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1.

001-es BibID:BIBFORM020090
Első szerző:Benyó Zoltán
Cím:Functional importance of neuronal nitric oxide synthase in the endothelium of rat basilar arteries / Zoltán Benyó, Zsombor Lacza, Tibor Hortobágyi, Christoph Görlach, Michael Wahl
Dátum:2000
ISSN:0006-8993
Megjegyzések:The function of the neuronal isoform of nitric oxide synthase (nNOS) was studied by comparing the effects of the specific nNOS blocker 7-nitro indazole monosodium salt (7-NINA) with that of the general NOS inhibitor N(G)-nitro-L-arginine (L-NA) in isolated rat basilar arteries (BAs). 7-NINA had no significant effect on the resting tone of the vessels, while both L-NA and 1H-[1,2,4]oxadiazolo[4, 3-a]quinoxalin-1-one (ODQ), a selective inhibitor of the soluble guanylyl cyclase, induced contraction. The relaxant effect of bradykinin was attenuated in the presence of L-NA but was not changed by 7-NINA. In contrast, 7-NINA markedly reduced the acetylcholine-induced, endothelium-dependent relaxation. These results demonstrate that nNOS contributes significantly to the relaxant effect of acetylcholine, indicating the functional importance of this isoenzyme in the cerebrovascular endothelium.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Brain Research. - 877 : 1 (2000), p. 79-84. -
További szerzők:Lacza Zsombor Hortobágyi Tibor (1965-) (patológus) Görlach, Christoph Wahl, Michael
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2.

001-es BibID:BIBFORM020080
Első szerző:Benyó Zoltán
Cím:Neuronal nitric oxide synthase in the cerebrovascular endothelium / Zoltán Benyó, Zsombor Lacza, Tibor Hortobágyi, Christoph Görlach, Péter Sándor, Michael Wahl
Dátum:2002
ISSN:0531-5131
Megjegyzések:The presence of the previous termneuronalnext term isoform of previous termnitricnext termprevious termoxidenext termprevious termsynthasenext term (nNOS) in astrocytes and neurons as well as in the perivascular nerves and previous termcerebrovascularnext termprevious termendotheliumnext term is well documented. The role of the nNOS, however, is not yet understood. In the present study, the function of previous termcerebrovascularnext term nNOS was investigated by comparing the effects of the specific nNOS blocker 7-nitro indazole monosodium salt (7-NINA) to that of the general NOS inhibitor NG-nitro-l-arginine (l-NA) in isolated rat basilar arteries (BAs). 7-NINA had no significant effect on the resting tone of the vessels, while l-NA induced strong contraction. The relaxant effect of bradykinin was attenuated in the presence of l-NA but was not changed by 7-NINA. In contrast, 7-NINA markedly reduced the acetylcholine-induced, previous termendotheliumnext term-dependent relaxation. These results demonstrate that nNOS contributes significantly to the relaxant effect of acetylcholine, indicating the functional importance of this isoenzyme in the previous termcerebrovascularnext termprevious termendotheliumnext term.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:International Congress Series. - 1235 (2002), p. 369-377. -
További szerzők:Lacza Zsombor Hortobágyi Tibor (1965-) (patológus) Görlach, Christoph Sándor Péter (1939-) Wahl, Michael
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3.

