Találati lista | Tudóstér

001-es BibID:	BIBFORM041210
035-os BibID:	PMID:11033413
Első szerző:	Csonka Csaba
Cím:	Effects of oxidative stress on the expression of antioxidative defense enzymes in spontaneously hypertensive rat hearts / Csaba Csonka, Tunde Pataki, Peter Kovacs, Sebastian L. Müller, Matthias L. Schroeter, Arpad Tosaki, Ingolf E. Blasig
Dátum:	2000
Megjegyzések:	Little is known concerning the effect of oxidative stress on the expression of antioxidative enzymes in the decompensated cardiac hypertrophy of spontaneously hypertensive rats (SHR), considered as a model of dilative cardiomyopathy in man. Superoxide dismutase (SOD), catalase, and glutathione peroxidase (GPx) were characterized in isolated perfused hearts of 18 month old SHR and the age-matched normotensive control Wistar-Kyoto (WKY) rats, before and after 30 min infusion of 25 microM H(2)O(2). After infusion of H(2)O(2), aortic flow decreased in WKY from 26.2 +/- 2.2 to 16.0 +/- 0.8 ml/min (p <.05) but not in SHR (18.2 +/- 1.9 vs. 20.7 +/- 2.2 ml/min). This protection was related to the higher myocardial activities of GPx, MnSOD and CuZnSOD in SHR, compared with those of the WKY group. Although total SOD activity in the SHR fell after H(2)O(2) exposure (to 1.81 +/- 0.13 from 3.56 +/- 0.49 U/mg of protein), catalase activity increased (to 2.46 +/- 0.34 from 1.56 +/- 0.29 k min(-1)mg(-1)protein), compared with the pre-infusion period (p <.05 in each case). In additional studies, hearts were subjected to 30 min of global ischemia followed by 30 min of reperfusion. The results obtained in ischemic/reperfused hearts show the same changes in enzyme activities measured as it was observed in H(2)O(2) perfused hearts, indicating that oxidative stress is independent of the way it was induced. The higher catalase activity derived from elevated mRNA synthesis. The antioxidative system in dilative cardiomyopathic hearts of SHR is induced, probably due to episodes of oxidative stress, during the process of decompensation. This conditioning of the antioxidative potential may help overcome acute stress situations caused by reactive oxygen species in the failing myocardium.
Tárgyszavak:	Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban külföldön készült közlemény
Megjelenés:	Free Radical Biology & Medicine 29 : 7 (2000), p. 612-619. -
További szerzők:	Pataki Tünde (1971-) (farmakológus, klinikai farmakológus) Kovács Péter (1939-) (farmakológus) Müller, Sebastian L. Schroeter, Matthias L. Tósaki Árpád (1958-) (kísérletes farmakológus, gyógyszerész) Blasig, Ingolf E.
Internet cím:	Intézményi repozitóriumban (DEA) tárolt változat DOI
Borító:
Saját polcon:

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