Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0001339 (acute pancreatitis)
10,593 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Trypsinogen activation peptide (TAP) concentration and alpha 2-macroglobulin-trypsin complex (alpha 2M-T) activity were measured in two experimental models of acute pancreatitis in rats to evaluate the significance of activation of trypsinogen in acute pancreatitis. TAP concentration and alpha 2M-T activity in serum rose significantly in trypsin-taurocholate-induced hemorrhagic acute pancreatitis, while in cerulein-induced edematous acute pancreatitis they did not rise in spite of a similar increase in immunoreactive trypsin. When rats in trypsin-taurocholate-induced pancreatitis were treated by protease inhibitor (FUT-175; nafamostat mesilate; FUT group), alpha 2M-T activity in serum was significantly lower than that in nontreated controls (mean +/- SEM, 20.8 +/- 1.43 U/L in the FUT group vs 79.1 +/- 24.5 in controls; p < 0.01). The survival rate at 24 h was significantly improved in the FUT group compared with the controls (70 vs 43%; p < 0.05). The increase in TAP concentration in the FUT group was similar to that in controls. The TAP concentration in pancreatic tissue at 24 h was significantly (p < 0.01) lower in the survival group (7.8 +/- 0.8 ng/ml) than in the lethal group (25.9 +/- 3.7 ng/ml). Activation of trypsinogen and its subsequent enzyme activity play an important role in the evolution of severe acute pancreatitis.
Pancreas 1995 Apr
PMID:Activation of trypsinogen in experimental models of acute pancreatitis in rats. 754 73

The purpose of the present work was to evaluate the efficacy of allopurinol in rat cerulein-induced acute pancreatitis, by studying amylase and lipase concentrations in bile-pancreatic juice and serum, blood leukocytes, and pancreatic histology. Supramaximal doses of cerulein, injected intraperitoneally twice with a 1-h interval (50 micrograms/kg), caused a reduction in juice amylase and lipase, high levels of the two enzymes in serum, leukocytosis, and severe histological damage to the pancreas, including the presence of diffuse cellular necrosis. These responses were not substantially altered by cotreatment with allopurinol (40 mg/kg i.p. twice with a 1-h interval) or by posttreatment with allopurinol (60 mg/kg i.p. 3 h after cerulein). In contrast, pretreatment with allopurinol (40 mg/kg allopurinol, 1 h, 20 mg/kg allopurinol + 50 micrograms/kg cerulein, 30 min, 40 mg/kg allopurinol, 30 min, 50 micrograms/kg cerulein) had a clear protective effect on pancreatic morphology and function, as shown by higher juice amylase and lipase values, lower serum amylase and lipase concentrations, and an almost normal histological picture of the pancreas. We concluded that allopurinol is effective in preventing the acute pancreatitis caused by administration of supramaximal doses of cerulein, by blocking the free radical generation in pancreatic tissue.
Pancreas 1995 Jul
PMID:Microsurgical evaluation of experimental pancreatitis after allopurinol: a secretory serological and morphological study. 754 94

Human pancreas-specific protein (PASP) has been characterized previously as a serum marker for pancreatitis. It was then identified as pancreatic procarboxypeptidase B (PCB). The aim of the present study was to verify the usefulness of PASP (PCB) as a serum marker in patients with acute (n = 20) and chronic (n = 12) pancreatitis and in those following endoscopic retrograde cholangiopancreaticography (ERCP) (n = 44). Serum PASP values were analyzed by radioimmunoassay, with a range of normal values between 15 and 111 ng/ml. Between April 1992 and September 1992, 20 subjects (19-86 years of age) with acute pancreatitis (alcoholic, 8; biliary, 8; other, 4) were studied. We found edematous pancreatitis in 17 cases and severe hemorrhagic pancreatitis in three cases. At admission, peak levels of PASP (average value, 1,976 +/- 329 ng/ml), pancreatic isoamylase (942 +/- 151 U/L) and lipase (2,946 +/- 534 U/L) were detected in 15 of 20, 16 of 20, and 12 of 20 cases, respectively. The etiology of the pancreatitis had no influence on the PASP values. Furthermore, 10 patients with alcoholic and two patients with nonalcoholic chronic pancreatitis (29-67 years of age) were studied. The average peak level of PASP was 1,229 +/- 434 ng/ml. In this group, PASP paralleled the time course of amylase and lipase. Maximal PASP, amylase, and lipase levels were found in 11 of 12, nine of 12, and five of 12 patients, respectively, on the day of admission. ERCP was performed in 44 patients (36-87 years of age), demonstrating common bile duct stones in 16 and bile or pancreatic ductal tumors in 15 cases.(ABSTRACT TRUNCATED AT 250 WORDS)
Pancreas 1995 Apr
PMID:"Human pancreas-specific protein" (procarboxypeptidase B): a valuable marker in pancreatitis? 762 99

