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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
Internet cím:	Szerző által megadott URL DOI Intézményi repozitóriumban (DEA) tárolt változat
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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
Internet cím:	DOI Intézményi repozitóriumban (DEA) tárolt változat
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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
Internet cím:	DOI Intézményi repozitóriumban (DEA) tárolt változat
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