes of platelet aggregation. These results indicate that AEP affects blood platelet function with the drop of their count.
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PMID:Does acute experimental pancreatitis affect blood platelet function? 252 19

The present study was undertaken to investigate the involvement of PAF in acute pancreatitis induced by cerulein in rats. Cerulein (two doses of 20 micrograms/rat, the first s.c. and the second i.v., 1 h apart) induced a significant increase in vascular permeability in the pancreas, evaluated by the Evans blue (EB) extravasation method. Plasma amylase levels were also significantly increased in this group. The PAF antagonists, BN-52021 (5 mg/kg) and WEB-2170 (1 and 10 mg/kg), both significantly reduced the extravasation of EB in the pancrease induced by i.v. injection of PAF (1 microgram/kg). At these concentrations, BN-52021 was effective at inhibiting cerulein-induced pancreatitis (60-70% of inhibition) whereas WEB-2170 had no significant effect. Although the inhibition induced by BN-52021 suggests the involvement of PAF in cerulein-pancreatitis, the lack of effect of WEB-2170 reported here does not allow a definite conclusion. Further studies are needed to elucidate the differential effect of the PAF antagonists.
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PMID:Effect of PAF antagonists on cerulein-induced pancreatitis. 753 59

In the present study we demonstrated that a single injection of endotoxin (lipopolysaccharides, E. Coli 0111-B4) into the superior pancreaticoduodenal artery of rabbits induced a dose-dependent acute necrotizing pancreatitis. The lesions observed by light microscopy were significant for 10 micrograms lipopolysaccharides and were maximal for 20 micrograms. After 24 h the main findings were edema, acinar cell vacuolisation, polymorphonuclear neutrophil infiltration and tissue necrosis. The pancreatic lesions developed strictly in the area supplied by the artery injected with lipopolysaccharides, without significant intestinal involvement. Since platelet-activating factor (1-O-hexadecyl-2-acetyl-sn-glycero-3- phosphocholine, PAF; 50-500 ng), a phospholipid mediator of endotoxin-induced inflammation and shock, was previously shown to cause an acute necrotizing pancreatitis in rabbits, the role of PAF in the development of acute pancreatitis induced by lipopolysaccharides was studied by evaluating: (1) the synergism between doses of lipopolysaccharides (5-10 micrograms), which produced a mild tissue injury, and doses of PAF (10 ng) not producing, per se, any significant injury, and (2) the effect of three structurally unrelated PAF receptor antagonists. The results obtained demonstrated that 10 ng of PAF significantly potentiated pancreatic tissue damage induced by 10 micrograms of lipopolysaccharides.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Role of platelet activating factor in acute pancreatitis induced by lipopolysaccharides in rabbits. 781 47

PLA2 is a family of regulatory enzymes that control eicosanoid synthesis and PAF production. PLA2 must be tightly regulated within the cell or cell destruction results. Circulatory release of PLA2 occurs in states of profound illness including sepsis, shock, severe injury, and pancreatitis, all of which are linked to the development of ARDS and MOF. Experimental and clinical evidence suggests that PLA2 may serve a primary regulatory role in the development of these inflammatory disorders. This evidence suggests that inhibitors of PLA2 activation could play an important role in future intensive care management.
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PMID:Phospholipase A2 regulates critical inflammatory mediators of multiple organ failure. 812 Nov 78

The pathophysiology of systemic organ failure in acute pancreatitis has been the subject of debate for many years but there is growing evidence that increase production of pro-inflammatory cytokines plays an important role. from this work and from the results of studies in experimental pancreatitis there exists a rationale for the use of PAF antagonists in the treatment of acute pancreatitis. Two pilot studies have now demonstrated a beneficial effect of the PAF antagonist Lexipafant on acute pancreatitis which may lead to an important advance in the treatment of these patients. A multicentre trial aiming to recruit 300 patients with severe acute pancreatitis is now underway in the UK, the results of which will be awaited with interest.
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PMID:The use of lexipafant in the treatment of acute pancreatitis. 913 Nov 75

17 Beagle's dogs were divided randomly into tree groups: pancreatitis group (PG, n = 6), pan+BN52021 group (BNG, n = 6), control group (CG, n = 5). The acute pancreatitic model of PG and BNG was established by injecting sodium taurocholate and trypsin into the main pancreatic duct. Animals of BNG were injected PAF receptor antagonist BN52021 (5 ml/kg) intravenously 5 minutes and 3 hours respectively after acute pancreatitis induction. Blood amylase activity was determined by Winslow's method. PAF in blood and pancreatic tissue was determined by the platelet accumulation method. Blood amylase activity of PG increased by 466.7 +/- 111.6 than the baseline at 8 hours and increased significantly than that of BNG and CG (P < 0.05). Blood PAF level of PG increased from 30 minutes to 11.81 +/- 0.78 ng/ml at 8 hours. BN52021 inhibited very significantly the increase of PAF level (P < 0.01). PAF level in pancreatic tissue of PG was significantly higher than that of BNG and CG (P < 0.01). PAF may play an important role in early acute pancreatitis.
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PMID:[The role of platelet activating factor in pathogenesis of acute pancreatitis in dogs]. 1037 89


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