We investigated peripheral lymphocyte subsets in 34 consecutive acute pancreatitis patients (21 males, 13 females; mean age, 57 years; range, 16-85 years) studied within 48 h of pain onset and for 5 consecutive days to understand better the immunological response during the course of the disease. The diagnosis was based on characteristic abdominal pain associated with a twofold increase in serum lipase and confirmed by imaging techniques in all patients. Acute pancreatitis was of biliary origin in 25 patients, due to alcohol abuse in 5, due to pancreas divisum in 1, and of unknown origin in 3. Fifteen patients had severe illness and 19 had mild disease. In all patients, total lymphocyte and lymphocyte subset counts were carried out on admission, as well as on the third and fifth day of hospitalization, using a flow cytometric analysis. Twenty-three patients (13 with severe illness and 10 with mild disease) also had a repeat count 1 month after recovery. Twenty-five healthy subjects and 27 patients with nonpancreatic acute abdomen comparable for sex and age were studied as controls. On the first day of the study, the leukocyte number was significantly higher in patients with acute pancreatitis and in those with nonpancreatic acute abdomen with respect to healthy subjects, whereas the number of total and CD4+, CD8+, CD3+ DR-, and CD3- DR+ lymphocytes was significantly lower in acute pancreatitis patients than in healthy subjects or in patients with nonpancreatic acute abdomen. These subject counts persisted on the third and fifth days of the study.(ABSTRACT TRUNCATED AT 250 WORDS)
Pancreas 1995 Jul
PMID:Circulating lymphocyte subsets in human acute pancreatitis. 766 48

Involvement of endogenous cholecystokinin (CCK) in the development of acute pancreatitis induced in rats by closed duodenal loop (CDL) was examined, and the effects of the potent and specific CCK receptor antagonist loxiglumide on this model of acute pancreatitis were evaluated. Plasma CCK bioactivity was markedly elevated 3 and 6 h after onset of acute pancreatitis. A single subcutaneous injection of 50 mg/kg body wt of loxiglumide 30 min before the induction of acute pancreatitis completely eliminated the hypercholecystokinemia. Loxiglumide given 3 h after the induction of acute pancreatitis suppressed plasma CCK bioactivity, which had risen up to 30-fold over basal value (0 h) at 3 h, to nearly the basal level. Loxiglumide pretreatment, in addition, significantly prevented the rise in serum amylase and lipase activity, as well as the increase in ascitic volume. It also ameliorated histological alterations of hemorrhagic and necrotizing pancreatitis. Reduction of plasma CCK bioactivity by loxiglumide after the onset of pancreatitis slowed the rate of progression of pancreatitis. However, pancreatic wet weight and cellular infiltration were not significantly influenced by loxiglumide treatment. These observations suggest that endogenous CCK is not involved in the initiation of acute hemorrhagic and necrotizing pancreatitis induced by CDL, but is involved in the development of pancreatitis in this model.
Pancreas 1993 Jan
PMID:Involvement of endogenous cholecystokinin in the development of acute pancreatitis induced by closed duodenal loop. 767 22

Hyperamylasemia has been reported in heroin addicts and ascribed to an increase of salivary isoamylase. Ours is the first report on acute pancreatitis in a heroin user. All prognostic parameters indicating a severe course of the disease were present, and computed tomography showed an edematous pancreatitis, but the acute pancreatitis took a benign clinical course.
Pancreas 1993 Jan
PMID:Acute pancreatitis: induced by heroin intoxication? 767 24

Recent investigations have suggested that digestive zymogens may become activated within the acinar cell during acute pancreatitis. While the molecular events responsible for intracellular zymogen activation remain unknown, several potential enzymatic pathways require an acidic pH to optimally proceed. We therefore proposed that manipulation of subcellular pH might alter the course of experimental pancreatitis. Chloroquine, a weak base that raises the pH of acidic subcellular compartments, was administered to young female mice in which pancreatitis was induced by a choline-deficient, ethionine-supplemented (CDE) diet. Control animals were maintained on regular laboratory chow. Examination of isolated pancreatic acini using acridine orange cytofluorescence demonstrated expansion of acidic subcellular compartments in animals fed the CDE diet. These compartments were effectively neutralized in animals receiving chloroquine. Animals receiving continuous infusions of high-dose chloroquine demonstrated a significant (p < 0.05) decrease in free pancreatic tryptic activity as well as improved survival. These changes were also associated with decreased trypsinogen content in animals treated with high-dose chloroquine, suggesting an additional potential effect of chloroquine on zymogen synthesis and accumulation. One explanation of these findings is that a low-pH compartment may be important in the pathogenesis of diet-induced pancreatitis.
Pancreas 1993 Jan
PMID:Influence of chloroquine on diet-induced pancreatitis. 767 27

