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J Németh

Publications and source records attributed to J Németh.

At least 19 recordsLinked to original sources
PubMed2006

Effects of the somatostatin receptor subtype 4 selective agonist J-2156 on sensory neuropeptide release and inflammatory reactions in rodents.

BACKGROUND AND PURPOSE: Substance P (SP) and calcitonin gene-related peptide (CGRP) released from capsaicin-sensitive sensory nerves induce local neurogenic inflammation; somatostatin exerts systemic anti-inflammatory actions presumably via sst4/sst1 receptors. This study investigates the effects of a high affinity, sst4-selective, synthetic agonist, J-2156, on sensory neuropeptide release in vitro and inflammatory processes in vivo. EXPERIMENTAL APPROACH: Electrically-induced SP, CGRP and somatostatin release from isolated rat tracheae was measured with radioimmunoassay. Mustard oil-induced neurogenic inflammation in rat hindpaw skin was determined by Evans blue leakage and in the mouse ear with micrometry. Dextran-, carrageenan- or bradykinin-induced non-neurogenic inflammation was examined with plethysmometry or Evans blue, respectively. Adjuvant-induced chronic arthritis was assessed by plethysmometry and histological scoring. Granulocyte accumulation was determined with myeloperoxidase assay and IL-1beta with ELISA. KEY RESULTS: J-2156 (10-2000 nM) diminished electrically-evoked neuropeptide release in a concentration-dependent manner. EC50 for the inhibition of substance P, CGRP and somatostatin release were 11.6 nM, 14.3 nM and 110.7 nM, respectively. J-2156 (1-100 microg kg(-1) i.p.) significantly, but not dose-dependently, inhibited neurogenic and non-neurogenic acute inflammatory processes and adjuvant-induced chronic oedema and arthritic changes. Endotoxin-evoked myeloperoxidase activity and IL-1beta production in the lung, but not IL-1beta- or zymosan-induced leukocyte accumulation in the skin were significantly diminished by J-2156. CONCLUSIONS AND IMPLICATIONS: J-2156 acting on sst4 receptors inhibits neuropeptide release, vascular components of acute inflammatory processes, endotoxin-induced granulocyte accumulation and IL-1beta synthesis in the lung and synovial and inflammatory cells in chronic arthritis. Therefore it might be a promising lead for the development of novel anti-inflammatory drugs.

Animals↗
PubMed2006

Effect of pituitary adenylate cyclase activating polypeptide-38 on sensory neuropeptide release and neurogenic inflammation in rats and mice.

Substance P (SP) and calcitonin gene-related peptide (CGRP), released from capsaicin-sensitive sensory nerves induce local neurogenic inflammation, while somatostatin exerts systemic anti-inflammatory actions. The aim of the present study was to investigate the release of pituitary adenylate cyclase activating polypeptide-38 (PACAP-38) and its effects on sensory neuropeptide release in vitro and acute neurogenic ear swelling in vivo. Capsaicin (10(-6) M) or electrical field stimulation (EFS; 40 V, 0.1 ms, 10 Hz, 120 s; 1200 impulses)-induced release of PACAP-38, SP, CGRP and somatostatin from isolated rat tracheae was measured with radioimmunoassay. Mustard oil-induced neurogenic inflammation in the mouse ear was determined with a micrometer and in the rat hind paw skin by the Evans Blue leakage technique. Capsaicin and EFS evoked 27% and more than twofold elevation of PACAP-38 release respectively, compared with the prestimulated basal values from isolated trachea preparation. Exogenously administered PACAP-38 (20-2000 nM) diminished both capsaicin- and EFS-evoked sensory neuropeptide release in a concentration-dependent manner. The maximal inhibitory effects of PACAP on capsaicin-induced substance P, CGRP and somatostatin release amounted to 75.4%, 73.3% and 90.0%, while EFS-evoked release of these peptides was 80.03%, 87.7% and 67.7%. In case of capsaicin stimulation the EC50 values for substance P, CGRP and somatostatin were 82.9 nM, 60.1 nM and 66.9 nM, respectively. When EFS was performed, these corresponding EC50 data were 92.1 nM, 67.8 nM and 20.9 nM. PACAP-38 (10, 100 and 1000 microg/kg i.p. in 200 microl volume) inhibited neurogenic ear swelling in the mouse. Furthermore, 100 microg/kg i.p. PACAP also significantly diminished mustard oil-evoked plasma protein extravasation in the rat skin. These results suggest that PACAP-38 is released from the stimulated peripheral terminals of capsaicin-sensitive afferents and it is able to inhibit the outflow of sensory neuropeptides. Based on this mechanism of action PACAP is also able to effectively diminish/abolish neurogenic inflammatory response in vivo after systemic administration.

