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1.

001-es BibID:BIBFORM020345
Első szerző:Bajza Ágnes (biológus)
Cím:Development of insulin resistance by nitrate tolerance in conscious rabbits / Ágnes Bajza, Barna Peitl, József Nemeth, Róbert Porszasz, György Rabloczky, Péter Literati-Nagy, Judit Szilvassy, Zoltán Szilvassy
Dátum:2004
Megjegyzések:Clinical evidence has been raised to suggest that transdermal nitroglycerin increases the sensitivity of peripheral tissues to the hypoglycemic effect of insulin. In this study we determined whether development of tolerance to the hypotensive effect of nitroglycerin also resulted in tolerance to the insulin-sensitizing effect in rabbits. Intravenous glucose disposal and hyperinsulinemic euglycemic glucose clamp studies were performed on naive and hemodynamic nitrate tolerant conscious New Zealand white rabbits. These rabbits were exposed to continuous "patch on" with nitroglycerin (0.07 mg/kg/h) or placebo patches over 7 days. Nitroglycerin treatment of 7 days produced a lack of hypotensive response to a single intravenous bolus of 30 microg/kg nitroglycerin, which caused a significant decrease in mean arterial blood pressure in control rabbits. A six-hour exposure to transdermal nitroglycerin significantly increased insulin sensitivity determined by hyperinsulinemic (100 microU/ml) euglycemic (5.5 mmol/l) glucose clamping as compared with that seen in rabbits treated with placebo patches. A significant decrease in insulin sensitivity was observed in the nitroglycerin patch-treated animals both in the presence and after the removal of the last patch when the patches were applied over 7 days. We conclude that acutely nitrate patches improve insulin sensitivity whereas a 7-day chronic treatment schedule that results in hemodynamic nitrate tolerance also produces insulin resistance.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
insulin tolerance
nitrate tolerance
Megjelenés:Journal of Cardiovascular Pharmacology. - 43 : 3 (2004), p. 471-476. -
További szerzők:Peitl Barna (1972-) (orvos, farmakológus) Németh József (Pécs) Pórszász Róbert (1965-) (farmakológus, klinikai farmakológus) Rablóczky György Literati Nagy Péter Szilvássy Judit (1960-2022) (fül- orr- gégész) Szilvássy Zoltán (1957-) (belgyógyász, farmakológus, klinikai farmakológus)
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2.

001-es BibID:BIBFORM028151
Első szerző:Bajza Ágnes (biológus)
Cím:Interaction between nitrate tolerance and insulin sensitivity in conscious rabbits / Bajza Ágnes, Peitl Barna, Porszász Róbert, Literáti-Nagy Péter, Szilvássy Zoltán
Dátum:2004
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idézhető absztrakt
Megjelenés:Fundamental & Clinical Pharmacology. - 18 (2004), p. 62. -
További szerzők:Peitl Barna (1972-) (orvos, farmakológus) Pórszász Róbert (1965-) (farmakológus, klinikai farmakológus) Literati Nagy Péter Szilvássy Zoltán (1957-) (belgyógyász, farmakológus, klinikai farmakológus)
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3.

001-es BibID:BIBFORM042635
Első szerző:Fürjes Gergely
Cím:Thrittene radioimmunoassay : description and application of a novel method / G. Fürjes, G. K. Tóth, B. Peitl, R. Pórszász, B. Lelesz, R. Sári, A. Tóth, Z. Szilvássy, J. Németh
Dátum:2012
Megjegyzések:In the present paper the development andapplication of a novel thrittene radioimmunoassay (RIA)are described. 125I-labeling of Tyr(0)-thrittene was performedby the iodogen-method and the mono-iodinatedpeptide, as RIA tracer, was separated by reversed-phasehigh performance liquid chromatography (HPLC). TheRIA results show that the antiserum used in the radioimmunoassayturned to be C-terminal specific, without significantaffinity to other members of the somatostatinpeptide hormone family. Detection limit of the assay was0.2 fmol/ml. This highly specific and sensitive thritteneRIA was used to investigate the distribution of thrittene inthe rat gastrointestinal tract and other tissue samples. Differentareas of the gastrointestinal tract and other tissueswere removed from rats and after extraction the sampleswere processed for thrittene radioimmunoassay. Highestconcentrations were found in the duodenum samplesfollowed by jejunum and ileum, however, all the examinedtissues contained highly enough thrittene for themeasurement.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény hazai lapban
Megjelenés:Journal of Radioanalytical and Nuclear Chemistry. - 292 : 1 (2012), p. 113-118. -
További szerzők:Tóth Gábor K. Peitl Barna (1972-) (orvos, farmakológus) Pórszász Róbert (1965-) (farmakológus, klinikai farmakológus) Lelesz Beáta (1989-) (molekuláris biológus) Sári Réka (farmakológus) Tóth Attila (1971-) (biológus) Szilvássy Zoltán (1957-) (belgyógyász, farmakológus, klinikai farmakológus) Németh József (1954-) (vegyész, analitikus)
Pályázati támogatás:75965
OTKA
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4.

