Endoscopic transgastric drainage of a pancreatic pseudocyst with mediastinal and cervical extensions.
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Abdominal Pain↗
Biomedical subjects
Ferenc László
Publications and source records attributed to Ferenc László.
Endotoxin can decrease isolated rat parotid acinar cell amylase secretion in a nitric oxide-independent manner.
Salivary mucus and amylase have an anti-bacterial nature. Bacterial endotoxin is considered to decrease mucus secreting cell activity by nitric oxide-dependent mechanisms. In this study, the actions of endotoxin on amylase secreting cell activity have been studied. Endotoxin (Escherichia coli lipopolysaccharide; 3 mg/kg, i.v., 5 h) evoked nitric oxide synthase 2 (NOS2) induction in the rat whole parotid tissue (assessed by Western blot and the citrulline assay) and in rat isolated parotid acinar cells (assessed by Western blot and immunohistochemistry), and reduced basal and acetylcholine-stimulated amylase secretion from these isolated cells. However, N(G)-nitro-L-arginine methyl ester (0.1 mg/ml, 4 days in drinking water, yielding a dose of 25 mg/kg/day) did not affect amylase release under basal or acetylcholine-stimulated conditions, either in control acinar cells or those from endotoxin challenged rats. Thus, basal, acetylcholine-evoked or endotoxin-decreased cellular amylase secretion from rat isolated parotid acinar cells does not appear to be modulated by endogenous nitric oxide.
Acetylcholine↗
Inhibitory effects of different galanin compounds and fragments on osmotically and histamine-induced enhanced vasopressin secretion in rats.
The effects of rat, porcine and human galanin, and the human 1-16 and human 16-30 terminal galanin fragments on vasopressin secretion were studied in rat. The plasma vasopressin level was determined by radioimmunoassay (RIA). There were no changes in the basal vasopressin secretion after galanin administration. A significant increase in vasopressin concentration was detected following 2.5% NaCl or histamine administration. I.c.v. injected rat, porcine or human galanin or the 1-16 N-terminal galanin fragment prevented the plasma vasopressin level enhancement. Following the i.v. administration of rat galanin or the i.c.v. injected 16-30 C-terminal galanin fragment, the vasopressin concentration did not return to the normal level. Administration of the galanin antagonist galantid (M15) i.c.v. before the rat galanin i.c.v. injection prevented the inhibitory effect on the increased plasma vasopressin level following 2.5% NaCl solution or histamine administration. The results indicate that there is no significant difference in the inhibitory effect of rat, porcine or human galanin or the 1-16 galanin fragment on the enhanced plasma vasopressin secretion induced by hyperosmosis or histamine administration. Our findings suggest that galanin, as a peptide modulator, is physiologically involved in the regulation of vasopressin release following different forms of stimulation: an osmotic response or histamine administration.
Animals↗
Endoscopic treatment of sphincterotomy-associated distal common bile duct strictures by using sequential insertion of multiple plastic stents.
BACKGROUND: A rare, late complication of endoscopic biliary sphincterotomy is the occurrence of short strictures extending from the papillary orifice to the distal parts of the extraduodenal common bile duct. METHODS: We evaluated the efficacy of the sequential insertion of multiple stents in the treatment of endoscopic biliary sphincterotomy associated common bile duct strictures. The design of the study is a prospective, single-arm observational study at a university-affiliated teaching hospital of 20 patients with distal common bile duct strictures because of choledocholithiasis-related endoscopic biliary sphincterotomy. Endoscopic treatment consisted of the sequential insertion of an increasing number of plastic stents with ever-larger diameters in 3-month follow-up intervals until stricture resolution. The primary outcome of the study was the rate of resolution of the stricture. The parameters measured were the duration of placement of stents, the maximum diameter, the total number of stents, and the total number of endoscopic sessions required for dilation of the strictures. RESULTS: After a median of 9.0 months of stent placement (range 3-22 months) and a median of 20F maximum stent diameter (range 10F-30F), 18 patients (90%) remained stent-free for a median of 14.5 months (range 6-38 months). Two patients (10%) had stricture recurrences at 10 and 24 months. Multivariate regression analysis demonstrated that the time elapsed after endoscopic biliary sphincterotomy was significantly associated with the stent-placement time (however, significance was removed by correction for multiple testing) and the number of ERCPs required for dilation. The initial common bile duct size was significantly associated with the total stent number and diameter needed for stricture resolution (however, significance was removed by correction for multiple testing). Limitations are the low case number and the single-arm, noncontrolled study design. CONCLUSIONS: Sequential insertion of an increasing number of biliary stents affords effective treatment of the distal biliary strictures that develop as a late complication of endoscopic biliary sphincterotomy.
