CCL

Összesen 5 találat.
#/oldal:
Részletezés:
Rendezés:

1.

001-es BibID:BIBFORM020515
Első szerző:Hegyi Péter Jenő (belgyógyász)
Cím:Pancreatic secretory responses in L-arginine-induced pancreatitis : comparison of diabetic and nondiabetic rats / Peter Hegyi, Laszlo Czako, Tamas Takacs, Zoltan Szilvassy, Janos Lonovics
Dátum:2000
ISSN:0885-3177
Megjegyzések:AbstractThe aim of this work was to study cholecystokinin-octapeptide (CCK-8)-stimulated pancreatic secretion after the induction of pancreatitis with L-arginine (ARG) in rats with or without streptozotocin (STZ) diabetes. One, 3, 7, and 14 days after pancreatitis induction, rats were surgically prepared with pancreatic duct and femoral vein cannulae under urethane anesthesia. Graded doses of CCK-8 ranging from 9 to 2,400 ng/kg/30 min were administered intravenously. In the control group, the step-wise increasing doses of CCK-8 resulted in a characteristic dose-response curve for the pancreatic volume, protein and amylase secretion (maximal volume, protein and amylase output at 600 ng/kg/30 min of CCK-8: 157 +/- 20.2 microl/30 min, 28.3 +/- 1.18 mg/30 min, and 3,750 +/- 92 IU/30 min, respectively). In rats with pancreatitis, the pancreatic volume (both basal and maximal) and amylase secretion were significantly elevated on day 1 versus the control group; then on days 3,7, and 14, the pancreatic secretory volume and amylase were progressively and significantly decreased versus the control group. However, the protein output was continuously decreased versus the control group on days 1, 3, 7, and 14. In diabetic rats, the maximal volume and protein and amylase output were all significantly decreased versus the control group throughout the experiment. In the diabetes + pancreatitis group, the maximal volume and protein and amylase output were all significantly increased versus the diabetes group on days 1, 3, 7, and 14. These results indicate that in the early phase of ARG-induced pancreatitis, the pancreatic secretion is characterized by increases in secretory volume and amylase, with a simultaneous decrease in protein output. Simultaneous diabetes seems to moderate the CCK-8-stimulated secretory changes in both the early and late phases after ARG-induced pancreatitis.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
pancreatic
L-arginine-induced
pancreatitis
Megjelenés:Pancreas. - 19 : 2 (1999), p. 167-174. -
További szerzők:Czakó László Takács Tamás (Szeged) Lonovics János (Szeged) Szilvássy Zoltán (1957-) (belgyógyász, farmakológus, klinikai farmakológus)
Internet cím:Szerző által megadott URL
Intézményi repozitóriumban (DEA) tárolt változat
Borító:

2.

001-es BibID:BIBFORM020462
Első szerző:Kovács Péter (belgyógyász, kardiológus, klinikai farmakológus)
Cím:Effect of transdermal nitroglycerin on glucose-stimulated insulin release in healthy male volunteers / P. Kovacs, Z. Szilvassy, P. Hegyi, J. Nemeth, P. Ferdinandy, Á. Tosaki
Dátum:2000
ISSN:0014-2972
Megjegyzések:Morpholinosydnonimine, a nitric oxide (NO) donor, has been reported to inhibit insulin release in isolated pancreatic islets. We studied whether transdermal application of nitroglycerin, another NO donor widely used for angina prophylaxis, influenced glucose-stimulated insulin release in healthy, young, male volunteers.METHODS AND RESULTS:Oral glucose tolerance tests [(OGTT) 75 g glucose in 200 mL of water) were performed in the presence of placebo patches or nitroglycerin-releasing 'active' patches (approx. 0.4 mg hour-1 nitroglycerin) in the same patients with a 2-week intertest interval. Venous blood samples were taken before and 15, 30, 60, 90, 120 and 180 min after the glucose load and evaluated for plasma glucose level and immunoreactive insulin responses (radioimmunoassay). Glucose-stimulated maximum increase in plasma insulin immunoreactivity were 36.3 +/- 5 and 78.8 +/- 6.1 mU mL-1 (P < 0.05) in the presence of active and placebo patches, respectively. Nevertheless, both fasting and postload blood glucose levels were the same at either patch. Active patches significantly decreased blood pressure with a marginal increase in heart rate.CONCLUSION:We conclude that inhibition of glucose-stimulated insulin release by transdermal nitroglycerin without causing hyperglycaemia may serve as a novel component of the antianginal mechanism of action of nitrates.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
transdermal nitroglycerin
glucose-stimulated insulin
Effect of transdermal nitroglycerin
Megjelenés:European Journal Of Clinical Investigation 30 : 1 (2000), p. 41-44. -
További szerzők:Szilvássy Zoltán (1957-) (belgyógyász, farmakológus, klinikai farmakológus) Hegyi Péter Jenő (belgyógyász) Németh József (Pécs) Ferdinándy Péter Tósaki Árpád (1958-) (kísérletes farmakológus, gyógyszerész)
Internet cím:Szerző által megadott URL
DOI
Intézményi repozitóriumban (DEA) tárolt változat
Borító:

3.