Animals↗
PubMed2006

HPLC-RIA analysis of the ectopic cortisol production in a cancerous pancreas tumor.

Steroidal pathophysiology of a malignant, ACTH-producing pancreas tumor was investigated via HPLC-RIA determinations of intratissular concentrations of eleven main steroid hormones. The tumor specimen underwent extraction procedure with ethyl acetate and the extract was purified on a C18 minicolumn. Steroids were isolated by HPLC (C18-silica reversed phase stationary phase and methanol-water eluent system) and quantified by specific RIAs. Cortisol content of the tumor specimen was 15,700 pmol/g, the further steroid hormones were found in much lower concentrations (< 1.5-28 pmol/g). The extremely high cortisol concentration in the tissue witnesses the synthesis of the main glucocorticoid steroid in the ACTH-producing pancreas tumor and suggests a stimulating paracrine effect of ACTH on cortisol production. The present data verify that the determination of intratissular steroid concentrations by HPLC-RIA methods may identify even the most peculiar hormone sources and the hormone profiles facilitate studying pathophysiology of ectopic endocrine tumors.

ACTH Syndrome, Ectopic↗
PubMed2004

[Vascular injuries in everyday practice].

BACKGROUND: It was the objective of this retrospective study to analyse the causes of injury, surgical approaches, outcome, and complications in patients with vascular trauma and to report our experience with vein homografts for arterial reconstruction in the upper and lower limbs and cervicothoracic region in patients operated on over a period between 1981-2001. PATIENTS: In 128 patients with peripheral arterial injuries the mechanism was direct penetration in 90 cases and blunt injury in 20 cases. In 4 cases a chronic damage (false aneurysm, AV fistula) was observed. Isolated vascular trauma was present in 97 patients (75.8%), 31 cases (24.2%) were aggravated by concomitant bone fractures, and nerve or soft tissue damage. Most frequently injured vessels were the superficial femoral (22.6%), crural (22.6%), and ulnar and radial (13.2%) arteries. 16 patients with penetrating cervicothoracic arterial injuries were registered during this period. 8 patients underwent emergency exploration and 8 patients angiography prior urgent exploration. RESULTS: Saphenous vein interposition grafting was applied with good results in 34 patients, polytetrafluoroethylene and Dacron grafts were used in eight cases, end to end anastomosis in 12 cases, venous bypasses in 5 cases, venous patches in 7 cases. 17 patients underwent arterial repair and 9 venous repair. Vein homografts as an arterial substitute were implanted in 8 patients. Five secondary amputations were performed and five patients died. The limb salvage rate was 95% and the primary patency rate of vein homografts was 75% (excluded primary amputations). The penetrating cervicothoracic injuries were all repaired with improvement in level of consciousness and neurological deficit when present. CONCLUSIONS: Most vascular injuries of the extremities can be managed successfully unless associated with severe concomitant damage of the bones, nerves and soft tissues. In the absence of suitable autologous vein grafts, homografts appear to be an interesting alternative for arterial repair. In penetrating cervicothoracic vascular injuries immediate operative repair offers the best chance of recovery.

Adolescent↗
PubMed2001

[Significance of anti-nucleosome (anti-chromatin) auto-antibodies in systemic lupus erythematosus].

