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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)
Internet cím:	Szerző által megadott URL Intézményi repozitóriumban (DEA) tárolt változat
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001-es BibID:	BIBFORM020274
Első szerző:	Horváth Péter
Cím:	Changes in tracheo-bronchial sensory neuropeptide receptor gene expression pattern in rats with cisplatin-induced sensory neuropathy / Péter Horváth, Zoltán Szilvássy, Barna Peitl, Judit Szilvássy, Zsuzsanna Helyes, János Szolcsányi, József Németh
Dátum:	2006
ISSN:	0143-4179
Megjegyzések:	AbstractAn attenuated neurogenic broncho-constriction underpinned by a decrease in sensory neuropeptide release has been shown to be characteristic of cisplatin-induced neuropathy. The present work was to explore if beyond neuropeptide release, cisplatin at a treatment schedule attaining sensory neuropathy, produced changes in the expression of the receptors of sensory neuropeptides such as somatostatin, calcitonin gene-related peptide (CGRP) and substance P (SP) in bronchial tissue of the rat. Twenty-four Wistar rats were divided into three groups. The animals in the "Treatment groups 1 and 2" were given cisplatin (1.5mgkg(-1)) and mannitol (75mgkg(-1)) over 5 days. The rats in the "Control" group were given mannitol+isotonic saline. Four animals from each group were used to study the expression pattern of the neuropeptide receptors in bronchial tissue. The levels of somatostatin receptor 4 (SSTR 4), neurokinin 1 (NK1), neurokinin 2 (NK2) and CGRP receptor expression were examined by quantitative real time polymerase chain reaction (RT-PCR) method, 11 and 22 days after the last cisplatin/vehicle dose. The cisplatin treatment significantly increased plasma somatostatin immunoreactivity and the expression of SSTR4 receptor detected both on the 11th and 22nd post-treatment days with no change in either CGRP, NK1, and NK2 receptor gene expression or plasma CGRP and substance P levels. We conclude that cisplatin neuropathy is accompanied by an increase in plasma somatostatin immunoreactivity with an increase in SSTR4 expression in rats.
Tárgyszavak:	Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban tracheo-bronchial neuropeptide receptor cisplatin-induced
Megjelenés:	Neuropeptides. - 40 : 1 (2006), p. 77-83. -
További szerzők:	Szilvássy Zoltán (1957-) (belgyógyász, farmakológus, klinikai farmakológus) Peitl Barna (1972-) (orvos, farmakológus) Szilvássy Judit (1960-2022) (fül- orr- gégész) Helyes Zsuzsanna Szolcsányi János (Pécs) Németh József (1954-) (vegyész, analitikus)
Internet cím:	Szerző által megadott URL DOI Intézményi repozitóriumban (DEA) tárolt változat
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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)
Internet cím:	Szerző által megadott URL DOI Intézményi repozitóriumban (DEA) tárolt változat
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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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