001-es BibID:BIBFORM020101
Első szerző:Görlach, Christoph
Cím:Neuronal nitric oxide synthase inhibitor has a neuroprotective effect in a rat model of brain injury / Christoph Görlach, Tibor Hortobágyi, Szabolcs Hortobágyi, Zoltán Benyó
Dátum:2000
Megjegyzések:Purpose: The aim of the present study was to assess the effects of neuronal nitric oxide synthase (NOS I) inhibitors and a combination of NOS I and NOS II inhibitors on lesion volume after experimental brain injury. Methods: Cold lesion of the brain was induced by application of a precooled (-78 degrees C) copper cylinder to the intact dura of the rat for 6 s. Brains were removed 24 h after the injury and lesion volume determined using the triphenyltetrazolium-chloride method. Results: The specific NOS I inhibitor 3-bromo-7-nitroindazole (Br-7-NI) reduced lesion volume significantly by 21 % compared with the vehicle control. In contrast, 7-nitroindazole had no effect on lesion volume. When aminoguanidine, a specific NOS II inhibitor, was adminis-tered after Br-7-NI, lesion volume was significantly reduced but not significantly more than with either compound alone. Conclusion: Brain injury after cold lesion is partly mediated by NOS I activity and can be attenuated successfully with Br-7-NI, while coin-hibition of NOS II does not improve the outcome significantly.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Restorative Neurology and Neuroscience. - 17 : 2-3 (2000), p. 71-76. -
További szerzők:Hortobágyi Tibor (1965-) (patológus) Hortobágyi Szabolcs Benyó Zoltán
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4.

001-es BibID:BIBFORM020089
Első szerző:Görlach, Christoph
Cím:Aminoguanidine reduces brain lesion volume after cold injury in the rat / C. Görlach, T. Hortobágyi, Z. Benyó, M. Wahl
Dátum:2000
ISSN:0031-6768
Megjegyzések:The aim of this study was to examine the effect of aminoguanidine (AG), which is thought to be an inducible nitric oxide synthase (iNOS) inhibitor, on lesion volume induced by cold injury in the parietal cortex of the rat. Cold lesion was induced by applying a precooled (-78 degrees C) copper cylinder (diameter: 3 mm) for 6 s to the intact dura. Lesion volume was determined using the triphenyltetrazolium-chloride method after 24 h. Pretreatment (1 h) and posttreatment (7.5 h) with AG [10 or 100 mg/kg body mass (BM)] reduced the lesion volume by 15 and 27%, respectively. However, posttreatment alone with AG (10 and 100 mg/kg BM) caused less of a reduction in lesion volume, by 8 and 20%, respectively. Pre- and posttreatment with AG also reduced the plasma nitrate/nitrite concentration compared with lesioned, saline-treated rats. Only a double therapy with AG (100 mg/kg BM) resulted in a significant reduction (48%) compared to saline alone, which was even larger (55%) compared to the sham group. The tissue nitrate/ nitrite concentration was significantly attenuated by pre- and posttreatment with AG (100 mg/kg BM) not only in the ipsilateral but also in the contralateral hemisphere. There was no difference regarding the parameter between shams and lesioned, saline-treated rats. Since combined pre- and posttreatment with AG reduced the lesion volume more than posttreatment alone and the plasma and tissue nitrate/nitrite concentrations were diminished during AG therapy compared to shams, we hypothesize that AG inhibits not only iNOS but also other enzymes, such as nNOS, diamine oxidase, and advanced glycation endproducts synthase.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Pflügers Archiv. - 440 : 2 (2000), p. 309-314. -
További szerzők:Hortobágyi Tibor (1965-) (patológus) Benyó Zoltán Wahl, Michael
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5.

001-es BibID:BIBFORM020084
Első szerző:Görlach, Christoph
Cím:Inhibition of endothelin-1 by the competitive ETA receptor antagonist Ro 61-1790 reduces lesion volume after cold injury in the rat / Christoph Görlach, Tibor Hortobágyi, Szabolcs Hortobágyi, Zoltan Benyó, Michael Wahl
Dátum:2001
ISSN:0031-6768
Megjegyzések:The aim of the present study was to investigate whether endothelin-1 (ET-1) in cerebral arteries is inhibited by the new, non-peptidergic ET(A) receptor antagonist Ro 61-1790 and, if it is, whether that inhibition reduces the lesion volume induced by cold injury in the parietal cortex. In vitro experiments were performed by measuring the isometric contractions of the rat middle cerebral and basilar arteries. A cold lesion was induced in vivo by the application of a pre-cooled (-78 degrees C) copper cylinder (diameter 3 mm) to the intact dura of rats for 6 s. After 24 h, lesion volume was determined by the triphenyltetrazolium method. In vitro, ET-1 (10(-12) - 3x10(-7) M) caused a dose-dependent contraction under resting conditions in the middle cerebral and basilar arteries of control rats. Ro 61-1790 (3x10(-9) M, 10(-7) M) shifted the concentration-effect curves for ET-1 in a parallel fashion (Emax unaltered). Post-treatment with Ro 61-1790 (10(-7)-10(-5) M) also inhibited the prior contraction elicited by ET-1 (3x10(-9) M) significantly. In vitro ET-1 application 3 h after the intracerebroventricular in vivo administration of Ro 61-1790 showed that the antagonist had reached the arteries and was bound to their ET(A) receptors. Intracerebroventricular pre-treatment of Ro 61-1790 reduced significantly the lesion volume by 23% after the injury. We conclude that ET-1 is involved in the development of secondary brain damage and that intracerebroventricular treatment with Ro 61-1790 reduces the size of the brain lesion caused by cold injury.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Pflügers Archiv. - 441 : 6 (2001), p. 844-849. -
További szerzők:Hortobágyi Tibor (1965-) (patológus) Hortobágyi Szabolcs Benyó Zoltán Wahl, Michael
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6.

