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

It has been reported that continuous intravenous infusion of nafamostat mesilate (FUT) produces hyperkalemia due to reduced urinary excretion of potassium. The present study was performed to see whether renin-aldosterone effect is involved in this inhibition of potassium excretion. Ten patients were studied who had been given this drug (4 mg.hr-1) to prevent postsurgical pancreatitis or DIC. Urine potassium output decreased significantly from 44 +/- 5 microEq.min-1 prior to administration of FUT to 18 +/- 4 microEq.min-1 in 3 hours, sodium/potassium ratio increased significantly from 1.7 +/- 0.7 prior to administration of FUT to 5.4 +/- 3.3 in 5 hours; and plasma aldosterone decreased significantly from 92 +/- 24 pg.ml-1 prior to administration of FUT to 63 +/- 22 pg.ml-1 in 6 hours. The results suggest that hyposecretion of aldosterone may be one of the main causes of hypokalemia. Reduced secretion of aldosterone may be due to other factors than the suppression of renin-angiotensin system.
 ...
PMID:[Effect of nafamostat mesilate on the renin-aldosterone system]. 156 May 70

Kinetics and distribution of i.v. human pancreatic phospholipase A2 (h-PLA2) were determined in intact and nephrectomized rats, and tissue localization of rat pancreatic PLA2 (r-PLA2) was studied by immunohistochemistry in experimental acute pancreatitis. The concentration of h-PLA2 and the catalytic activity of phospholipase A2 in plasma decreased exponentially in intact and nephrectomized animals after the injection. The initial 15-min half-life was considerably longer in nephrectomized animals, and higher h-PLA2 concentrations and PLA2 catalytic activities were found in plasma. h-PLA2 was localized in endocytotic vesicles and apical cytoplasmic vacuoles in proximal tubule cells of the kidney. The intensity of the immunoreaction decreased considerably between 15 and 50 min in these cells. No signs of tubular damage were seen by light microscopy. Neither immunoreactive h-PLA2 nor PLA2 catalytic activity was found in urine. r-PLA2 was observed in proximal tubule cells 15 min after an injection of sodium taurocholate (necrotizing pancreatitis group) or saline (edematous pancreatitis group) into the pancreatic duct. Signs of tubular damage were present in necrotizing pancreatitis, but tubular morphology was normal in the animals with edematous pancreatitis. We conclude that the proximal tubule cells of the kidney participate in the metabolism of circulating pancreatic PLA2, and considerably higher PLA2 levels persist in plasma in nephrectomized animals. Endogenous pancreatic PLA2 is detected in kidneys in acute pancreatitis.
 ...
PMID:Pancreatic phospholipase A2 in proximal tubules of rat kidney in experimental acute pancreatitis and after intravenous injection of the enzyme. 159 53

The possible risk factors for failure of medical therapy were examined in 23 patients with pancreatic ascites or effusion. The ascites or effusion resolved completely in 10 patients after a mean (+/- SEM) of 30 +/- 2 days of conventional medical treatment. In five patients in whom conventional medical therapy failed, the addition of an octreotide (SMS 201-995) analogue to the medical therapy led to a resolution of the ascites (three patients) or effusion (two patients). Six patients underwent surgery after failed medical therapy, one patient died while receiving conservative therapy, and one patient refused hospital treatment. Serum sodium and albumin levels were significantly lower, and the ratio of total fluid protein to total serum protein was significantly higher in the group that failed to heal in response to conventional medical therapy. Nine of 11 patients with mild to moderately severe chronic pancreatitis healed in response to conservative therapy. Only one of 10 patients with advanced pancreatitis healed in response to conventional medical therapy. Our results suggest that a selective surgical approach is warranted to treat pancreatic ascites and effusion. In patients with mild or moderately severe pancreatitis, medical therapy is recommended. Patients with advanced pancreatic disease should be selected for early surgery. Octreotide may be useful in the patient in whom surgery may be associated with a prohibitive morbidity or mortality.
 ...
PMID:Pancreatic ascites and effusion. Risk factors for failure of conservative therapy and the role of octreotide. 159 72