001-es BibID:BIBFORM028188
Első szerző:Kolonics Attila
Cím:BGP-15, a new type of insulin sensitizer / Kolonics A., Literati-Nagy P., Peitl B., Bajza A., Jaszlits L., Laszlo L., Horvath T., Kulcsar E., Porszasz R., Paragh G., Bernath S., Literati B., Koranyi L., Szilvassy Z., Tory K.
Dátum:2006
ISSN:0012-1797
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idézhető absztrakt
Megjelenés:Diabetes. - 55 : Suppl.1 (2006), p. 483. -
További szerzők:Literati Nagy Péter Peitl Barna (1972-) (orvos, farmakológus) Bajza Ágnes (1970-) (biológus) Jaszlits László László Lajos Horváth Tünde Kulcsár Enikő Pórszász Róbert (1965-) (farmakológus, klinikai farmakológus) Paragh György (1953-) (belgyógyász) Bernáth Sándor Literáti-Nagy Botond Korányi László Szilvássy Zoltán (1957-) (belgyógyász, farmakológus, klinikai farmakológus) Tory Kálmán
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5.

001-es BibID:BIBFORM044909
035-os BibID:PMID:10385246
Első szerző:Peitl Barna (orvos, farmakológus)
Cím:Capsaicin-insensitive sensory-efferent meningeal vasodilatation evoked by electrical stimulation of trigeminal nerve fibres in the rat / Barna Peitl, Gábor Pethő, Róbert Pórszász, József Németh, János Szolcsányi
Dátum:1999
ISSN:0007-1188
Megjegyzések:Antidromic vasodilatation and plasma extravasation to stimulation of the trigeminal ganglion or its perivascular meningeal fibres was investigated by laser-Doppler flowmetry and 125I-labelled bovin serum albumin in the dura mater and in exteroceptive areas (nasal mucosa, upper eyelid) of anaesthetized rats pretreated with guanethidine and pipecuronium. 2 Trigeminal stimulation at 5 Hz for 20 s elicited unilateral phasic vasodilatation in the dura and lasting response in the nasal mucosa. Resiniferatoxin (1-3 microg kg(-1) i.v.), topical (1%) or systemic capsaicin pretreatment (300 mg kg(-1) s.c. plus 1 mg kg(-1) i.v.) did not inhibit the meningeal responses but abolished or strongly inhibited the nasal responses. Administration of vinpocetine (3 mg kg(-1) i.v.) increased both basal blood flow and the dural vasodilatation to perivascular nerve stimulation. 3. Dural vasodilatation to trigeminal stimulation was not inhibited by the calcitonin gene-related peptide-1 receptor (CGRP-1) antagonist hCGRP8-37 (15 or 50 microg kg(-1) i.v), or the neurokinin-1 receptor antagonist RP 67580 (0.1 mg kg(-1) i.v.) although both antagonists inhibited the nasal response. Neither mucosal nor meningeal responses were inhibited by atropine (5 mg kg(-1) i.v.), hexamethonium (10 mg kg(-1) i.v.) or the vasoactive intestinal polypeptide (VIP) antagonist (p-chloro-D-Phe6-Leul7)VIP (20 microg kg(-1) i.v.). 4. Plasma extravasation in the dura and upper eyelid elicited by electrical stimulation of the trigeminal ganglion was almost completely abolished in rats pretreated with resiniferatoxin (3 microg kg(-1) i.v.). 5. It is concluded that in the rat meningeal vasodilatation evoked by stimulation of trigeminal fibres is mediated by capsaicin-insensitive primary afferents, while plasma extravasation in the dura and upper eyelid and the vasodilatation in the nasal mucosa are mediated by capsaicin-sensitive trigeminal fibres.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
egyetemen (Magyarországon) készült közlemény
Megjelenés:British Journal of Pharmacology. - 127 : 2 (1999), p. 457-467. -
További szerzők:Pethő Gábor Pórszász Róbert (1965-) (farmakológus, klinikai farmakológus) Németh József (Pécs) Szolcsányi János (Pécs)
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6.

