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1.

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)
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2.

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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Intézményi repozitóriumban (DEA) tárolt változat
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3.

001-es BibID:BIBFORM020441
Első szerző:Sári Réka (farmakológus)
Cím:Impairment by lovastatin of neural relaxation of the rabbit sphincter of Oddi / Reka Sari, Jozsef Nemeth, Robert Porszasz, Peter Horvath, Ingolf E. Blasig, Peter Ferdinandy, Istvan Nagy, Janos Lonovics, Zoltan Szilvassy
Dátum:2001
Megjegyzések:AbstractWe sought whether inhibition of cholesterol biosynthesis by lovastatin influenced the nitrergic relaxation response of the sphincter of Oddi. Rabbit sphincters of Oddi rings were tested for changes in isometric tension in response to field stimulation in the presence of 4 microM guanethidine and 1 microM atropine. Tissue samples were then analyzed for cAMP and cGMP content by radioimmunoassay for nitric oxide concentration by electron spin resonance and for vasoactive intestinal peptide and calcitonin gene-related peptide (CGRP) release by radioimmunoassay. Membrane G(salpha) protein was determined by Western blot analysis. Field stimulation relaxed the preparations with an increase in nitric oxide, cAMP and cGMP concentrations at increased calcitonin gene-related peptide and vasoactive intestinal polypeptide (VIP) release. Preparations from rabbits pre-treated with lovastatin (5 mg/kg/day intragastrically, over 5 days) contracted under the same conditions with an attenuated cGMP-increase at preserved increase in NO content and neuropeptide release. The relaxation was recaptured combining lovastatin with farnesol (1 mg/kg intravenously, twice a day for 5 days). The field stimulation-induced increase in cyclic nucleotides was also restored. Lovastatin decreased membrane G(salpha) protein content, which was re-normalized by farnesol. Farnesol treatment reinstates neurogenic relaxation of the sphincter of Oddi deteriorated by lovastatin possibly by normalizing G-protein coupling.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
Impairment by lovastatin
lovastatin
neural relaxation
Megjelenés:European Journal of Pharmacology. - 432 : 1 (2001), p. 91-97. -
További szerzők:Németh József (Pécs) Pórszász Róbert (1965-) (farmakológus, klinikai farmakológus) Horváth Péter Blasig, Ingolf E. Ferdinándy Péter Nagy István (orvos) Lonovics János (Szeged) Szilvássy Zoltán (1957-) (belgyógyász, farmakológus, klinikai farmakológus)
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Intézményi repozitóriumban (DEA) tárolt változat
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4.

001-es BibID:BIBFORM020459
Első szerző:Szilvássy Judit (fül- orr- gégész)
Cím:Impaired bronchomotor responses to field stimulation in guinea-pigs with cisplatin-induced neuropathy / Judith Szilvássy, Istvan Sziklai, Tamas Racz, Peter Horvath, Gyorgy Rabloczky, Zoltan Szilvassy
Dátum:2000
Megjegyzések:AbstractPre-treatment with cisplatin (3 mg/kg) i.p. once a day over 6 days induced sensory neuropathy as confirmed by femoral nerve conduction velocity test and significantly decreased contractions induced by electrical field stimulation (100 stimuli, 20 V, 0.1 ms, 20 Hz) in isolated main bronchial rings from guinea-pigs. The field stimulation-induced non-adrenergic, non-cholinergic (NANC) relaxations, however, were amplified in rings from animals with cisplatin neuropathy. The NANC relaxation response was completely blocked by 30 microM N(G)-nitro-L-arginine methyl ester in preparations from both control and cisplatin-treated animals. Superoxide dismutase (40 units/ml) was without effect on NANC relaxation in control rings, however, it substantially decreased NANC relaxation in preparations from animals with cisplatin neuropathy. These results show that cisplatin-induced sensory neuropathy is accompanied by attenuation of neural bronchoconstriction and an enhanced NANC relaxation. The latter is in part attained by an increased peripheral superoxide production.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
Impaired bronchomotor responses
bronchomotor responses
field stimulation
cisplatin-induced neuropathy
Megjelenés:European Journal of Pharmacology. - 403 : 3 (2000), p. 259-265. -
További szerzők:Sziklai István (1954-) (fül-orr-gégész) Rácz Tamás (1961-) (fül-orr-gégész) Horváth Péter Rablóczky György Szilvássy Zoltán (1957-) (belgyógyász, farmakológus, klinikai farmakológus)
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Intézményi repozitóriumban (DEA) tárolt változat
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5.

001-es BibID:BIBFORM020438
Első szerző:Szilvássy Judit (fül- orr- gégész)
Cím:Feeble bronchomotor responses in diabetic rats in association with decreased sensory neuropeptide release / Judit Szilvássy, Istvan Sziklai, Peter Horvath, Maria Szilasi, József Németh, Péter Kovács, Zoltán Szilvássy
Dátum:2002
Megjegyzések:AbstractType I diabetes is associated with a low incidence of asthma. We tested whether a decrease in sensory neuropeptide release is associated with an attenuated bronchoconstrictive response to field stimulation (FS; 100 stimuli, 20 V, 0.1 ms, 20 Hz) in streptozotocin (STZ)-induced diabetes. The organ fluid of the preparations were also tested for substance P, calcitonin gene-related peptide (CGRP), and somatostatin concentrations by RIA. Preparations were from either normal rats or those pretreated with 50 mg/kg STZ iv 8 wk before experiment. A group of STZ-treated animals was supplied with insulin delivery (4 IU/day sc) implants between 4 and 8 wk. A subgroup was formed to study the effect of capsaicin desensitization. The atropine-resistant contraction was attenuated by diabetes without capsaicin-sensitive relaxation response. Exogenous CGRP and substance P potentiated, whereas somatostatin inhibited (1 nM-10 microM) the FS-induced contractions in rings from either group. FS released somatostatin, CGRP, and substance P from 0.17 +/- 0.024, 0.15 +/- 0.022, and 1.65 +/- 0.093 to 0.58 +/- 0.032, 0.74 +/- 0.122, and 5.34 +/- 0.295 in preparations from normal, and from 0.19 +/- 0.016, 0.11 +/- 0.019, and 0.98 +/- 0.116 to 0.22 +/- 0.076, 0.34 +/- 0.099, and 1.84 +/- 0.316 fmol/mg wet wt in preparations from diabetic rats. Insulin supplementation restored neuropeptide release in rings from STZ-treated rats. The results show that the decreased FS-induced contractions occurred with a decrease in sensory neuropeptide release in STZ-diabetic rats.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
bronchomotor responses
decreased sensory
neuropeptide
Megjelenés:American Journal of Physiology. - 282 : 5 (2002), p. 1023-1030. -
További szerzők:Sziklai István (1954-) (fül-orr-gégész) Horváth Péter Szilasi Mária (1953-) (tüdőgyógyász, klinikai immunológus, allergológus, belgyógyász) Németh József (Pécs) Kovács Péter (1939-) (farmakológus) Szilvássy Zoltán (1957-) (belgyógyász, farmakológus, klinikai farmakológus)
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Intézményi repozitóriumban (DEA) tárolt változat
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