Systemic lupus erythematosus is characterised by the presence of antinuclear autoantibodies (ANA). Native DNA, histone proteins and small nuclear ribonucleoproteins (snRNP) are the main targets of these ANA-s, but some of them may derive against the entire chromatin, which is composed of the listed elements, and also against its fundamental unit, that is nucleosome. Authors investigated at the first time the frequency and the concentration of anti-nucleosome antibodies in a group of 107 consecutively selected Hungarian lupus patients. They calculated correlation between these parameters and the activity as well as organ--mainly kidney--manifestations of the disease. The frequencies of positive anti-nucleosome, anti-dsDNA and anti-histone antibodies were 39.2, 28.0 and 47.6%, respectively. All the three autoantibodies were present more frequently in cases with lupus nephritis, and this correlation was significant by statistical respect. Also a positive correlation was found between the concentration of these autoantibodies and activity of the diseases (SLE-DAI). Results suggest that long disease duration (mean 8.5 year) and consequently low disease activity (mean DAI: 3.28) may stand at the background of the relatively low occurrence of the measured ANA-s. Besides anti-dsDNA, the determination of anti-nucleosome and anti-histone antibodies can be useful in the diagnosis and monitoring of SLE. Authors discuss the possible role of anti-nucleosome autoantibodies in the pathogenesis of lupus nephritis.

Adult↗
PubMed2001

Cholecystokinin fails to promote pancreatic regeneration in diabetic rats following the induction of experimental pancreatitis.

The aim of the present study was to investigate the spontaneous and cholecystokinin-octapeptide (CCK-8)-promoted laboratory changes and morphological alterations in rats with arginine (Arg)-induced pancreatitis in which diabetes had been induced with streptozotocin (STZ). Male Wistar rats were used in our experiments. Pancreatitis was induced by arginine, diabetes by STZ and regeneration was promoted by CCK-8. The serum amylase, glucose and insulin levels, the pancreatic contents of protein, DNA, amylase, trypsinogen and lipase, the pancreatic weight/body- weight ratio (pw/bw) and the plasma glucagon level were examined 1, 3, 7, 14 and 28 days after pancreatitis induction. Pancreatic tissue samples were examined by light microscopy and immunostaining on paraffin-embedded sections. The insulin and glucagon-containing cells were visualized by using monoclonal antibodies. The administration of low doses of CCK-8 accelerated the processes of regeneration following Arg-induced pancreatitis, but in rats that were also diabetic, pancreatic regeneration was not observed. The administration of low doses of CCK-8 seems to reduce the pancreatic beta -cell number and function in diabetic rats. The pancreatic endocrine function was further deteriorated by simultaneous Arg-induced pancreatitis. The diabetic state appeared to shift the normal pancreatic enzyme content (decreased amylase and increased trypsinogen) in this study.

Animals↗
PubMed2001

Central retinal vessel trunk exit and location of glaucomatous parapapillary atrophy in glaucoma.

OBJECTIVE: To evaluate whether the position of the central retinal vessel trunk exit on the lamina cribrosa spatially correlates with the location of parapapillary atrophy in glaucoma. DESIGN: Clinic-based, observational, cross-sectional study. PATIENTS: Color stereo optic disc photographs of 95 patients with primary or secondary open-angle glaucoma and 65 healthy persons were morphometrically evaluated. The intrapapillary and parapapillary region was divided into four quadrants. We determined the position of the central retinal vessel trunk exit on the lamina cribrosa surface and measured the area of parapapillary atrophy and neuroretinal rim in the four quadrants. MAIN OUTCOME MEASURES: The area of neuroretinal rim and parapapillary atrophy and the position of the central retinal vessel trunk exit. RESULTS: Comparing measurements between opposite disc quadrants showed that beta zone of parapapillary atrophy was significantly (P < 0.05) larger and that the neuroretinal rim was significantly smaller when beta zone and neuroretinal rim were measured in the disc quadrant most distant to the central retinal vessel trunk exit, than if the beta zone and neuroretinal rim were measured in the quadrant containing the vessel trunk exit. Comparing measurements in the disc quadrants between eyes with different positions of the central retinal vessel trunk exit revealed that, in the respective disc quadrant, the beta zone was significantly larger and the neuroretinal rim was smaller in eyes with the vessel trunk exiting in the opposite disc quadrant than in eyes with the vessel trunk exit located in the respective disc quadrant where the measurements were obtained. CONCLUSIONS: Position of the central retinal vessel trunk exit on the lamina cribrosa influences the location of parapapillary atrophy in glaucoma. The longer the distance to the central retinal vessel trunk exit, the more enlarged is parapapillary atrophy and the smaller is the neuroretinal rim. This relationship agrees with the spatial relationship between glaucomatous neuroretinal rim loss and enlarged parapapillary atrophy in glaucoma. Diagnostically, it may indicate that, in eyes with an abnormal configuration of parapapillary atrophy or with an abnormal position of the central retinal vessel trunk exit, early glaucomatous rim changes should be looked for in the disc sector that is most distant to the central retinal vessel trunk exit and where parapapillary atrophy may be relatively large.