001-es BibID:BIBFORM020328
Első szerző:Peitl Barna (orvos, farmakológus)
Cím:Sensory nitrergic meningeal vasodilatation and non-nitrergic plasma extravasation in anaesthesized rats / Barna Peitl, József Németh, János Szolcsányi, Zoltán Szilvássy, Róbert Pórszász
Dátum:2004
Megjegyzések:The aim of the present study was to evaluate the role of nitric oxide (NO) of sensory neural origin in neurogenic inflammatory response in the trigeminovascular system. Antidromic vasodilatation and plasma extravasation in response to electrical stimulation (15 V, 5 Hz, 0.5 ms, 100 impulses) of the trigeminal ganglion were investigated in the dura mater and nasal mucosa/upper eyelid by laser Doppler flowmetry and [(125)I]-labelled bovine serum albumin, respectively. Electrical stimulation of the trigeminal ganglion of rats elicited a reproducible ipsilateral enhancement of both meningeal and nasal mucosal blood flow. N(omega)-nitro-L-arginine (L-NNA; 4, 8, and 16 mg/kg, i.v.), a nonselective inhibitor of nitric oxide synthase (NOS), inhibited antidromic vasodilatation both in the dura mater (15.86+/-2.05%, 22.82+/-2.51%, and 36.28+/-4.37%) and nasal mucosa (35.46+/-8.57%, 58.72+/-9.2%, and 89.99+/-8.94%) in a dose-dependent manner. Specific inhibitors of neuronal NOS, 7-nitroindazole (7-NI; 20 mg/kg, i.v.) and 3-bromo-7-nitroindazole (3Br-7NI; 10 mg/kg, i.v.) were administered to assess the possible role of NO released from the trigeminal sensory fibres. The meningeal vasodilatation was inhibited by both 3Br-7NI and 7-NI (63.36+/-7.7% and 49+/-6.5%, respectively). The nasal hyperaemic response was also reduced by 3Br-7NI (78.26+/-8.7%). Plasma extravasation in the dura mater and upper eyelid evoked by electrical stimulation of the trigeminal ganglion (25 V, 5 Hz, 0,5 ms, 5 min), expressed as extravasation ratios (ERs) of the stimulated vs. nonstimulated sides, was 1.80+/-0.8 and 4.63+/-1.24, respectively. This neurogenic oedema formation was not inhibited by neither L-NNA nor 3Br-7NI. It is concluded that neural nitrergic mechanisms are involved in the meningeal vasodilatation evoked by electrical stimulation of the trigeminal ganglion.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
meningeal vasodilatation
non-nitrergic
plasma extravasation
Megjelenés:European Journal of Pharmacology. - 497 : 3 (2004), p. 293-299. -
További szerzők:Németh József (Pécs) Szolcsányi János (Pécs) Szilvássy Zoltán (1957-) (belgyógyász, farmakológus, klinikai farmakológus) Pórszász Róbert (1965-) (farmakológus, klinikai farmakológus)
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7.

