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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:BIBFORM020306
Első szerző:Djazayeri, Katayoun
Cím:Accelerated recovery of 5-fluorouracil-damaged bone marrow after rosiglitazone treatment / Katayoun Djazayeri, Zoltán Szilvássy, Barna Peitl, József Németh, László Nagy, Attila Kiss, Boglárka Szabó, Ilona Benkő
Dátum:2005
Megjegyzések:AbstractOur preliminary data indicate that rosiglitazone may be myeloprotective. We investigated whether it can modify bone marrow recovery. Five-day pre-treatment with rosiglitazone significantly accelerated recovery of 5-fluorouracil-damaged bone marrow in mice. Frequency and femoral content of granulocyte-macrophage progenitors reached mean baseline faster in pre-treated groups than in 5-fluorouracil-treated controls. Consequently, neutropenia was milder. Five-day insulin pre-treatment had similar effects in vivo. Insulin supports in vitro hematopoiesis. The observed myeloprotection demonstrated the importance of insulin in vivo. Clinical use of insulin to moderate myelotoxicity is impractical but rosiglitazone, an insulin sensitizer, could offer hope. Although rosiglitazone tends to increase plasma insulin levels, the significant myeloprotection was partly due to direct effects on progenitors. In vitro rosiglitazone enhanced the survival of both murine progenitor and human mobilized blood stem cells in the presence of 5-fluorouracil, the effect of which was neutralized by a peroxisome-proliferator-activated receptor-gamma antagonist.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
5-fluorouracil
5-fluorouracil-damaged
bone marrow
rosiglitazone
Megjelenés:European Journal of Pharmacology. - 522 : 1-3 (2005), p. 122-129. -
További szerzők:Peitl Barna (1972-) (orvos, farmakológus) Németh József (Pécs) Nagy László (1966-) (molekuláris sejtbiológus, biokémikus) Kiss Attila (1942-) (belgyógyász, haematológus) Szabó Boglárka Benkő Ilona (1954-) (orvos, farmakológus) Szilvássy Zoltán (1957-) (belgyógyász, farmakológus, klinikai farmakológus)
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3.

001-es BibID:BIBFORM019120
Első szerző:Horváth Péter
Cím:Decreased sensory neuropeptide release in isolated bronchi of rats with cisplatin-induced neuropathy / Peter Horvath, Judit Szilvassy, Jozsef Nemeth, Barna Peitl, Maria Szilasi, Zoltan Szilvassy
Dátum:2005
ISSN:0014-2999
Megjegyzések:We studied if attenuated neurogenic bronchoconstriction was associated with a change in sensory neuropeptide release in preparations from rats with cisplatin-induced neuropathy. Electrical field stimulation (100 stimuli, 20 V, 0.1 ms, 20 Hz) induced an increase in the release of somatostatin, calcitonin gene-related peptide (CGRP) and substance P determined by radioimmunoassay from baseline 0.18+/-0.01, 0.17+/-0.01 and 0.86+/-0.02, to 0.59+/-0.02, 1.77+/-0.04 and 5.96 fmol/mg wet tissue weight, respectively, in organ fluid of tracheal tubes from rats. This was significantly attenuated to post-stimulation values of 0.36+/-0.02, 0.45+/-0.02, 4.68+/-0.24 fmol/mg wet tissue weight for somatostatin, CGRP, and substance P, respectively, with a significant decrease in field stimulation-induced contraction of bronchial preparations from animals 11 days after a 5-day treatment period with cisplatin (1.5 mg/kg i.p. once a day). The cisplatin-treated animals developed sensory neuropathy characterized by a 40% decrease in femoral nerve conduction velocity. The results show that a decrease in tracheo-bronchial sensory neuropeptide release associates with feeble bronchomotor responses in rats with cisplatin-induced sensory neuropathy.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
neuropeptide
neuropeptide release
bronchi
cisplatin-induced neuropathy
Megjelenés:European Journal Of Pharmacology 507 : 1-3 (2005), p. 247-252. -
További szerzők:Szilvássy Judit (1960-2022) (fül- orr- gégész) Németh József (Pécs) Peitl Barna (1972-) (orvos, farmakológus) Szilasi Mária (1953-) (tüdőgyógyász, klinikai immunológus, allergológus, belgyógyász) Szilvássy Zoltán (1957-) (belgyógyász, farmakológus, klinikai farmakológus)
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4.

