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

Pancreatic microvasculature in cerulein-induced pancreatitis was studied at the electron and light microscopic level. Using a modified model of in situ india ink perfusion, focally a marked reduction of the number of india-ink-filled microvessels was found. The numerical density (NA) of filled microvessels was reduced by 66.7% in pancreatitis. The morphological correlate for this extreme numeric reduction might be a collapse of the lumen of pancreatic microvessels. In the presence of cerulein pancreatitis 42% of pancreatic capillaries had a collapsed lumen as shown by electron microscopy. The endothelium of capillaries in acute pancreatitis demonstrated surface blebbing, the formation of cytoplasmatic vacuoles, edema, and swollen mitochondria. Some capillaries had irregularities at the interendothelial junction, and the majority of examined vessels were surrounded by marked perivascular edema. No strict correspondence between histological signs of pancreatitis and light microscopic and/or ultrastructural microvascular alterations could be demonstrated. Our study emphasizes that alterations of microvasculature are present early in experimental edematous pancreatitis. Therefore, alterations of pancreatic microcirculation seem to be of great importance in the pathogenesis of pancreatic inflammation, and should be the subject of further studies.
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PMID:Structural alterations of pancreatic microvasculature in cerulein-induced pancreatitis in the rat. 208 36

Severe potassium permanganate poisoning (more than 10 g of potassium permanganate) is invariably associated with massive systemic upset and death. Multiple organ damage has been recognized as an inevitable consequence of such an overdose, although pancreatitis has not been previously reported. Death due to cardiovascular collapse and profound hypotension is a common end point in those who reach hospital, but the pathogenesis is uncertain. We report a case of haemorrhagic pancreatitis following an overdose of potassium permanganate and suggest that this complication may be an unrecognized factor contributing to the extremely high mortality rate associated with this condition.
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PMID:Haemorrhagic pancreatitis--a cause of death in severe potassium permanganate poisoning. 221 35

Acute pancreatitis associated with the passage of gallstones through the sphincter of Oddi might be caused by obstruction of pancreatic exocrine secretion or by duodenopancreatic reflux. Possible complicating factors are discussed, which are necessary in order to turn the interstitial edematous inflammation caused by pancreatic duct obstruction into hemorrhagic necrotizing pancreatitis. Furthermore, clinical and experimental data are reviewed concerning a possible collapse of the protective mechanisms which usually prevent contact of duodenal contents and pancreatic tissue.
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PMID:The pathogenesis of acute biliary pancreatitis: a controversial issue. Part II: The concepts of duodenopancreatic reflux and of obstruction of pancreatic exocrine secretion. 269 72

Lipocortins, a group of corticosteroid-induced phospholipase-inhibitory proteins, are thought to play a prominent role in the mediation of the anti-inflammatory effects of steroids. The synthesis and release of these proteins may represent a major endogenous mechanism of regulation of extracellular phospholipase A2 (PLA2) activity. Because soluble PLA2 activity has been associated with circulatory collapse in hyperphospholipasemic conditions, such as septic shock and pancreatitis, we examined the relationship between circulating PLA2 activity and adrenocortical function. In a prospective study of 10 episodes of septic shock, serum PLA2 and cortisol levels correlated significantly in all survivors (p less than 0.0001), whereas such a correlation was absent in all nonsurvivors (p less than 0.07). No significant correlation of cortisol and adrenocorticotropic hormone (ACTH), or PLA2 and ACTH, was found in any patient, suggesting that the stimulus for cortisol release arises from outside the hypothalamic-pituitary axis. These data suggest that, in human beings, the regulation of soluble PLA2 activity may be mediated by adrenocortical hormones, perhaps through the intermediary action of lipocortins.
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PMID:Concordance of endogenous cortisol and phospholipase A2 levels in gram-negative septic shock: a prospective study. 283 77

Circulating phospholipase A2 (PLA2) has been recognized as a mediator of circulatory collapse in experimental endotoxic shock. To assess the role of serum PLA2 in septic shock in man, we determined serum PLA2 profiles in a prospective study in 12 patients with septic shock. During the hypotensive phase of sepsis, serum PLA2 levels were consistently elevated as high as 33,428 U/ml (normal range 115 +/- 12 [SE]; n = 101). In all 12 patients, PLA2 levels correlated directly with the magnitude and duration of circulatory collapse (p less than .001), with a progressive fall of serum PLA2 levels during convalescence. In contrast, serum PLA2 levels in patients with cardiogenic shock secondary to myocardial infarction remained low. In pancreatitis, PLA2 levels paralleled fluctuations of serum amylase and lipase, whereas in septic shock without pancreatic involvement, PLA2 changes were discordant with changes in pancreatic enzymes. As well, septic shock serum PLA2 failed to crossreact by radioimmunoassay with antiserum against human pancreatic PLA2. These data are consistent with an extrapancreatic source of intravascular PLA2 release during sepsis. Since endogenous serum PLA2 levels correlate directly with the magnitude of hypotension in both experimental endotoxic shock and clinical septic shock, and since parenteral administration of purified exogenous PLA2 reproduces hypotension in experimental models, we conclude that high levels of intravascular PLA2 may contribute similarly to the circulatory collapse in septic shock in man.
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PMID:Pathogenesis of hypotension in septic shock: correlation of circulating phospholipase A2 levels with circulatory collapse. 333 73