The plasma bradykinin (BK) and serum amylase levels and histological changes in rats during the course of acute pancreatitis induced by a large dose of cerulein were examined. Animals were given four intraperitoneal injections of 20 micrograms/kg body wt of cerulein at hourly intervals. The plasma concentration of BK-like immunoreactivity (BK-LI), measured by a highly sensitive and specific radioimmunoassay established in this study, was found to reach a peak 6 h after the first injection of cerulein and then to remain elevated. On the other hand, the serum amylase and the histological alterations (i.e., interstitial edema, vacuolization, and inflammatory infiltration) were maximal 9 h after the first injection and returned to nearly normal after 24 h. These observations suggest that the BK generation is indicative of the participation of the kallikrein-kinin system in the pathophysiological change and that the plasma BK-LI level is a good marker of cellular damage and inflammation within the pancreas during the course of acute pancreatitis.
Pancreas 1993 Mar
PMID:Radioimmunoreactive plasma bradykinin levels and histological changes during the course of cerulein-induced pancreatitis in rats. 768 81

Our previous data showed that the pancreatitis induced in rats by cerulein develops into hemorrhagic pancreatitis following water-immersion stress. The present study examined the effects of water-immersion stress and high doses of cerulein (intraperitoneal injection) on pancreatic blood flow. Five hours of water-immersion stress reduced the local pancreatic blood flow to approximately 30% of the initial value (253.75 +/- 12.58 ml/min/100 g) without causing any histological alterations. Blood flow was decreased as early as 1 h after the immersion and reached the lowest value (30% of initial value) 3 h after the immersion. The administration of 40 micrograms/kg body wt cerulein as two intraperitoneal injections reduced the pancreatic blood flow by 40% 5 h after the first cerulein injection. The injections of cerulein combined with water-immersion stress did not reduce the pancreatic blood flow more than did water-immersion stress alone. The systemic blood pressure was unaffected during 5 h of water immersion after the cerulein injections. These findings suggest that in rats the stress-induced decrease of local pancreatic blood flow may not produce pancreatitis, but may aggravate an existing acute pancreatitis.
Pancreas 1993 Jul
PMID:Role of local pancreatic blood flow in development of hemorrhagic pancreatitis induced by stress in rats. 768 31

Cholecystokinin (CCK) receptor antagonists are shown to have therapeutic as well as preventive effects in some types of acute pancreatitis. However, there is a possibility that administration of CCK receptor antagonists with a high inhibitory potency on the endocrine pancreas to patients with acute pancreatitis exacerbates the associated glucose intolerance. In the present study we simultaneously examined the effects of the newly developed benzodiazepine derivative FK480 and proglumide-related antagonist KSG-504 on CCK octapeptide (CCK-8)-stimulated exocrine and endocrine function in the isolated perfused rat pancreas. FK480 and KSG-504 inhibited CCK-8-stimulated pancreatic juice flow, protein output, and insulin release in a dose-dependent manner. FK480 was approximately 10 times more potent than KSG-504 in inhibiting exocrine and endocrine secretion. Both antagonists inhibited CCK-8-stimulated insulin release more potently than exocrine secretion. FK480 caused a dose-dependent residual inhibition of exocrine secretion after its removal from the perfusate, whereas insulin release was only slightly impaired even at the highest dose. In contrast, termination of KSG-504 infusion resulted in an immediate increase in both exocrine and insulin responses without causing any residual inhibition. With regard to the residual inhibition, therefore, KSG-504 had no significant influences on exocrine and insulin release, whereas FK480 inhibited exocrine secretion more potently than insulin response. These results suggest that FK480 might become a useful therapeutic agent for pancreatitis with respect to its long-duration inhibitory effect on exocrine secretion and short-duration inhibitory effect on insulin release.
Pancreas 1995 Mar
PMID:Different inhibitory effects of the newly developed CCK receptor antagonists FK480 and KSG-504 on pancreatic exocrine and endocrine secretion in the isolated perfused rat pancreas. 771 33


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