001-es BibID:BIBFORM020083
Első szerző:Görlach, Christoph
Cím:Bradykinin B2, but not B1, receptor antagonism has a neuroprotective effect after brain injury / Christoph Görlach, Tibor Hortobágyi, Szabolcs Hortobágyi, Zoltán Benyó, Jane Relton, Eric Taylor Whalley, Michael Wahl
Dátum:2001
ISSN:0897-7151
Megjegyzések:The aim of the present study was to measure the therapeutic effects of bradykinin antagonists on lesion volume and brain swelling induced by cold injury in the parietal cortex of rat and mouse, respectively. Cold lesion was induced by application of a precooled (-78 degrees C) copper cylinder (3 mm diameter) to the intact dura of rat and mouse for 6 and 30 sec, respectively. At 24 h after the injury, the brains were removed and lesion volume was determined by the triphenyltetrazolium chloride method in rats. In the mouse, brain swelling was expressed as percentage increase in weight of the injured hemisphere which is compared to the contralateral side. After a subcutaneous priming dose of 18 microg/kg, a 1-h pretreatment and 24-h posttreatment using osmotic minipumps (300 ng/kg x min) was applied. Hoe140, a bradykinin receptor 2 antagonist, revealed a 19% reduction of lesion volume (p < 0.05) in the rat and a 14% diminution of brain swelling (p < 0.05) in the mouse. In contrast, the bradykinin receptor 1 antagonist, B 9858, had no effect on lesion volume compared to sham treated rats. When B 9858 was given in combination with Hoe140, a significant reduction in lesion volume was seen which was equivalent to and not different from that seen with Hoe140 alone in the rat. We conclude that brain injury after cold lesion is partially mediated by bradykinin and can be successfully treated with B2 antagonists.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Journal of Neurotrauma. - 18 : 8 (2001), p. 833-838. -
További szerzők:Hortobágyi Tibor (1965-) (patológus) Hortobágyi Szabolcs Benyó Zoltán Relton, Jane Whalley, Eric Taylor Wahl, Michael
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7.