Adult↗
Synergistic interaction of endogenous platelet-activating factor and vasopressin in generating angina in rats.
We examined the involvement of endogenous vasopressin and platelet-activating factor (PAF) in the pathogenesis of two types of experimental angina in urethane-anaesthetised male Wistar rats. In the first model, epinephrine (10 microg kg(-1)) was injected into the tail vein, followed at the development of the maximum blood pressure response, i.e., 30 s later, by phentolamine (15 mg kg(-1)). In the second model, the vasopressin V1 receptor agonist ornithine-vasopressin (ornipressin; 0.5 IU kg(-1), i.v.) was administered. The heart rate, mean arterial blood pressure and surface electrocardiogram (ECG, standard lead II) were registered simultaneously. As a measure of myocardial ischaemia, at 1 min after phentolamine or ornipressin administration, we found significant ST-segment depression, lasting for more than 10 or 5 min, respectively. Pretreatment (15 min, s.c.) with the vasopressin V1 receptor antagonist Mca1,Tyr(Me)2AVP (the Manning peptide; 0.02-0.2 microg kg(-1)) or the platelet-activating factor receptor antagonist ginkgolide B (BN 52021; 0.25-2.5 mg kg(-1)) alone caused a dose-dependent reduction of the ST-segment depression. Concurrent administration of the two antagonists in their threshold doses (0.02 microg kg(-1) and 0.25 mg kg(-1)) also attenuated the ST-segment depression in both models. Neither antagonist affected the blood pressure or heart rate changes throughout the studies. Our results suggest that endogenous vasopressin and platelet-activating factor interact synergistically in provoking myocardial ischaemia in vivo in experimental angina in the rat.
Angina Pectoris↗
Raloxifene lowers ischaemia susceptibility by increasing nitric oxide generation in the heart of ovariectomized rats in vivo.
We studied the effects of a 2-week period of oral raloxifene therapy on the cardiac level of nitric oxide (NO) and on the susceptibility to angina in ovariectomized rats. Ovariectomy decreased the activity of Ca2+-dependent nitric oxide synthase (NOS) in the left ventricle, an effect restored by raloxifene (0.2-5 mg kg(-1) day(-1)) or 17beta-oestradiol (0.3 mg kg(-1) day(-1)). Ovariectomy led to a significant ST segment depression after the injection of (1) ornithine-vasopressin (0.5 IU kg(-1), i.v.) or (2) epinephrine (10 microg kg(-1), i.v.), followed 30 s later by phentolamine (15 mg kg(-1), i.v.); both effects were reversed by raloxifene or 17beta-oestradiol treatment. Inhibition of nitric oxide synthase (with NG-nitro-L-arginine methyl ester [L-NAME]; 5 mg kg(-1), s.c.) augmented the ST segment depression in the ovariectomized rat and abolished the anti-ischaemic effect of 17beta-oestradiol or raloxifene. Thus, an oestrogen deficiency down-regulates the cardiac constitutive nitric oxide synthase, which increases the susceptibility of the heart to ishaemia because both actions can be blocked by exogenous administration of the natural oestrogen 17beta-oestradiol or the selective oestrogen-receptor modulator (SERM) raloxifene. In the present in vivo system, raloxifene exerts oestrogen-agonist properties.
Administration, Oral↗
Medium-term results of endoscopic treatment of common bile duct strictures in chronic calcifying pancreatitis with increasing numbers of stents.