Adult↗
PubMed2001

Corneal topography changes after a 15 second pause in blinking.

PURPOSE: To examine the effect of a short pause in blinking on the quantitative topographic parameters of the corneal surface. SETTING: Refractive corneal surgery unit of a university eye hospital. METHODS: Using a TMS-1 instrument (Computed Anatomy, Inc.), corneal topographic parameters were measured 5 and 15 seconds after a complete blink in 12 healthy subjects. The main outcome measures were changes in the surface regularity index (SRI) and the surface asymmetry index (SAI). RESULTS: During the pause in blinking, the mean SRI value increased from 0.18 +/- 0.19 (SD) to 0.30 +/- 0.19 (P <.02) and the SAI from 0.21 +/- 0.08 to 0.24 +/- 0.10 (P =.079, not statistically significant). There were no significant changes in the values for potential visual acuity, corneal refractive power, or astigmatism. CONCLUSION: The results indicated a significant change in corneal topography during even a short pause in blinking. In follow-up studies using corneal topography, all measurements should be done at a fixed time after a complete blink.

Adult↗
PubMed2001

Anti-inflammatory effect of synthetic somatostatin analogues in the rat.

1. Somatostatin (6.11 nmol kg(-1) i.p.) inhibited neurogenic plasma extravasation evoked by 1% mustard oil and non-neurogenic oedema induced by 5% dextran in the rat skin. 2. Cyclic synthetic octapeptide (TT-248 and TT-250) and heptapeptide (TT-232) somatostatin analogues proved to be more effective in reducing neurogenic and non-neurogenic inflammatory reactions but octreotide had no influence on either neurogenic or non-neurogenic inflammation. 3. TT-232 administered i.p. or i.v. (1.06 - 42.40 nmol kg(-1)) inhibited in a dose-dependent manner the plasma extravasation evoked by mustard oil in the rat's paw. Neither diclofenac (15.78 - 315.60 micromol kg(-1)) nor the selective COX-2 inhibitor meloxicam (2.95 - 569.38 micromol kg(-1)) attenuated the mustard oil-induced neurogenic plasma extravasation. 4. TT-232, diclofenac and meloxicam dose-dependently diminished non-neurogenic dextran-oedema of the paw the ED(35) values were 1.73 nmol kg(-1) for TT-232 and 34.37 micromol kg(-1) for diclofenac. 5. TT-232 inhibited in the dose range of 1.06 - 21.21 nmol kg(-1) the bradykinin-induced plasma extravasation in the skin of the chronically denervated paw. 6. Mustard oil-induced cutaneous plasma extravasation was dose-dependently diminished by s.c. TT-232 1, 2, 4, 6 or 16 h after the treatment. TT-232 (2 x 106, 2 x 212 and 2 x 530 nmol kg(-1) per day s.c. for 18 days) caused dose-dependent inhibition of chronic Freund adjuvant-induced arthritis during the experimental period. 7. TT-232 (200 and 500 nM) inhibited the release of SP, CGRP and somatostatin from the rat isolated trachea induced by electrical field stimulation (40 V, 0.1 ms, 10 Hz, 120 s) or by capsaicin (10(-7) M), but did not influence the basal, non-stimulated peptide release. 8. It is concluded that somatostatin analogues without endocrine functions as TT-232 are promising compounds with a novel site of action for inhibition of non-neurogenic and neurogenic inflammatory processes.

