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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:BIBFORM020389
Első szerző:Németh József (Pécs)
Cím:Impaired capsaicin-induced decrease in heart rate and coronary flow in isolated heart of diabetic rats / J. Németh, Z. Szilvássy, G. Oroszi, R. Pórszász, B. Jakab, J. Szolcsányi
Dátum:2001
ISSN:1588-2683
Megjegyzések:AbstractThe effect of capsaicin (0.1 microM) on heart rate and coronary flow was studied in Langendorff-perfused heart from streptozotocin-induced (50 mg/kg i.v.) diabetic rats where sensory neuropathy developed. In hearts from animals 4- and 8-week diabetes baseline heart rate and coronary flow decreased from 317.9 +/- 2.9 b.p.m. and 13.4 +/- 0.7 m/min to 255.1 +/- 12.7 and 219.8 +/- 2.8 b.p.m. and 8.9 +/- 0.6 and 10.0 +/- 0.1 ml/min (P<0.05), respectively. Capsaicin significantly decreased both variables in either normal or 4-week diabetic animals its effects, however, on coronary flow or heart rate were missing in preparations from 8-week diabetic rats. Endothelin-1 (0.1 nM), the putative mediator of the capsaicin effect, significantly decreased heart rate and coronary flow irrespective of the presence or absence of diabetes. In the femoral nerve of streptozotocin-treated animals conduction velocity involving both fast conducting A- and slow-conducting C-fibres was decreased proportional to the duration of the pre-existing diabetic state. It is concluded that in insulin deficient diabetes the diminished responses evoked by capsaicin on heart rate and coronary flow are signs of sensory neuropathy. This is related to a feeble endothelin release from sensory nerve endings without changes in post-receptor mechanisms mediating the endothelin effects.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény hazai lapban
Impaired capsaicin-induced
decrease in heart rate
coronary flow
decrease in coronary flow
Megjelenés:Acta Physiologica Hungarica. - 88 : 3-4 (2001), p. 207-218. -
További szerzők:Szilvássy Zoltán (1957-) (belgyógyász, farmakológus, klinikai farmakológus) Oroszi Gábor (Pécs) Pórszász Róbert (1965-) (farmakológus, klinikai farmakológus) Jakab Balázs (Pécs) Szolcsányi János (Pécs)
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3.

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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4.

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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5.

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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6.

001-es BibID:BIBFORM043723
Első szerző:Pintér Erika
Cím:Pharmacological characterisation of the somatostatin analogue TT-232 : effects on neurogenic and non-neurogenic inflammation and neuropathic hyperalgesia / Pintér E., Helyes Zs., Németh J., Pórszász R., Pethő G., Thán M., Kéri G., Horváth A., Jakab B., Szolcsányi J.
Dátum:2002
ISSN:0028-1298
Megjegyzések:The putative anti-inflammatory and anti-nociceptive activity of the heptapeptide somatostatin analogue TT-232 ( D-Phe-Cys-Tyr- D-Thr-Lys-Cys-Thr-NH(2)) was investigated in the rat and mouse, as well as its effect on neuropathic hyperalgesia, gastric ulceration and the release of sensory neuropeptides. In the rat, carrageenin-induced paw oedema was inhibited dose dependently by TT-232 (3x2.5-20 microg/kg i.v.). Evans blue accumulation induced by intraarticular bradykinin injection (0.5 nmol in 0.1 ml) was slightly, but significantly inhibited by a single TT-232 dose (5-20 microg/kg). Cutaneous neutrophil accumulation over a 3-h period after intradermal (i.d.) injection of carrageenin (1 mg/site) or interleukin 1beta (IL-1beta, 3 pmol/site) was inhibited significantly by TT-232 (3x80 microg/kg i.v.), while diclofenac (3x10 mg/kg i.v.) elicited significant inhibition only in the IL-1beta test. In the mouse, TT-232 potently decreased oedema formation induced by 2.5% capsaicin applied topically to the ear. Mechano-nociception in the rat hind-paw during neuropathic pain induced by partial sciatic nerve injury (model of Seltzer) was measured using the Randall-Selitto test. TT-232 (5-20 microg/kg i.p. on the 7th day after the operation) dose-dependently inhibited the mechano-nociceptive hyperalgesia. In vitro release of substance P (SP), calcitonin gene-related peptide (CGRP) and somatostatin from the isolated rat trachea in response to electrical field stimulation (40 V, 0.1 ms, 10 Hz, 120 s) of its nervous elements was inhibited significantly by 500 nM TT-232. The role of G protein-coupled receptors in the effect of TT-232 was indicated by the prevention of its inhibitory action on the release of sensory neuropeptides by incubation the tissue for 1 or 6 h with pertussis toxin (100 ng/ml). The release of sensory neuropeptides to in response to electrical nerve stimulation was not inhibited by a potent tyrosine kinase inhibitor, genistein (50 microM). TT-232 (up to 5 mg/kg i.p.) did not induce mucosal lesions in either the stomach or the duodenum. These data suggest that TT-232, a somatostatin analogue devoid of endocrine effects, is a promising lead molecule in the search for novel, broad-spectrum anti-inflammatory and analgesic agents.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Naunyn-Schmiedebergs Archives Of Pharmacology. - 366 : 2 (2002), p. 142-150. -
További szerzők:Helyes Zsuzsanna Németh József (Pécs) Pórszász Róbert (1965-) (farmakológus, klinikai farmakológus) Pethő Gábor Thán Márta Kéri György Horváth Anikó Jakab Balázs (Pécs) Szolcsányi János (Pécs)
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7.