001-es BibID:BIBFORM020464
Első szerző:Németh József (Pécs)
Cím:Impairment of neurogenic inflammatory and anti-inflammatory responses in diabetic rats / József Németh, Márta Thán, Réka Sári, Barna Peitl, Gábor Oroszi, Beatrix Farkas, János Szolcsányi, Zoltán Szilvássy
Dátum:1999
Megjegyzések:AbstractThe effect was studied of a primary (preconditioning) neurogenic inflammatory challenge induced by electrical stimulation of the peripheral stump of the sciatic nerve (20 V, 0.5 ms, 5 Hz, for 5 min) on neurogenic oedema (5 min later) induced by stimulation of the contralateral sciatic nerve. Plasma extravasation due to the second stimulation was decreased by 52.7+/-3.1% (P<0.01) in normal animals and by 29.7+/-2.2 and 18.1+/-1.5% with 50 mg/kg streptozotocin pretreatment i.v. 4 and 8 weeks previously, respectively. Subsequently, bilateral sciatic nerve stimulation increased baseline plasma somatostatin levels from 6.4+/-0.3, 11. 7+/-1.4, and 16.8+/-3.8 to 28.3+/-2.9 (P<0.01), 17.9+/-3.7, and 25. 1+/-1.7 pmol/l in normal, and 4- and 8-week diabetic animals, respectively. We conclude that experimental diabetes impairs the capability of a preconditioning neurogenic inflammatory episode to elicit a systemic anti-inflammatory effect. This is accompanied by a deficiency in elevation of the plasma somatostatin level in response to nerve stimulation, although the baseline plasma somatostatin level increases proportionally to the duration of experimental diabetes.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
neurogenic inflammatory
neurogenic inflammatory responses
anti-inflammatory
anti-inflammatory responses
Megjelenés:European Journal of Pharmacology. - 386 : 1 (1999), p. 83-88. -
További szerzők:Thán Márta Sári Réka (farmakológus) Peitl Barna (1972-) (orvos, farmakológus) Oroszi Gábor (Pécs) Farkas Beatrix Szolcsányi János (Pécs) Szilvássy Zoltán (1957-) (belgyógyász, farmakológus, klinikai farmakológus)
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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:BIBFORM020242
Első szerző:Peitl Barna (orvos, farmakológus)
Cím:Meal-induced enhancement in insulin sensitivity is not triggered by hyperinsulinemia in rats / Barna Peitl, Róbert Döbrönte, József Németh, Csaba Pankucsi, Réka Sári, Angelika Varga, Zoltán Szilvássy
Dátum:2009
Megjegyzések:Several reports confirmed the phenomenon of postprandial increase in whole-body insulin sensitivity. Although the initial step of this process is unknown, the pivotal role of postprandial hyperinsulinemia has strongly been suggested. The aim of the present study was to determine whether hyperinsulinemia per se induces insulin sensitization in healthy male Wistar rats. Rapid insulin sensitivity test (RIST) were performed in fasted, anesthetized rats before and during stable hyperinsulinemia achieved by hyperinsulinemic euglycemic glucose clamping (HEGC) with insulin infused either through the jugular vein (systemic HEGC) or into the portal circulation (portal HEGC) at a rate of 3 mU/(kg min). Insulin sensitivity expressed by the rapid insulin sensitivity (RIST) index (in milligrams per kilogram) was characterized by the total amount of glucose needed to maintain prestudy blood glucose level succeeding an intravenous bolus infusion of 50 mU/kg insulin over 5 minutes. In fasted animals, the RIST index was 37.4 +/- 3.1 mg/kg. When hyperinsulinemia mimicking the postprandial state was achieved by systemic HEGC, the RIST index (39.7 +/- 10.6 mg/kg) showed no significant changes as compared with the pre-HEGC values. Hyperinsulinemia achieved by portal insulin infusion also failed to modify the RIST index (35.7 +/- 4.3 mg/kg). The results demonstrate that acute hyperinsulinemia, no matter how induced, does not yield any sensitization to the hypoglycemic effect of insulin.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
insulin
insulin sensitivity
hyperinsulinemia
Megjelenés:Metabolism: Clinical and Experimental. - 58 : 3 (2009), p. 328-332. -
További szerzők:Döbrönte Róbert Németh József (Pécs) Pankucsi Csaba (farmakológus) Sári Réka (farmakológus) Varga Angelika (1977-) (biológus) Szilvássy Zoltán (1957-) (belgyógyász, farmakológus, klinikai farmakológus)
Pályázati támogatás:HO7-BEL 74162
Egyéb
K75965
OTKA
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7.

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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8.

001-es BibID:BIBFORM017767
Első szerző:Peitl Barna (orvos, farmakológus)
Cím:The prandial insulin sensitivity-modifying effect of vagal simulation in rats / Barna Peitl, Róbert Döbrönte, József Németh, Géza Mezey, Péter Kovács, György Paragh, Zoltán Szilvássy
Dátum:2005
ISSN:0026-0495
Megjegyzések:The effect of left cervical vagal nerve stimulation was studied on insulin sensitivity to test the proposed permissive insulin-sensitizing role of hepatic vagal parasympathetic efferent pathways in fasted and fed anesthetized rats. In fed animals, electrical stimulation (square impulses: 25 V, 5 Hz, 0.5 milliseconds over 15 minutes) of the vagal nerve induced hyperglycemia and an increase in plasma insulin immunoreactivity. Atropine (1.0 mg/kg intravenously) induced insulin resistance estimated by rapid insulin sensitivity testing. This was amplified when the vagal nerve was stimulated. The insulin-resistant state developed by fasting was not modified by either treatment with atropine or electrical stimulation. We conclude that both parasympathetic cholinergic and noncholinergic vagal efferents modulate postprandial neurogenic insulin sensitivity adjustments.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
prandial insulin
vagal stimulation
modifying effect
Megjelenés:Metabolism-Clinical and Experimental. - 54 : 5 (2005), p. 579-583. -
További szerzők:Döbrönte Róbert Németh József (Pécs) Mezey Géza (1978-) (idegsebész) Kovács Péter (1947-) (belgyógyász, kardiológus, klinikai farmakológus) Paragh György (1953-) (belgyógyász) Szilvássy Zoltán (1957-) (belgyógyász, farmakológus, klinikai farmakológus)
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9.

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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