Animals↗
PubMed2001

Retinal microcirculation correlates with ocular wall thickness, axial eye length, and refraction in glaucoma patients.

PURPOSE: To examine the correlations of refraction, axial eye length, and posterior eye wall thickness with retinal microcirculation. PATIENTS AND METHODS: In a prospective study, 25 patients with primary open-angle glaucoma, 12 patients with ocular hypertension, and 12 healthy subjects were examined; only one eye of each participant was considered in the analysis. Posterior eye wall thickness and axial eye length were measured with standardized A-scan ultrasonography. Retinal microcirculation temporal to the optic disc was determined by a scanning laser Doppler flowmeter using automatic full-field perfusion image analyzer software. RESULTS: In glaucoma patients, temporal retinal mean flow exhibited significant correlation to the eye wall thickness (r = 0.470, P = 0.042), axial eye length (r = -0.570, P = 0.011), and refraction of the eye (r = 0.520, P = 0.022). In glaucomatous eyes, the temporal retinal mean flow was significantly lower than in healthy subjects or in ocular hypertensive patients (P = 0.01). CONCLUSIONS: Myopic eyes have longer axial eye length and thinner ocular wall than emmetropic eyes. In glaucoma patients, the longer the axial eye length and the thinner the ocular wall, the more reduced the retinal microcirculation. The reduced microcirculation found in myopic glaucomatous eyes might contribute to the development of glaucomatous damage in these eyes.

Blood Flow Velocity↗
PubMed2001

Impaired capsaicin-induced decrease in heart rate and coronary flow in isolated heart of diabetic rats.

The effect of capsaicin (0.1 microM) on heart rate and coronary flow was studied in Langendorff-perfused heart from streptozotocin-induced (50 mg/kg i.v.) diabetic rats where sensory neuropathy developed. In hearts from animals 4- and 8-week diabetes baseline heart rate and coronary flow decreased from 317.9 +/- 2.9 b.p.m. and 13.4 +/- 0.7 m/min to 255.1 +/- 12.7 and 219.8 +/- 2.8 b.p.m. and 8.9 +/- 0.6 and 10.0 +/- 0.1 ml/min (P<0.05), respectively. Capsaicin significantly decreased both variables in either normal or 4-week diabetic animals its effects, however, on coronary flow or heart rate were missing in preparations from 8-week diabetic rats. Endothelin-1 (0.1 nM), the putative mediator of the capsaicin effect, significantly decreased heart rate and coronary flow irrespective of the presence or absence of diabetes. In the femoral nerve of streptozotocin-treated animals conduction velocity involving both fast conducting A- and slow-conducting C-fibres was decreased proportional to the duration of the pre-existing diabetic state. It is concluded that in insulin deficient diabetes the diminished responses evoked by capsaicin on heart rate and coronary flow are signs of sensory neuropathy. This is related to a feeble endothelin release from sensory nerve endings without changes in post-receptor mechanisms mediating the endothelin effects.

Animals↗
PubMed2000

Systemic anti-inflammatory effect of somatostatin released from capsaicin-sensitive vagal and sciatic sensory fibres of the rat and guinea-pig.

The systemic anti-inflammatory effect induced by antidromic sensory nerve stimulation was investigated in rats and guinea-pigs. In atropine-pretreated rats, bilateral antidromic stimulation of vagal afferent fibres (8 Hz, 20 min, at C-fibre strength) inhibited plasma extravasation induced by 1% mustard oil on the acutely denervated hindlegs by 36.45+/-3.95%. Both the prevention of this inhibitory effect by cysteamine pretreatment and the stimulation-evoked rise of plasma somatostatin-like immunoreactivity in the two species suggest a mediator role of neural somatostatin. Since this response was blocked by systemic capsaicin pretreatment and slightly reduced after subdiaphragmal vagotomy, participation of thoracic capsaicin-sensitive afferents is indicated. In guinea-pigs pretreated with guanethidine and pipecuronium, antidromic sciatic nerve stimulation induced 45.46+/-5.08% inhibition on the contralateral leg and increased plasma somatostatin-like immunoreactivity. It is concluded that somatostatin released from the activated vagal capsaicin-sensitive sensory nerve terminals of the rat and somatic nerves of the guinea-pigs exerts a systemic humoral function.