001-es BibID:BIBFORM045973
035-os BibID:PMID:12871836
Első szerző:Pórszász Róbert (farmakológus, klinikai farmakológus)
Cím:Hepatic insulin sensitizing substance : a novel 'sensocrine' mechanism to increase insulin sensitivity in anaesthetized rats / Robert Porszasz, Gyorgyi Legvari, Tunde Pataki, Judith Szilvassy, Jozsef Nemeth, Peter Kovacs, Gyorgy Paragh, Janos Szolcsanyi, Zoltan Szilvassy
Dátum:2003
ISSN:0007-1188
Megjegyzések:We recently described the sensory nitrergic nature of the hepatic insulin sensitizing substance (HISS) mechanism linked to postprandial activation of anterior hepatic plexus fibres in rabbits. This study is designed to assess the involvement of the sensory pathways in this mechanism. 2. Selective sensory denervation of the anterior hepatic plexus (AHP) was achieved by a 3-day perineurial treatment with 2% capsaicin solution in Wistar rats (230-250 g). After 1 week, hyperinsulinaemic (100 micro U kg(-1)) euglycaemic (5.5 mmol kg(-1)) glucose clamp studies were performed to estimate insulin sensitivity. 3. The rats with regional AHP sensory denervation exhibited a significantly decreased insulin sensitivity, that is, 9.1+/-1.0 mg kg(-1) min(-1) glucose reinstalled euglycaemia vs 13.3+/-1.9 mg kg(-1) min(-1) glucose (P<0.01) in control rats. 4. Acute partial hepatic denervation by AHP cut was without effect on insulin sensitivity, whereas chronic hepatic denervation induced insulin resistance was similar to that achieved by regional AHP capsaicin treatment. 5. Intraportal administration of L-NAME (10 mg kg(-1)) decreased, whereas capsaicin (0.3 mg kg(-1) min(-1)) increased insulin sensitivity. Neither atropine (1 mg kg(-1)) nor acetylcholine (1-10 micro g mg min(-1)) produced any significant effect. In animals with preceding regional capsaicin desensitization, none of the pharmacological manoeuvres modified the resulting insulin-resistant state. 6. Cysteamine (200 mg kg(-1) s.c.) is known to cause functional somatostatin depletion-induced insulin resistance similar to that produced by either chronic partial hepatic denervation or perineurial AHP capsaicin desensitization. Intraportal capsaicin (0.3 mg kg(-1) min(-1)) was unable to modify insulin resistance achieved by cysteamine. 7. We conclude that capsaicin-sensitive sensory fibres play a crucial role in neurogenic insulin sensitization known as the HISS mechanism without involvement of anatomical reflex-mediated circuits. The results also suggest that HISS is identical to somatostatin of AHP sensory neural origin.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:British Journal of Pharmacology. - 139 : 6 (2003), p. 1171-1179. -
További szerzők:Légvári Györgyi Pataki Tünde (1971-) (farmakológus, klinikai farmakológus) Szilvássy Judit (1960-2022) (fül- orr- gégész) Németh József (Pécs) Kovács Péter (1939-) (farmakológus) Paragh György (1953-) (belgyógyász) Szolcsányi János (Pécs) Szilvássy Zoltán (1957-) (belgyógyász, farmakológus, klinikai farmakológus)
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8.