001-es BibID:BIBFORM020088
Első szerző:Hortobágyi Tibor (patológus)
Cím:A novel brain trauma model in the mouse : effects of dexamethasone treatment / T. Hortobágyi, S. Hortobágyi, C. Görlach, T. Harkany, Z. Benyó, T. Görögh, W. Nagel, M. Wahl
Dátum:2000
ISSN:0031-6768
Megjegyzések:We describe a novel methodological approach for inducing cold lesion in the mouse as a model of human cortical contusion trauma. To validate its reproducibility and reliability, dexamethasone (Dxm) was repeatedly applied to demonstrate possible antioedematous drug effects. Following the induction of anaesthesia with halothane, the dura was exposed via trephination. Using a micromanipulator a pre-cooled (-78 degrees C) copper cylinder, 3 mm in diameter, was pressed down to a depth of 1 mm onto the dura for 30 s under microscopic control. The body temperature was held constant at 37 degrees C throughout the procedure. Blood pressure (BP), measured by a modified photosensor-monitored tail-cuff method, and acid-base status were not significantly different when analysed before and after cold lesion and prior to sacrifice. However, there was a marginal mixed respiratory and metabolic acidosis. The antioedematous action of Dxm was studied in four standard pre-and post-treatment paradigms: 2x0.5 mg/kg (II), 2x12.5 mg/kg (III) and 4x6.25 mg/kg (IV: 3x pre-, 1x post-treatment: V: 1x pre-, 3x post-treatment). Physiological saline injections served as controls. High doses of Dxm (III-V) significantly attenuated the cold-lesion-induced loss of body mass. Dxm treatment also resulted in a reduction of brain water content (III; P<0.05), and brain swelling (IV; P<0.05) in the lesioned hemisphere, relative to controls. In conclusion, we have characterized a novel cold lesion model in the mouse to mimic traumatic brain injury and the beneficial effect of Dxm treatment on the extent of brain oedema.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Pflügers Archiv. - 441 : 2-3 (2000), p. 409-415. -
További szerzők:Hortobágyi Szabolcs Görlach, Christoph Harkány Tibor Benyó Zoltán Görögh Tibor Nagel, W. Wahl, Michael
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8.

001-es BibID:BIBFORM020071
Első szerző:Hortobágyi Tibor (patológus)
Cím:Inhibition of neuronal nitric oxide synthase-mediated activation of poly(ADP-ribose) polymerase in traumatic brain injury : neuroprotection by 3-aminobenzamide / T. Hortobágyi, C. Görlach, Z. Benyó, Z. Lacza, S. Hortobágyi, M. Wahl, T. Harkany
Dátum:2003
ISSN:0306-4522
Megjegyzések:Focal traumatic injury to the cerebral cortex is associated with early activation of the neuronal isoform of nitric oxide synthase (nNOS), where high concentrations of nitric oxide-derived free radicals elicit extensive DNA damage. Subsequent activation of the nuclear repair enzyme poly(ADP-ribose) polymerase (PARP) causes a severe energy deficit leading to the ultimate demise of affected neurons. Little is known about the temporal relationship of nNOS and PARP activation and the neuroprotective efficacy of their selective blockade in traumatic brain injury. To determine the relationship of nNOS and PARP activation, brain injury was induced by cryogenic lesion to the somatosensory cortex applying a pre-cooled cylinder after trephination for 6 s to the intact dura mater. Pre-treatment with 3-bromo-7-nitroindazole (BrNI; 25 mg/kg, i.p.), and pre- or combined pre- and post-treatment with 3-aminobenzamide (AB; 10 mg/kg (i.c.v.) or 10 mg/kg/h (i.p.)) were used to inhibit nNOS and PARP, respectively. Cold lesion-induced changes in the somatosensory cortex and neuroprotection by BrNI and AB were determined using immunocytochemistry and immunodot-blot for detection of poly(ADP-ribose; PAR), the end-product of PARP activation, and the triphenyltetrazolium-chloride assay to assess lesion volume. PAR immunoreactivity reached its peak 30 min post-lesion and was followed by gradual reduction of PAR immunolabeling. BrNI pre-treatment significantly decreased the lesion-induced PAR concentration in damaged cerebral cortex. Pre-treatment by i.c.v. infusion of AB markedly diminished cortical PAR immunoreactivity and significantly reduced the lesion volume 24 h post-injury. In contrast, i.p. AB treatment remained largely ineffective. In conclusion, our data indicate early activation of PARP after cold lesion that is, at least in part, related to nNOS induction and supports the relevance of nNOS and/or PARP inhibition to therapeutic approaches of traumatic brain injury.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Neuroscience. - 121 : 4 (2003), p. 983-990. -
További szerzők:Görlach, Christoph Benyó Zoltán Lacza Zsombor Hortobágyi Szabolcs Wahl, Michael Harkány Tibor
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9.