OBJECTIVES: The goal of this study was to evaluate our medium-term results on common bile duct stenting with increasing numbers of stents on strictures due to chronic calcifying pancreatitis. BACKGROUND: Common bile duct strictures frequently complicate the course of chronic calcifying pancreatitis. The effectiveness of endoscopic stenting to resolve definitely these strictures is still debated. STUDY: Twenty-nine patients with common bile duct stricture due to chronic calcifying pancreatitis were stented and followed up. Biliary sphincterotomy, dilation of the stricture, and insertion of plastic biliary stents (7.5-10 F) were performed. Patients were scheduled for elective stent changing/restenting at 3-month intervals or any time when it was urgently indicated. Our basic intention was to insert the maximum possible number of stents to reach as large diameter as the stricture allowed. All stents were removed after the disappearance of common bile duct dilatation or left in place in cases of persisting strictures. RESULTS: Eighteen patients (60%) had complete radiologic and serologic recovery after a mean of 21.1 months overall stenting time and had a stent free follow-up period for a mean of 12.1 months without recurrence of stricture. Five patients (16%) still have stents in place after 26 months. Three patients (13%) required surgery. There were 3 deaths (10%): 1 for unrelated cause and 2 with septic shock of biliary origin. CONCLUSIONS: Most chronic calcifying pancreatitis patients with common bile duct strictures respond to the increasing numbers of endoscopic stents, and remain stent free for medium term periods. Less patients (30%) does not benefit of biliary stenting, who are candidates for surgery.
Adult↗
Importance of cytokines, nitric oxide, and apoptosis in the pathological process of necrotizing pancreatitis in rats.
OBJECTIVES: Ischemia-reperfusion injury can be involved in the pathophysiology of acute necrotizing pancreatitis. The aim of our study was to determine the production of cytokines, tumor necrosis factor (TNF) and interleukin-6 (IL-6), the activation of the inducible nitric oxide synthase (iNOS), and the development of apoptosis during this pathologic process. METHODS: Acute pancreatitis was produced in male Wistar rats by injection of 200 microL of 6% taurocholic acid into the main pancreatic duct in combination with the temporary (15 minutes) occlusion of the inferior splenic artery. Six and 24 hours later, the histologic damage was evaluated, and serum amylase, TNF, IL-6 levels, and iNOS and apoptotic activity from pancreatic and pulmonary tissues were determined. RESULTS: Twenty-four hours after the induction of pancreatitis, the mortality rate was 63%. During this period, the serum TNF and IL-6 levels were permanently high (50 +/- 12 and 58 +/- 10 U/mL and 7083 +/- 1610 and 6790 +/- 850 U/mL after 6 and 24 hours, respectively). The iNOS activity showed an increasing tendency in the pancreas, and a decrease following an initial increase in the lung (from 4.2 +/- 0.6 to 5 +/- 0.4 and from 6.8 +/- 0.6 to 3.8 +/- 0.5 pmol/min/mg protein after 6 and 24 hours, respectively). Histologic examination confirmed severe necrotizing pancreatitis. In the pancreas, the apoptotic activity increased significantly (from 4 +/- 4 to 27 +/- 5/mm at 6 and 24 hours), while in the lungs, following an initial increase it declined during the course of necrotizing pancreatitis (from 49 +/- 4 to 11 +/- 6/mm at 6 and 24 hours). CONCLUSION: Our results indicate that intraductal taurocholic acid and ischemia-reperfusion provokes severe acute necrotizing pancreatitis with a high mortality rate and leads to systemic inflammatory reaction, which appears to be the consequence of the activation of the cytokine cascade and iNOS. The degree of NO overproduction by iNOS corresponds with the apoptotic process in the pancreas and the lung.
Animals↗
Autoimmune pancreatitis associated with immune-mediated inflammation of the papilla of Vater: report on two cases.