001-es BibID:BIBFORM043852
035-os BibID:PMID:7715824
Első szerző:Pórszász Róbert (farmakológus, klinikai farmakológus)
Cím:Antidromic vasodilatation in the striated muscle and its sensitivity to resiniferatoxin in the rat / Róbert Pórszász, János Szolcsányi
Dátum:1994
ISSN:0304-3940
Megjegyzések:Antidromic stimulation at the L4-L5 dorsal roots elicited a blood flow increase in ipsilateral muscles of lower extremities in rats measured by laser-Doppler flowmetry. Stimulation with 0.5 Hz; 20 V; 0.5 ms; 50 impulses was much less effective in muscle (18.9 +/- 6.4 area under the curve (%); mean +/- S.E.) than in the glabrous skin (80.5 +/- 8.25; P < 0.001). No significant difference was seen at 10 Hz (51.6 +/- 10.6 muscle; 60.6 +/- 17.3 skin). In the muscle the latency period of the response was long (37.4 +/- 3.1 s; mean +/- S.E.) at 0.5 Hz stimulation and was much shorter (8.8 +/- 0.8 s) at the higher frequency of 10 Hz, unlike in the skin where latency values at both frequencies were similar (9.7 +/- 0.8 s and 8.9 +/- 0.9 s, respectively). Antidromic vasodilatation in the muscle and the skin was abolished by resiniferatoxin (RTX) in an i.v. dose of 1.0 microgram/kg. These results provide a direct evidence for the existence of antidromic vasodilatation in striated muscle and suggest a mediating role for capsaicin/RTX sensitive afferents.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Neuroscience Letters 182 : 2 (1994), p. 267-270. -
További szerzők:Szolcsányi János (Pécs)
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9.

001-es BibID:BIBFORM043854
035-os BibID:PMID:1844797
Első szerző:Pórszász Róbert (farmakológus, klinikai farmakológus)
Cím:Circulatory and respiratory effects of capsaicin and resiniferatoxin on guinea pigs / R. Pórszász, J. Szolcsányi
Dátum:1991
ISSN:0237-6261
Megjegyzések:The cardiorespiratory effects of capsaicin and its novel analogue resiniferatoxin (RTX) have been investigated in urethan anaesthetized guinea pigs. Intravenously administered capsaicin (5-20 micrograms/kg) failed to elicit the full pulmonary chemoreflex, but after a latency of 2 seconds caused a short period of tachypnea (6-9 sec) and hypotension without bradycardia. An initial tachypnea was observed in response to 1 microgram/kg intravenously administered RTX, which was followed by a slowly developing shallow breathing, accompanied by an increase in blood pressure after a transient hypotensive effect. RTX inhibited the reflex response evoked by capsaicin for about 10 minutes. After bilateral vagotomy neither tachypnea nor hypotension was observed in response to capsaicin. These results show that in the guinea pig the vagally mediated pulmonary chemoreflex evoked by capsaicin and inhibited by RTX is qualitatively different from that described on other mammalian species (cat, dog, rat, etc.)
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény hazai lapban
Megjelenés:Acta Biochimica et Biophysica Hungarica. - 26 : 1-4 (1991), p. 131-138. -
További szerzők:Szolcsányi János (Pécs)
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10.

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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11.

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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12.

001-es BibID:BIBFORM094831
Első szerző:Szolcsányi János (Pécs)
Cím:Capsaicin and pharmacology of nociceptors / J. Szolcsányi, R. Pórszász, G. Pethő
Dátum:1994
ISBN:2-7420-0081-X
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok könyvfejezet
könyvrészlet
Megjelenés:Frontiers in pain research : peripheral neurons in nociception. Physio-pharmacological aspects / J. M. Besson, G. Guilbaud, H. Ollat. - p. 109-124. -
További szerzők:Pórszász Róbert (1965-) (farmakológus, klinikai farmakológus) Pethő G.
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
Borító:
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