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1.

001-es BibID:BIBFORM043850
035-os BibID:PMID:8813543
Első szerző:Abdel Salam, Omar M. E.
Cím:Effect of capsaicin and resiniferatoxin on gastrointestinal blood flow in rats / Omar M. E. Abdel Salam, János Szolcsányi, Róbert Pórszász, Gyula Mózsik
Dátum:1996
ISSN:0014-2999
Megjegyzések:The effect of capsaicin and resiniferatoxin on gastrointestinal blood flow was studied in anaesthetized rats by laser Doppler flowmetry. Resiniferatoxin injected into the jugular vein (0.08-1.6 nmol/kg) produced a marked and dose-dependent increase in gastric blood flow, while the effect of capsaicin (0.33-19.6 nmol/kg) was transient, variable and accompanied by profound systemic blood pressure changes. After acute bilateral cervical vagotomy combined with sympathetic neurone blockade (guanethidine 16 mumol/kg) or alpha-adrenoceptor blockade (phentolamine 1.6 mumol/kg), the vasodilator response to injected resiniferatoxin was more pronounced, indicating that the resiniferatoxin-induced gastric vasodilatation is not due to reflexes via parasympathetic or sympathetic efferent fibres. Resiniferatoxin given i.v. (0.08-0.64 nmol/kg) evoked a similar increase in the blood flow of the jejunum. Capsaicin (0.33-33 microM) or resiniferatoxin (0.16-1.6 microM) applied topically to the serosal surface of the stomach or jejunum produced a pronounced and long-lasting increase in blood flow after vagotomy and guanethidine treatment. The blood flow and blood pressure responses to capsaicin and resiniferatoxin were absent in rats desensitized with systemic capsaicin pretreatment. These laser Doppler data provide the first evidence for the effect of resiniferatoxin on gastrointestinal microcirculation and indicate the advantages of this agent and technique to study the sensory-efferent function of capsaicin-sensitive fibres.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:European Journal of Pharmacology. - 305 : 1-3 (1996), p. 127-36. -
További szerzők:Szolcsányi János (Pécs) Pórszász Róbert (1965-) (farmakológus, klinikai farmakológus) Mózsik Gyula
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2.

001-es BibID:BIBFORM043722
Első szerző:Benkó Rita
Cím:Effect of experimental diabetes on cholinergic, purinergic and peptidergic motor responses of the isolated rat bladder to electrical field stimulation or capsaicin / Benkó R., Lázár Z., Pórszász R., Somogyi G. T., Barthó L.
Dátum:2003
ISSN:0014-2999
Megjegyzések:An attempt has been made to pharmacologically isolate cholinergic, P(2) purinoceptor-mediated and peptidergic (capsaicin-sensitive, tachykinin-mediated) contraction of the guanethidine-treated rat bladder detrusor preparation, in vitro. The effect of experimental diabetes was assessed on these types of contraction. Responses were evoked by electrical field stimulation (single shocks or 1 Hz for 30 s or 10 Hz for 40 s). Single shocks and 1-Hz stimulation were applied in the presence of (a). atropine (1 microM) or (b). P(2) purinoceptor antagonists (50 microM pyridoxalphosphate-6-azophenyl-2',4'-disulfonic acid) [PPADS] plus 100 microM suramin. Long-term electrical field stimulation (10 Hz for 40 s) (c). was applied with both atropine and the P(2) purinoceptor antagonists present in the organ bath. The effects of capsaicin (d). and ATP (e). were also studied. Three groups of experimental animals were used: streptozotocin-treated (50 mg.kg(-1) i.p., 8 weeks before the experiment), parallel solvent-treated and untreated rats. (a). Responses to electrical field stimulation in the presence of atropine were reduced by half by PPADS plus suramin, but were resistant to capsaicin tachyphylaxis. They were enhanced in preparations taken from diabetic rats. (b). Contractions to electrical field stimulation in the presence of PPADS plus suramin were reduced by 2/3 by atropine, but were left unchanged by capsaicin or diabetes. (c). Contractions to long-term stimulation had a quick and a sustained phase. Especially the latter was inhibited by capsaicin tachypyhlaxis; it was also strongly reduced in preparations taken from diabetic rats. (d). Contractions to capsaicin (30 nM and 1 microM) were resistant to tetrodotoxin, strongly reduced by a combination of tachykinin NK(1) and NK(2) receptor antagonists, and slightly reduced in preparations from diabetic animals. Capsaicin (1 microM) had no acute inhibitory action on cholinergic or purinergic responses, nor did it cause relaxation in precontracted preparations treated with tachykinin receptor antagonists. (e) ATP-induced contractions were strongly reduced by PPADS plus suramin (50 plus 100 microM) and to a similar degree by 100 plus 200 microM, respectively. It is concluded that experimental diabetes selectively impairs peptidergic, capsaicin-sensitive responses (especially those that involve impulse conduction) in the rat detrusor preparation. The contractile response to electrical field stimulation that remains after atropine plus the P(2) purinoceptor antagonists has a yet unknown transmitter background.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:European Journal Of Pharmacology. - 478 : 1 (2003), p. 73-80. -
További szerzők:Lázár Zsófia Pórszász Róbert (1965-) (farmakológus, klinikai farmakológus) Somogyi George T. Barthó Loránd
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3.