Autoimmune pancreatitis (AIP) is defined histologically by periductal and interacinar lymphocytic infiltration. Immunohistochemically, the majority of these lymphocytes are identified as T cells. Epithelial HLA-DR antigen expression was also described as a marker of autoimmunity in this type of chronic pancreatitis. We report 2 cases, a 56-year-old man and a 29-year-old woman, with AIP associated with immune-mediated inflammation of the main duodenal papilla (MDP). Serologically, antinuclear antibody positivity was detected in the male patient. The female patient, treated medically for ulcerative proctitis, had no serological evidence of autoimmune disease. Macroscopic papillitis was present only in the male patient, and endoscopic biopsy samples were taken from this swollen MDP. Since we could not exclude malignancy, a pancreatic head resection was performed in both patients. The histologic and immunohistochemical studies of the resected specimens showed periductal T-lymphocytic infiltration in the pancreatic and papillary tissues. Furthermore, HLA-DR-antigen expression was also demonstrated in epithelial cells of the pancreas and MDP. The immunohistological features of endoscopic biopsy samples from the swollen MDP were identical as in the surgically resected specimens. Immune-mediated inflammation of the MDP may be associated with AIP.
Adult↗
The role of nitric oxide in edema formation in L-arginine-induced acute pancreatitis.
INTRODUCTION: Nitric oxide (NO) has been implicated in the regulation of the pancreatic circulation, the promotion of the capillary integrity, and the inhibition of leukocyte adhesion. AIMS: To investigate the rates of changes in the pancreatic constitutive NO synthase (cNOS) and inducible NOS (iNOS) activities and the role of NO in the vascular permeability changes during the development of L-arginine (Arg)-induced acute pancreatitis. METHODOLOGY: Acute pancreatitis was induced in male Wistar rats by injecting 250 mg/100 g body weight of Arg i.p. twice at an interval of 1 hour, as a 20% solution in 0.15 NaCl (group I). The control rats received the same quantity of glycine (group II). In group III, 30 mg/kg N -nitro-L-arginine methyl ester (L-NAME) was injected i.p. 19 hours after the first Arg injection. The rats were killed at 6, 12, 24, or 48 hours following Arg administration, and the plasma amylase concentration and the pancreatic weight/body weight (pw/bw) ratios were evaluated. NOS activity was determined via the conversion of L- C-Arg monohydrochloride to C-citrulline. The vascular permeability was examined by means of the extravasation of Evans blue dye (20 mg/kg bw) into the pancreatic tissue. RESULTS: The serum amylase level was already increased at 6 hours in group I animals, peaked at 12 hours after the Arg injection (11.800 +/- 590 versus 6.618 +/- 252 U/L in group II), and returned to the control level at 48 hours. The pw/bw ratio peaked at 24 hours in group I (6.63 +/- 0.52 versus 4.02 +/- 0.22 mg/g in group II) and returned to the control level at 48 hours. The cNOS activity was depleted at 6 hours in group I (0.02 +/- 0.003 versus 0.23 +/- 0.02 pmol/min/mg protein in group II); it then gradually increased to a level significantly higher than that in group II and decreased thereafter (0.45 +/- 0.03 and 0.13 +/- 0.01 pmol/min/mg protein at 24 and 48 hours). The iNOS activity was significantly increased at 24 and 48 hours versus that in group II (0.15 +/- 0.05 and 0.07 +/- 0.01 versus 0.04 +/- 0.01 pmol/min/mg protein). The pancreatic concentration of Evans blue dye was significantly higher in group I than in group II (138.59 +/- 11.04 versus 43.57 +/- 2.67 (g/dry weight). Treatment with L-NAME significantly reduced the amylase activity, pw/bw, Evans blue concentration, and cNOS activity of the pancreas but did not exert any beneficial effect on the histologic score at 24 hours after the onset of pancreatitis, as compared with those values in group I (6.528 +/- 673 U/L, 4.56 +/- 0.65 mg/g, 86.84 +/- 3.9 (g/dry weight, 0.14 +/- 0.04 pmol/min/mg protein). CONCLUSION: Endogenous NO is involved in the formation of pancreatic edema in Arg-induced acute pancreatitis by increasing the vascular permeability and protein extravasation. L-NAME treatment decreased the cNOS activity and edema formation but did not prevent the histologic damage in Arg-induced acute pancreatitis.
Acute Disease↗