001-es BibID:BIBFORM046502
Első szerző:Pálvölgyi Attila
Cím:Interplay between nitric oxide and VIP in CCK-8-induced phasic contractile activity in the rabbit sphincter of Oddi / Attila Pálvölgyi, Réka Sári, József Németh, Annamária Szabolcs, István Nagy, Péter Hegyi, János Lonovics, Zoltán Szilvássy
Dátum:2005
ISSN:1007-9327
Megjegyzések:AIM: The sphincter of Oddi (SO) plays an important role indelivery of bile into the duodenum. To establish whethervasoactive intestinal polypeptide (VIP) and nitric oxide (NO)were involved in phasic contractile activity of the rabbitSO stimulated by cholecystokinin-octapeptide (CCK-8).METHODS: Isolated SO muscle rings were cleaned of fatand mounted horizontally on two small L-shaped hooksone of which was connected to a force transducer for themeasurement of isometric tension. The experiments werecarried out in a thermostatically controlled (37?0.2 )organ bath (5 mL) containing Krebs solution. The organfluid was gassed with 95% O2 and 50 mL/L CO2 to keepthe pH at 7.40?0.05. Contractile responses to CCK-8(1 ?mol/L) were evaluated in the presence and absenceof NG-nitro-L-arginine (LNNA), an inhibitor of NO synthase(100 ?mol/L), and (p-chloro-D-Phe6-Leu17)-VIP (VIPa,30 ?mol/L), a VIP receptor antagonist.RESULTS: CCK-8 stimulated the phasic activity of the SO.NO synthase inhibition increased the frequency and amplitudeof contractions with a slight increase in developed tension.Pre-incubation with VIPa also attenuated this CCK-8 effect.The combined application of LNNA and VIPa abolishedthe phasic activity of the muscle rings with a marked increasein tension in response to CCK-8.CONCLUSION: VIP and NO together contribute to anincrease in phasic activity of SO.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Sphincter of Oddi
CCK
VIP
NO
LNNA
Megjelenés:World Journal of Gastroenterology. - 11 : 21 (2005), p. 3264-3266. -
További szerzők:Sári Réka (farmakológus) Németh József (Pécs) Szabolcs Annamária Nagy István Hegyi Péter Jenő (belgyógyász) Lonovics János (Szeged) Szilvássy Zoltán (1957-) (belgyógyász, farmakológus, klinikai farmakológus)
Pályázati támogatás:3.2.2.-2004-07-0001/3.0
GVOP
Internet cím:Szerző által megadott URL
Intézményi repozitóriumban (DEA) tárolt változat
Borító:

4.