In 76 male wistar rats with a median weight of 340 g acute pancreatitis was induced by injection of 2% sodium taurocholate into a temporarily closed duodenal loop. 40 animals received an additional cecostomy (group B), the others served as controls (group A). The postoperative figures for amylase, leucocyte count, and hemoglobin were nearly identical in both groups. According to histologic criteria acute pancreatitis was comparable in both groups, too. In nine rats endotoxin was found elevated postoperatively (13.4%). Seven animals belonged to the control (22.6%) and only two to the cecostomy group (5.6%). The difference was statistically significant (p less than 0.05). Also the differences between the median serum endotoxin levels reached statistic significance (79 ng/l in group B vs. 219 ng/l in group A). Mortality was significantly increased in endotoxin-positive animals (42.9% vs. 19.4%). Additionally, among the animals of the control group alterations of the colonic mucosa were observed more frequently than in the cecostomy group. The results are in favour of a translocation of endotoxin from the gut lumen into the circulation during acute experimental pancreatitis.
 ...
PMID:[Effect of cecostomy on the pathophysiology and prognosis of acute experimental pancreatitis]. 161 79

The present studies were done to evaluate the therapeutic potential of several antioxidants and free radical scavengers in three different models of acute pancreatitis. (a) Edematous pancreatitis with acinar cells necrosis was induced by seven hourly intraperitoneal injections of 50 micrograms of caerulein per kg in mice. (b) Hemorrhagic pancreatitis was induced by feeding a choline-deficient, ethionine-supplemented (CDE) diet in mice. (c) Hemorrhagic pancreatitis was induced by retrograde infusion of 0.6 ml of 5% sodium taurocholate into the pancreatic duct in rats. The following antioxidants and free radical scavengers were given at various doses intravenously, subcutaneously, or intraperitoneally before the onset of pancreatitis: Ebselen [2-phenyl-1,2-benzisoselenazol-3(2H)-one], superoxide dismutase, catalase, deferoxamine (Desferal), dimethyl sulfoxide, or allopurinol. The severity of pancreatitis was assessed at various times after its onset by determination of serum amylase and pancreatic weight (edema), by grading of histological alterations, and by determination of survival (survival determined in models of hemorrhagic pancreatitis). In general, free radical scavengers and antioxidants ameliorated edema and inflammation to a greater degree than necrosis and the increase in serum amylase. Superoxide dismutase (as did Ebselen in previous studies) exerted beneficial effects on survival in diet-induced pancreatitis in the absence of marked effects on pancreatic necrosis, suggesting that these beneficial effects are due to amelioration of extrapancreatic complications that often contribute to mortality in acute pancreatitis. None of the antioxidants had major beneficial effects in taurocholate-induced hemorrhagic pancreatitis. Thus, formation of free radicals may be important for progression and outcome in diet-induced and, to a lesser degree, in caerulein-induced pancreatitis but not at all in taurocholate-induced pancreatitis. Different models of pancreatitis may, therefore, involve different degrees and mechanisms of free radical formation. Despite the amelioration of edema and the beneficial effects on mortality seen for some antioxidants in some of the models, antioxidants and free radical scavengers appear to have only a limited potential for treatment of acute pancreatitis.
 ...
PMID:Effects of antioxidants and free radical scavengers in three different models of acute pancreatitis. 164 91

Malonic dialdehyde as an indirect marker of the lipid peroxidation was found increased in the acute pancreatitis compared with persons of the same age and sex. Its concentrations inversely correlated to those of the serum calcium during the course of the disease and additionally they proved to be indicator of the prognosis. Postulating that the acute pancreatitis must be a "free radical disease", in a randomized clinical study the adjuvant therapy of the acute necrotizing pancreatitis (n = 8) with sodium selenite was carried out in a daily dose of 500 micrograms. The lethality of the control group was 89% (8 out of altogether 9 patients), no patient died in the therapy group. By the selenium therapy within 24 hours a normalization of the serum calcium and a decrease of the increased MDA-values could be achieved. It was concluded that by selenium increased activities of the phospholipid-hydroperoxide-glutathione peroxidase were induced, by means of which a peroxidation protection of membrane fatty acids, an inhibition of the activity of phospholipase A2 and an interruption of the arachidonic acid cascade must have been reached.
 ...
PMID:[Acute pancreatitis--a free radical disease. Decrease in fatality with sodium selenite (Na2SeO3) therapy]. 131 23