Afferent Pathways↗
PubMed2000

Anti-nociceptive effect induced by somatostatin released from sensory nerve terminals and by synthetic somatostatin analogues in the rat.

In rats anaesthetized with urethan and pretreated with pipecuronium bromide nocifensive reaction of blood pressure elevation evoked by intraarterial capsaicin injection was inhibited over 40 min by bilateral antidromic stimulation of the sensory fibres of the sciatic nerves. Rise in blood pressure, heart rate and respiratory frequency evoked by capsaicin were markedly diminished after smearing 1% mustard oil on the acutely denervated hindpaws indicating a release of mediators with anti-nociceptive action from cutaneous nociceptors. Intravenous injection of the putative mediator somatostatin (10 microg/kg) or its analogues RC-160 and TT-232, but not octreotide inhibited the cardiorespiratory and blood pressure responses evoked by topical cutaneous application of mustard oil or capsaicin instillation into the eye. It is concluded, that the endocrine and the anti-nociceptive effects of somatostatin are mediated through distinct receptor subtypes and therefore, TT-232, a novel heptapeptide analogue without endocrine action, is a promising analgesic compound.

Analgesics↗
PubMed2000

Effect of L-aminocarnitine, an inhibitor of mitochondrial fatty acid oxidation, on the exocrine pancreas and liver in fasted rats.

Fasting induces pancreatic secretory lipase, possibly through an increased utilization of fatty acids and/or ketone bodies by the acinar cells. To test this hypothesis, the effects of L-aminocarnitine (ACA), an inhibitor of mitochondrial beta-oxidation and ketone body formation, on the pancreatic enzyme composition were studied in rats. The characteristics and reversibility of the hepatic steatosis produced by ACA in fasted animals were also investigated. In fasted rats, ACA decreased the plasma levels of beta-hydroxybutyrate, glucose and insulin, but increased that of glucagon. Fasting for 3 days increased the pancreatic lipase content by 80%. Administration of ACA (3, 10 or 30 mg kg(-1) daily) for 3 days to fasted rats led to dose-related decreases in pancreatic lipase content, the fasting-induced increase was prevented even by the lowest dose. Nevertheless, ACA in the fasted rats likewise decreased the pancreatic contents of protein, amylase and trypsinogen to varying degrees, suggesting a general defect of protein synthesis. The 3-day treatment with ACA during fasting led to dose-related, marked increases in hepatic weight and triglyceride content. Light and electron microscopy revealed lipid vesicles of varying sizes in the hepatocytes; the fat deposition was predominant in the periportal zones of the hepatic lobules. By means of electron microscopy, lipid vacuoles were observed in the centroacinar cells, but not in the acinar cells of the pancreas. In rats treated with 30 mg kg(-1) of ACA daily for 3 days while they were fasted, cessation of ACA treatment and refeeding with normal chow led to normalization of the pancreatic enzyme contents within 6 days, and gradual and complete disappearance of the hepatic steatosis within 24 days. Microscopy also demonstrated complete recovery in both the liver and the pancreas. The results indicate that pancreatic secretory lipase induction during the adaptive phase of starvation is dependent on an unhindered mitochondrial beta-oxidation of fatty acids and ketogenesis. The dose-related degree of hepatic triglyceride accumulation which can be produced readily by administration of ACA during short-term starvation in the rat may serve as a new, convenient experimental model for studies of fatty liver.

Animals↗
PubMed2000

Assessment of pancreatic enzyme secretory capacity by a modified Lundh test.