001-es BibID:BIBFORM046503
035-os BibID:PMID:15526367
Első szerző:Sári Réka (farmakológus)
Cím:Ethanol inhibits the motility of rabbit sphincter of Oddi in vitro / Réka Sári, Attila Pálvölgyi, Zoltán Rakonczay Jr, Tamás Takács, János Lonovics, László Czakó, Zoltán Szilvássy, Péter Hegyi
Dátum:2004
ISSN:1007-9327
Megjegyzések:AIM: The role of the sphincter of Oddi (SO) in ethanol(ETOH)-induced pancreatitis is controversial. Our aim wasto characterise the effect of ETOH on basal and stimulatedSO motility.METHODS: SOs removed from white rabbits were placedin an organ bath (Krebs solution, pH7.4, 37 ). The effectsof 2 mL/L, 4 mL/L, 6 mL/L and 8 mL/L of ETOH on thecontractile responses of the sphincter were determined.SOs were stimulated with either 0.1 ?mol/L carbachol, 1?mol/L erythromycin or 0.1 ?mol/L cholecystokinin (CCK).RESULTS: ETOH at a dose of 4 mL/L significantly decreasedthe baseline contractile amplitude from 11.98?0.05 mN to11.19?0.07 mN. However, no significant changes in thecontractile frequency were observed. ETOH (0.6%)significantly decreased both the baseline amplitude and thefrequency compared to the control group (10.50?0.01 mN,12.13?0.10 mN and 3.53?0.13 c/min, 5.5?0.13 cycles(c)/min,respectively). Moreover, 0.8% of ETOH resulted in completerelaxation of the SO. Carbachol (0.1 ?mol/L) or erythromycin(1 ?mol/L) stimulated the baseline amplitudes (by 82%and 75%, respectively) and the contractile frequencies(by 150% and 106%, respectively). In the carbachol orerythromycin-stimulated groups 2-6 mL/L of ETOH significantlyinhibited both the amplitude and the frequency. Interestingly,a 4-5 min administration of 6 mL/L ETOH suddenly andcompletely relaxed the SO. CCK (0.1 ?mol/L) stimulatedthe baseline amplitude from 12.37?0.05 mN to 27.40?1.82mN within 1.60?0.24 min. After this peak, the amplitudedecreased to 17.17?0.22 mN and remained constant duringthe experiment. The frequency peaked at 12.8?0.2 c/min,after which the constant frequency was 9.43?0.24 c/minthroughout the rest of the experiment. ETOH at a doseof 4 mL/L significantly decreased the amplitude from16.13?0.23 mN to 14.93?0.19 mN. However, no significantchanges in the contractile frequency were observed. ETOHat a dose of 6 mL/L inhibited both the amplitudes and thefrequencies in the CCK-stimulated group, while 8 mL/L ofETOH completely relaxed the SO.CONCLUSION: ETOH strongly inhibits the basal, carbachol,erythromycin, and CCK-stimulated rabbit SO motility.Therefore, it is possible that during alcohol-intake therelaxed SO opens the way for pancreatic fluid to flow outinto the duodenum in rabbits. This relaxation of the SOmay protect the pancreas against alcohol-induced damage.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
ethanol
effect of ETOH
CCK-stimulated
SO
erythromycin
Megjelenés:World Journal of Gastroenterology. - 10 : 23 (2004), p. 3470-3474. -
További szerzők:Pálvölgyi Attila Rakonczay Zoltán Jr. Takács Tamás (Szeged) Lonovics János (Szeged) Czakó László Szilvássy Zoltán (1957-) (belgyógyász, farmakológus, klinikai farmakológus) Hegyi Péter Jenő (belgyógyász)
Internet cím:Szerző által megadott URL
Intézményi repozitóriumban (DEA) tárolt változat
Borító:

5.

001-es BibID:BIBFORM020340
Első szerző:Sári Réka (farmakológus)
Cím:Cyclic GMP-mediated activation of a glibenclamide-sensitive mechanism in the rabbit sphincter of Oddi / Reka Sari, Barna Peitl, Peter Kovacs, Janos Lonovics, Attila Palvolgyi, Peter Hegyi, Istvan Nagy, Jozsef Nemeth, Zoltan Szilvassy, Robert Porszasz
Dátum:2004
Megjegyzések:AbstractWe investigated whether glibenclamide-sensitive potassium channels are involved in cyclic GMP (cGMP)-mediated relaxation of the rabbit Oddi's sphincter. Changes in isometric tension were measured in the presence of atropine (1 microM) and guanethidine (4 microM). Concentration-response curves for nitroglycerin, vasoactive intestinal polypeptide (VIP), and sodium nitroprusside (SNP) were shifted to the right in the presence of (p-chloro-D-Phe6, Leu17)-VIP (VIPa), a VIP receptor antagonist. Glibenclamide (1 microM) attenuated the relaxations to VIP, nitroglycerin, or 8-bromo cGMP. In the presence of tetrodotoxin (TTX), glibenclamide attenuated relaxations to VIP without effect on those to nitroglycerin. Furthermore, nitroglycerin increased both cAMP and cGMP concentrations, however, it failed to increase the tissue cAMP concentration in the presence of TTX. VIPa also blocked the increase in content of either cyclic nucleotide. VIP increased cAMP with a TTX-sensitive increase in cGMP content. 8-Bromo cGMP (1 microM) significantly increased the tissue cAMP content. This was blocked by either TTX or VIPa (both 1 microM). We conclude that ATP-sensitive potassium channel (KATP) activation contributes to cGMP-mediated relaxation of the Oddi's sphincter of the rabbit. Activation of KATP results from a cyclic AMP-mediated process due to cGMP-dependent VIP release from neurons.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
Cyclic GMP
GMP-Mediated Activation
Glibenclamide-Sensitive
Megjelenés:Digestive Diseases and Sciences. - 49 : 3 (2004), p. 514-520. -
További szerzők:Peitl Barna (1972-) (orvos, farmakológus) Kovács Péter (1947-) (belgyógyász, kardiológus, klinikai farmakológus) Lonovics János (Szeged) Pálvölgyi Attila Hegyi Péter Jenő (belgyógyász) Nagy István (orvos) Németh József (Pécs) Szilvássy Zoltán (1957-) (belgyógyász, farmakológus, klinikai farmakológus) Pórszász Róbert (1965-) (farmakológus, klinikai farmakológus)
Internet cím:Szerző által megadott URL
DOI
Intézményi repozitóriumban (DEA) tárolt változat
Borító:
Rekordok letöltése1 
Corvina könyvtári katalógus v8.2.27 © 2023 Monguz kft. Minden jog fenntartva.