The authors make a retrospective analysis of 95 cases of acute pancreatitis hospitalized between 1975 and 1979. In 3,8% of all the cases the acute pancreatitis was associated with hyperlipoproteinemia. The study of the 4 patients involved revealed the primary origin of hyperlipoproteinemia as a result of alimentary abuse in 3 of the cases. In a fourth case the increased serum lipoproteins were due to prolonged use of contraceptives. From the clinical viewpoint, pancreatitis associated with hyperlipoproteinemia was more severe, with signs of shock and collapse, respiratory failure, high serum nitrogen an hyperglycemia. The blood and the serum had a lactescent aspect, with a thick layer of chylomicrons. The serum and blood values for lipids were higher than 4000 mg%. The increase in the amount of lipids was especially due to high triglycerides values. From the anatomopathologic viewpoint the 4 patients presented as acute cases of cholecysto-pancreatitis with major and extensive haemorrhagic necrosis which involved almost the entire pancreas. The evolution of the four patients was difficult. Two of the patients recovered after a long hospitalization, and had definitive sequels - insulin-dependent diabetes. The other two patients died following septic complications (bronchopneumonia and visceral gangrene), and hypovolemia due to upper digestive haemorrhage.
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PMID:[Hyperlipoproteinemia, a factor of severity in acute pancreatitis]. 646 Feb 73

Three patients with pancreatic ascites documented by ascitic fluid protein greater than 2.5 g/dl and elevated amylase in their peritoneal fluid were treated by peritoneo-jugular shunting (PJS). Patient 1 was so treated inadvertently; Patient 2 had resolving amylase levels but increasing amounts of ascites; Patient 3 had clear, active pancreatic ascites. None incurred untoward effects from this procedure. Ventilatory compromise from reduced diaphragmatic excursion was ameliorated in all patients. Two patients required no further therapy. The third patient was greatly improved in preparation for definitive surgical therapy for a leaking pancreatic pseudocyst. The infusion of enzyme-rich fluids into the circulation may be responsible for certain systemic effects of pancreatitis. Coagulation defects are a known complication of PJS for the ascites of Laennec's cirrhosis. There was no evidence of histamine-mediated cardiovascular collapse, exacerbation of respiratory failure, or coagulation defects in these patients. We conclude that these complications are not the inevitable results of PJS of pancreatic ascites.
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PMID:Outcome after peritoneo-jugular shunting of pancreatic ascites. 674 24

This article reports a case of acute pancreatitis in a patient taking the oral contraceptive pill. A 32 year old mother had been on combined contraceptive pills since 1975. In 1978 she started having upper abdominal and retrosternal pain. She became critically ill with peripheral circulatory collapse, dyspnoea and cyanosis. A superficial thrombophlebitis was noted on the medial aspect of the right thigh. The diagnosis of pancreatitis was considered with history of recurrent abdominal pain. After several tests and supportive therapy (intravenous fluids, antibiotics, steriods), the woman started showing improvements in 48 hours and recovered in 10 days. This case differs from previously described cases in that the cholesterol and triglyceride levels were normal. The hypoglycemia has not been described previously.
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PMID:Contraceptive pills and acute pancreatitis. 732 5

The article analyzes the experience of treatment of 1003 patients with acute pancreatitis for 17 years. The method of choice was the early complex intensive conservative treatment performed in full detail. It proved to be effective in 87.3% of patients (876). There were no lethal outcomes. In 12.7% of patients (127) with acute pancreatitis operations were performed with clinical picture of apparent pancreatitis, pancreatonecrosis with progressing collapse, purulent pancreatitis and cholecystopancreatitis. In most patients (111) the method of surgery consisted in external drainage of the bile-excretory ducts, tamponage and drainage of the bursa omentalis and the retroperitoneal space. The postoperative lethality was 24%. The postoperative lethality of pancreatonecrosis and purulent pancreatitis was 30%. General lethality was 3%.
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PMID:[Treatment experiences with acute pancreatitis]. 742 90

The objective of this study was to determine whether the observed vascular collapse and other pathologic features of severe pancreatitis may be related to the induction of nitric oxide synthase (NOS). The rat model of pancreatitis reported by Schmidt et al. was employed. Rats in the experimental groups received pretreatment with known NOS inhibitors, N-Monomethylarginine (NMMA) or Aminoguanidine (AG). Controls included sham-operated rats without pancreatic insult and a diseased control group which received pretreatment with normal saline (NS). Arterial blood pressure was continuously recorded with a femoral arterial catheter connected to a transducer and monitor. Fluid resuscitation for hypotension followed a strict protocol with the administration of 5.0 cc NS for sustained decreases in systolic blood pressure (SBP) below 90 mm Hg at 5-minute intervals. Laboratory parameters and histopathology confirmed the induction of pancreatitis, with 6 to 15-fold increases in serum amylase levels and an average of approximately 20% decrease in serum ionized Ca++ levels. Immunohistochemical studies of the pancreas revealed that pancreatic insult resulted in the induction of NOS. Rats in the saline control group (n = 5) became hypotensive (SBP less than 90 mm Hg) between 3 and 4 hours post pancreatic insult and required an average of 110.0 cc (3-4 x blood volume) of NS fluid resuscitation. Rats which were not resuscitated (n = 5) did not survive.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:First place winner of the Conrad Jobst Award in the gold medal paper competition. Nitric oxide synthase inhibitors N-monomethylarginine and aminoguanidine prevent the progressive and severe hypotension associated with a rat model of pancreatitis. 753 Apr 15


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