001-es BibID:BIBFORM020086
Első szerző:Lacza Zsombor
Cím:NO synthase blockade induces chaotic cerebral vasomotion via activation of thromboxane receptors / Zsombor Lacza, Péter Hermán, Christoph Görlach, Tibor Hortobágyi, Péter Sándor, Michael Wahl, Zoltán Benyó
Dátum:2001
ISSN:0039-2499
Megjegyzések:BACKGROUND AND PURPOSE: Instability of the vascular tone (vasomotion) develops in several cerebrovascular diseases associated with endothelial dysfunction. The aim of the present study was to characterize cerebral vasomotion induced by diminished NO production with quantitative evaluation and chaos analysis. We tested the hypothesis that activation of thromboxane receptors mediates chaotic vasomotion after NO synthase (NOS) inhibition. METHODS: Measurements of vascular tension were carried out in isolated rat middle cerebral arteries. The extent of vasomotion was characterized by tension instability, whereas vasomotion complexity was assessed by chaos analysis. RESULTS: Blocking the basal NO release by N(omega)-nitro-L-arginine (L-NA) induced vasomotion, which was further enhanced and became irregular after UTP administration. The NO donor sodium nitroprusside was able to reverse this effect, and stable steady-state conditions reappeared. The guanylyl cyclase inhibitor 1H-(1,2,4)oxadiazolo[4,3-a]quinoxaline-1-one (ODQ) or coapplication of ODQ and L-NA had an effect identical to that of L-NA alone. Vasoconstriction by K(+) failed to induce vasomotion in intact vessels or in the presence of L-NA or ODQ. The thromboxane receptor antagonist ICI 192605 dose-dependently attenuated the vasomotion induced by L-NA and UTP, and the thromboxane-receptor agonist U-46619 induced significant vasomotion in intact vessels. CONCLUSIONS: The lack of NO in cerebral vessels provokes vulnerability to chaotic vasomotion, which can be triggered by the administration of UTP, whereas excess NO reverses it to stable conditions. The vasomotion after blockade of the NO-cGMP pathway is mediated by activation of thromboxane receptors.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Stroke. - 32 : 11 (2001), p. 2609-2614. -
További szerzők:Hermán Péter Görlach, Christoph Hortobágyi Tibor (1965-) (patológus) Sándor Péter (1939-) Wahl, Michael Benyó Zoltán
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10.

001-es BibID:BIBFORM020300
Első szerző:Wahl, Michael
Cím:Effects of bradykinin in the cerebral circulation / M. Wahl, C. Görlach, T. Hortobágyi, Z. Benyó
Dátum:1999
Megjegyzések:All components of an intracerebral kallikrein-kinin system have been described. Thus, bradykinin (BK) acting from the parenchymal side as well as from the blood side may influence cerebral microcirculation. BK is a potent dilator of extra- and intraparenchymal cerebral arteries when acting from the perivascular side. The vasomotor effect of BK is mediated by B2 receptors which appear to be located at the abluminal membrane of the endothelial cell. Signal transmission from the endothelial to the smooth muscle cell is mediated by NO, prostanoids, free radicals or H2O2 depending on the animal species and on the location of the artery. Selective opening of the blood-brain barrier for small tracers (Na+-fluorescein: MW, 376) has been found in cats during cortical superfusion or intraarterial application of BK. This leakage is mediated by B2 receptors located at the luminal and abluminal membrane of the endothelial cells and probably mediated by an opening of tight junctions. Formation of brain edema has been found after ventriculo-cisternal perfusion or interstitial infusion of BK. This can be explained by increase of vascular permeability and cerebral blood flow due to arterial dilatation thus enhancing driving forces for the extravasation. An increase of the BK concentration in the interstitial space of the brain up to concentrations which induce extravasation, dilatation and edema formation has been found under several pathological conditions. Thus, BK may be involved in edema and necrosis formation after cold lesion, concussive brain injury, traumatic spinal cord and ischemic brain injury.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény hazai lapban
Megjelenés:Acta Physiologica Hungarica. - 86: : 2 (1999), p. 155-160. -
További szerzők:Görlach, Christoph Hortobágyi Tibor (1965-) (patológus) Benyó Zoltán
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