001-es BibID:BIBFORM044988
035-os BibID:PMID:10081702
Első szerző:Pethő Gábor
Cím:Spike generation from dorsal roots and cutaneous afferents by hypoxia or hypercapnia in the rat in vivo / Gábor Pethő, Róbert Pórszász, Barna Peitl, János Szolcsányi
Dátum:1999
Megjegyzések:The present study aimed at investigating the responsiveness of different parts of the primary afferent neurones to a brief hypoxia, hypercapnia or ischaemia under in vivo conditions. Action potentials were recorded in separate groups of anaesthetized rats from (i) the peripheral end of the central stump of the cut L3, L4 or L5 dorsal root (dorsal root preparation); (ii) the central end of the peripheral stump of the cut saphenous nerve (saphenous-receptor preparation); (iii) the distal end of a segment of the saphenous nerve cut at both ends (axon preparation). In paralysed animals interruption of artificial ventilation for 20-60 s elicited or increased the frequency of action potentials in both the dorsal root and saphenous-receptor preparations. Activation of these preparations was also achieved by inspiration of gas mixtures containing 10-0% oxygen (mixed with nitrogen) or 20-50% carbon dioxide (mixed with oxygen) which elicited in the blood a decrease in PO2 or an increase in PCO2 with a fall in pH. Occlusion of the femoral artery for 3 min also caused spike generation in the saphenous-receptor preparations with little alteration in blood pressure. All these stimuli failed to evoke action potentials in the axon preparations. Systemic (300 mg kg-1 s.c.) or perineural (2%) capsaicin pretreatment failed to inhibit the effect of hypoxia, hypercapnia or ischaemia, indicating a significant contribution of capsaicin-insensitive neurones to the responses. It is concluded that central and peripheral terminals but not axons of primary afferent neurones are excited by a brief hypoxia or hypercapnia and the peripheral terminals by a short local ischaemia as well. Excitation of central terminals by hypoxia or hypercapnia revealed in this way an antidromic activation of dorsal roots in response to natural chemical stimuli.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Experimental Physiology. - 84 : 1 (1999), p. 1-15. -
További szerzők:Pórszász Róbert (1965-) (farmakológus, klinikai farmakológus) Peitl Barna (1972-) (orvos, farmakológus) Szolcsányi János (Pécs)
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8.

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)
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9.

001-es BibID:BIBFORM020269
Első szerző:Szilvássy Judit (fül- orr- gégész)
Cím:Neurogenic insulin resistance in guinea-pigs with cisplatin-induced neuropathy / Judit Szilvássy, István Sziklai, Réka Sári, József Németh, Barna Peitl, Robert Porszasz, János Lonovics, Zoltán Szilvássy
Dátum:2006
Megjegyzések:The aim of the present work was to study whether neurotoxicity produced by cisplatin modified tissue insulin sensitivity in guinea-pigs. One week after selective sensory denervation of the anterior hepatic plexus by means of perineurial 2% capsaicin treatment, hyperinsulinaemic euglycaemic glucose clamp were performed to estimate insulin sensitivity in male guinea-pigs. The guinea-pigs underwent regional sensory denervation of the anterior hepatic plexus exhibited insulin resistance, whereas systemic capsaicin desensitization increased insulin sensitivity. Intraportal administration of L-nitro-arginine methyl ester (L-NAME decreased, whereas capsaicin increased insulin sensitivity. Neither atropine nor acetylcholine produced any significant effect. In animals with preceding regional capsaicin desensitization, none of the pharmacological maneuvers modified the resulting insulin resistant state. Cisplatin pretreatment induced sensory neuropathy and decreased insulin sensitivity. Insulin sensitivity did not change after either regional or systemic capsaicin desensitization in the cisplatin-treated animals. CGRP(8-37), a nonselective calcitonin gene-related peptide (CGRP) antagonist (50 microg/kg i.v.), significantly increased insulin sensitivity in normal animals but only a tendency to insulin sensitization was seen after cisplatin treatment. Cisplatin treatment, similar to regional capsaicin desensitization of the anterior hepatic plexus, produced a significant decrease in insulin-stimulated uptake of 2-deoxy-D [L-14C] glucose in cardiac and gastrocnemius muscle with no effect on percentage suppression of endogenous glucose production by hyperinsulinaemia. We conclude that the majority of cisplatin-induced insulin resistance is related to functional deterioration of the hepatic insulin sensitizing substance (HISS) mechanism.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
neurogenic insulin
insulin resistance
cisplatin-induced
neuropathy
Megjelenés:European Journal of Pharmacology. - 531 : 1-3 (2006), p. 217-225. -
További szerzők:Sziklai István (1954-) (fül-orr-gégész) Sári Réka (farmakológus) Németh József (1954-) (vegyész, analitikus) Peitl Barna (1972-) (orvos, farmakológus) Pórszász Róbert (1965-) (farmakológus, klinikai farmakológus) Lonovics János (Szeged) Szilvássy Zoltán (1957-) (belgyógyász, farmakológus, klinikai farmakológus)
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