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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4.

001-es BibID:BIBFORM020420
Első szerző:Pórszász Róbert (farmakológus, klinikai farmakológus)
Cím:The sensory nitrergic nature of the hepatic insulin sensitizing substance mechanism in conscious rabbits / Robert Porszasz, Gyorgyi Legvari, Jozsef Nemeth, Peter N. Literati, Janos Szolcsanyi, Zoltan Szilvassy
Dátum:2002
Megjegyzések:AbstractFunctional deterioration of sensory fibres in the anterior hepatic plexus or intraportal administration of 7-nitro indazole (1 mg/kg), a selective inhibitor of neural nitric oxide (NO) synthase, caused insulin resistance as determined by hyperinsulinaemic (100 micro U/ml) euglycaemic (5.5 mmol/l) glucose clamping in chronically instrumented conscious rabbits. Intraportal nitroglycerin restored insulin sensitivity in either case. We conclude that NO of sensory neural origin plays a major role in endogenous neurogenic insulin sensitizing mechanisms.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
sensory nitrergic nature
hepatic insulin
sensitizing substance mechanism
Megjelenés:European Journal of Pharmacology. - 443 : 1-3 (2002), p. 211-212. -
További szerzők:Légvári Györgyi Németh József (Pécs) Literati Nagy Péter Szolcsányi János (Pécs) Szilvássy Zoltán (1957-) (belgyógyász, farmakológus, klinikai farmakológus)
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5.

001-es BibID:BIBFORM020414
Első szerző:Pórszász Róbert (farmakológus, klinikai farmakológus)
Cím:Capsaicin-induced nonneural vasoconstriction in canine mesenteric arteries / Robert Pórszász, Ágnes Porkoláb, Andrea Ferencz, Tünde Pataki, Zoltán Szilvássy, János Szolcsányi
Dátum:2002
Megjegyzések:AbstractProlonged cold storage (4 degrees C) of canine mesenteric arteries was used to reveal the role of nonneural mechanisms in capsaicin-induced vascular contraction. The EC(50) values of capsaicin were 3.0 microM, 670 and 104 nM in preparations made fresh, after a 1- or 2-week period of cold storage, respectively, indicating an enhanced contractile responsiveness of the denervated tissue to capsaicin. A similar exaggerated contractile response was seen with phenylephrine exclusively after a 1-week cold storage. For fresh, 1- and 2-week cold-stored arteries, the EC(50) of phenylephrine were 248, 38 and 30 nM, respectively. The maximum contraction produced by tyramine was decreased with time. The results suggest that capsaicin may attain vasoconstriction independent of neural elements.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
Capsaicin-induced
nonneural vasoconstriction
Megjelenés:European Journal of Pharmacology. - 441 : 3 (2002), p. 173-175. -
További szerzők:Porkoláb Ágnes (Pécs) Ferencz Andrea Pataki Tünde (1971-) (farmakológus, klinikai farmakológus) Szilvássy Zoltán (1957-) (belgyógyász, farmakológus, klinikai farmakológus) Szolcsányi János (Pécs)
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6.

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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7.

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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