BACKGROUND: The Lundh test is a usual means of estimating the enzyme secretory capacity of the gland. During this procedure, however, a major proportion of the test meal is removed from the duodenum together with the gastric, duodenal, and pancreatic secretions and the bile. This study was undertaken to compare the pancreatic enzyme secretion induced by the Lundh procedure with that resulting from stimulation of the normal digestive process, by reinfusion of the aspirated duodenal juice. METHODS: Nine men (mean age: 46.7, range 42-55 yr) free from pancreatic disease were studied. Pancreatic secretion was measured via a multiple lumen tube by aspiration of the duodenal juice. After a basal period the Lundh test meal was placed in the stomach and the duodenal juice was completely aspirated. On a separate day, the procedure was repeated, but the aspirated duodenal juice was reinfused into the upper jejunum. RESULTS: In the first 30 min of the test period, the enzyme outputs were the same on both test days. In the 30-60-min period, the lipase output, and in the 75-90-min period, the amylase output was significantly lower during the Lundh test compared with the jejunal reinfusion test. The CCK levels were significantly above the basal level at 20 and 40 min, but the increase was significantly lower during the traditional Lundh test. No significant difference in gastrin release was observed during either the Lundh or the reinfusion test. CONCLUSIONS: In the traditional Lundh test, the trypsin secretory capacities of the gland are measured appropriately, but the lipase and amylase secretory capacity and the CCK release are not fully represented compared with the reinfusion test. An association between the lower CCK release and lipase amylase secretion is suggested.

Adult↗
PubMed2000

Stimulated gastrointestinal hormone release and gallbladder contraction during continuous jejunal feeding in patients with pancreatic pseudocyst is inhibited by octreotide.

BACKGROUND: Continuous enteral feeding, the old-new therapeutic modality in the treatment of patients with acute pancreatitis and those with complications is considered to bypass the cephalic, the gastric, and (at least in part) the intestinal phase of pancreatic secretion. The aim of this study was to test the GI hormonal changes and gallbladder motility during CJF in patients with pancreatic pseudocysts following acute pancreatitis, with or without octreotide pretreatment. PATIENTS AND METHODS: In 15 patients with pancreatic pseudocysts, an 8-French (8F) nasojejunal catheter was positioned into the jejunum distal to the ligament of Treitz during duodenoscopy. On test d 1, blood samples were taken for CCK, gastrin, insulin-like immunoreactivity (IRI), glucagon, and glucose measurements prior to and at 20, 40, 60, and 120 min following jejunal saline infusion at a rate of 2 mL/min. The gallbladder volumes were determined simultaneously by ultrasonography. On test d 2, CJF (175 kcal/h) was started by the same route and at the same infusion rate. Analogous measurements were performed as indicated above. On test d 3, 100 microg of octreotide was administered subcutaneously and the previous procedure was repeated. The plasma level of CCK and glucagon and the serum levels of IRI and gastrin were determined by bioassay and radioimmunoassay (RIA), respectively. RESULTS: Significant changes in hormone levels were not observed during jejunal saline perfusion. However, the levels of CCK (5.7+/-0.9 pmol), gastrin (10.6+/-1.3 pmol/L), IRI (27.2+/-5.8 microIU/mL), glucagon (322.8+/-32.4 pg/mL), and glucose (5.8+/-1.0 mmol/L) were significantly increased at 20 min during CJF vs the saline controls (2.0+/-0.3 pmol, 6.8+/-1.1 pmol/L, 7.8+/-0.4 microIU/mL, 172.8+/-33.4 pg/mL, and 4.5+/-0.5 mmol/L, respectively) and remained elevated at 40, 60, and 120 min. Octreotide pretreatment eliminated the increases in CCK, gastrin, IRI, and glucagon levels observed during CJF alone. The significant decrease in gallbladder volume during CJF was also prevented by octreotide pretreatment. CONCLUSION: Continuous jejunal feeding (CJF) elicited significant increases in gastrointestinal (GI) regulatory hormone (cholecystokinin [CCK], gastrin, IRI, and glucagon) levels and evoked a consecutive gallbladder contraction. These biological responses are eliminated by octreotide pretreatment. Further clinical studies are needed to assess the eventual therapeutic effect of octreotide during CJF in patients with pancreatic pseudocyst.

Adult↗