Morphologic disorders in the liver during the acute pancreatitis are an important aspect of multiorgan disturbances seen in this disease. The study aimed at evaluating ultrastructural disorders in the of the experimental pancreatitis. The study involved 24 male Wistar rats. The acute experimental pancreatitis has been produced by the injection of a 5% sodium taurocholate during sterile laparotomy. Samples for examination have been taken after 1, 3, 6, and 12 hours. Collected samples have been examined systematically. Mitochondrial pleomorphism, partial RER degranulation, decrease in glycogen content, and autophagocytosis have been noted already within 1 and 3 hours. The degree of these disorders has increased within 6 hours, reaching its peak after 12 hours. Marked degeneration of mitochondria, high autophagocytosis, nearly complete disappearance of glycogen, impaired sinusal endothelium, and Kupffer's cells stimulation, in which increased phagocytic activity has been noted made a complete picture of the ultrastructural disorders. Such morphologic changes in the liver have indicated its damage in the early stages of the acute pancreatitis. It may be of importance for the development of multiorgan complications of this disease.
 ...
PMID:[Ultrastructural changes in rat liver in early stages of experimental acute pancreatitis]. 166 89

One hundred and ninety-three nephrotic children with a total of 271 admissions during the past decade, from 1980 to 1989, were retrospectively reviewed for acute complications and unusual features of nephrotic syndrome. One hundred and forty-nine patients were male, 44 female. Hypertension was found in 41 children (21.2%). Nine patients (4.7%) had a total of 11 episodes of hypovolemic shock. These shock patients had a more severe hemoconcentration (mean hemoglobin concentration 19.6 +/- 1.5 g/dl) and hyponatremia (mean serum sodium 127.5 +/- 8.5 mmole/L). Bacterial infections occurred in 28 children (14.5%) with primary peritonitis in 13, sepsis in 6, cellulitis in 4, urinary tract infection in 4 and osteomyelitis in 1. Almost all infections were caused by gram-negative bacilli. Other complications or features included tetany in 4 (2.1%), thromboembolism in 2 (1.0%), pancreatitis in one (0.5%) and Fanconi syndrome in one (0.5%).
 ...
PMID:Complications of nephrotic syndrome in children. 168 Oct 1

The hemorheologic alterations were studied in experimental acute hemorrhagic necrotizing pancreatitis (AHNP) which was induced by injection of 5% sodium taurocholate into the main pancreatic duct. The results showed that during the early stage of AHNP, all of hemorheologic parameters were significantly elevated, and continually increased at the rest intervals. The authors suggested that the blood viscosity and hematocrit increase, red blood cells tend to aggregate, and erythrocyte deformation decrease are the causation of pancreatic microcirculatory disturbances and promoting pancreatic progressive necrosis. After using low molecular dextran and Salvia miltiorrhizae, the hemorheologic alterations in AHNP were recovered, and the histologic observation improved. Our data indicate the hemorheologic disturbances is one of the key factors in the pathogenesis of AHNP.
 ...
PMID:[The role of hemorheologic changes in the pathogenesis of acute hemorrhagic necrotizing pancreatitis]. 169 13

Bile salts in the intestinal lumen act to inhibit the release of cholecystokinin (CCK). Recent studies have shown that CCK may play a permissive role in the development of acute pancreatitis. In this study, the amount of luminal bile salts in female Swiss Webster mice was either decreased by feeding 4% (wt/wt) cholestyramine or increased by feeding 0.5% sodium taurocholate for 1 wk. Plasma levels of CCK were stimulated by cholestyramine and inhibited by taurocholate. Then, acute pancreatitis was induced either by caerulein injections, or by feeding a choline-deficient, ethionine-supplemented (CDE) diet. Feeding of cholestyramine significantly decreased survival from 25% to 0% in the CDE pancreatitis, and increased the magnitude of elevation of serum amylase levels and the extent of pancreatic necrosis in both models of pancreatitis; CCK-receptor blockade with CR-1409 completely abolished the adverse effects of cholestyramine. In contrast, feeding of taurocholate significantly increased survival to 100% and decreased the elevation of serum amylase and pancreatic necrosis; CCK-8 antagonized these actions of taurocholate. Luminal bile salts appear to provide a physiologic protection against necrotizing pancreatitis, at least in part, both by inhibiting the release of CCK and by promoting resistance of the pancreas to CCK excessive stimulation in vivo.
 ...
PMID:Protective action of luminal bile salts in necrotizing acute pancreatitis in mice. 169 66


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>