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1.

001-es BibID:BIBFORM020511
Első szerző:Csonka Csaba
Cím:Heme oxygenase and cardiac function in ischemic/reperfused rat hearts / Csaba Csonka, Edit Varga, Peter Kovacs, Peter Ferdinandy, Ingolf E. Blasig, Zoltan Szilvassy Árpád Tosaki
Dátum:1999
Megjegyzések:AbstractWe investigated whether the expression of heme oxygenase (HO) isozymes was related to the occurrence of ventricular fibrillation (VF) induced by ischemia/reperfusion in nondiabetic and diabetic myocardium. To study the role of HO-1 and HO-2 mRNA expression in VF, isolated hearts obtained from nondiabetic and 8-week diabetic rats were subjected to 30 min of ischemia followed by 2 h of reperfusion. Expression of HO-1 and HO-2 mRNA was studied in fibrillated and nonfibrillated myocardium using Northern blotting and reverse transcription polymerase chain reaction (RT-PCR). The effect of zinc protoporphyrin IX (Zn-PPIX), a potent inhibitor of HO activity, on HO activity was also studied in ischemic/reperfused hearts. Upon reperfusion, an expression of HO-1 was observed in nonfibrillated myocardium. HO-1 mRNA expression was significantly reduced in hearts showed VF. Zn-PPIX (5 microM) treatment reduced HO activity from its control values of 398+/-27 (in nondiabetics) and 370+/-20 pmol bilirubin/h (in diabetics) to 69+/-14 (in nondiabetics, p<.05) and 60+/-11 pmol bilirubin/h (in diabetics, p<.05), respectively, and all hearts, upon reperfusion, showed VF in both nondiabetic and diabetic subjects. HO-2 expression was unchanged in nonfibrillated and fibrillated myocardium. Postischemic function showed no correlation with the expression of these genes. Our data show that the mechanism(s) of ischemia/reperfusion-induced VF involves the downregulation of HO-1 mRNA and a reduction in HO activity. Furthermore, the mechanism(s) of VF at molecular level involving HO isozymes does not show a significant difference between nondiabetics and diabetics.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
heme oxygenase
cardiac function
ischemic heart
reperfused heart
Megjelenés:Free Radical Biology and Medicine 27 : 1-2 (1999), p. 119-126. -
További szerzők:Varga Edit (gyógyszerész) Kovács Péter (1947-) (belgyógyász, kardiológus, klinikai farmakológus) Ferdinándy Péter Blasig, Ingolf E. Szilvássy Zoltán (1957-) (belgyógyász, farmakológus, klinikai farmakológus) Tósaki Árpád (1958-) (kísérletes farmakológus, gyógyszerész)
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2.

001-es BibID:BIBFORM020473
Első szerző:Csonka Csaba
Cím:Classic preconditioning decreases the harmful accumulation of nitric oxide during ischemia and reperfusion in rat hearts / Csaba Csonka, Zoltán Szilvássy, Ferenc Fülöp, Tibor Páli, Ingolf E. Blasig, Árpád Tósaki, Richard Schulz, Péter Ferdinandy
Dátum:1999
Megjegyzések:The role of NO in the mechanism of preconditioning is not understood. Therefore, we studied the effect of preconditioning and subsequent ischemia/reperfusion on myocardial NO content in the presence of an NO synthase (NOS) inhibitor.METHODS AND RESULTS:Isolated working rat hearts were subjected to preconditioning protocols of 3 intermittent periods of rapid pacing or no-flow ischemia of 5 minutes' duration each followed by a test 30 minutes of global no-flow ischemia and 15 minutes of reperfusion. Test ischemia/reperfusion resulted in a deterioration of myocardial function and a considerable increase in cardiac NO content as assessed by electron spin resonance. Preconditioning improved postischemic myocardial function and markedly decreased test ischemia/reperfusion-induced NO accumulation. In the presence of 4.6 micromol/L N(G)-nitro-L-arginine (LNA), basal cardiac NO content decreased significantly, although test ischemia/reperfusion-induced functional deterioration and NO accumulation were not affected in nonpreconditioned hearts. However, the protective effects of preconditioning on both test ischemia/reperfusion-induced functional depression and NO accumulation were abolished. When 4.6 micromol/L LNA was administered after preconditioning, it failed to block the effect of preconditioning. In the presence of 46 micromol/L LNA, ischemia/reperfusion-induced NO accumulation was significantly decreased and postischemic myocardial function was improved in nonpreconditioned hearts.CONCLUSIONS:Our results show that (1) although NO synthesis by the heart is necessary to trigger classic preconditioning, preconditioning in turn attenuates the accumulation of NO during ischemia/reperfusion, and (2) blockade of ischemia/reperfusion-induced accumulation of cardiac NO by preconditioning or by an appropriate concentration of NOS inhibitor alleviates ischemia/reperfusion injury as demonstrated by enhanced postischemic function.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
Classic preconditioning
accumulation of nitric oxide
nitric oxide
ischemia
reperfusion
Megjelenés:Circulation 100 : 22 (1999), p. 2260-2266. -
További szerzők:Szilvássy Zoltán (1957-) (belgyógyász, farmakológus, klinikai farmakológus) Fülöp Ferenc (Szeged) Páli Tibor Blasig, Ingolf E. Tósaki Árpád (1958-) (kísérletes farmakológus, gyógyszerész) Schulz, Richard Ferdinándy Péter
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3.

001-es BibID:BIBFORM046506
Első szerző:Ferdinándy Péter
Cím:Loss of pacing-induced preconditioning in rat hearts : role of nitric oxide and cholesterol-enriched diet / Peter Ferdinandy, Zoltan Szilvassy, Laszlo I. Horvath, Tamas Csont, Csaba Csonka, Erzsebet Nagy, Reka Szentgyorgyi, Istvan Nagy, Matyas Koltai, Laszlo Dux
Dátum:1997
ISSN:0022-2828
Megjegyzések:We examined whether the inhibition ofnitric oxide (NO) synthesis by NG-nitro-L-arginine (LNNA) abolished pacing-induced preconditioning, and ifprolonged exposure to cholesterol-enriched diet led to the loss of preconditioning due to decreased cardiac NOformation. Therefore, Wistar rats fed 2% cholesterol-enriched diet or standard diet for 24 weeks were treatedwith a single dose of 1 mg/kg LNNA or its solvent at the end of the week 24, respectively. Isolated hearts fromall groups were subjected to either preconditioning induced by three consecutive periods of pacing at 600 beats/min for 5 min, with 5-min interpacing periods, or time-matched non-preconditioning perfusion, followed by a10-min coronary occlusion, respectively. In the control group, coronary occlusion after a non-preconditioningprotocol decreased aortic flow (AF) from 45.4?2.4 to 15.6?1.5 ml/min, and resulted in a lactate dehydrogenase(LDH) release of 219?55 mU/min/g, however, preconditioning attenuated the consequences of coronary occlusion[AF: 27.3?1.7 ml/min (P<0.05); LDH: 44?14 mU/min/g (P<0.05)]. Preconditioning did not confer protectionin the LNNA-treated (AF: 17.4?1.5 ml/min; LDH: 151?21 mU/min/g), and/or in the high-cholesterol-fed groups(AF: 15.7?1.2 ml/min; LDH: 168?22 mU/min/g). Preconditioning was preserved however, when hearts weretreated with LNNA after the preconditioning protocol [AF: 29.6?2.2 ml/min (P<0.05); LDH: 48?17 mU/min/g (P<0.05)]. Both LNNA treatment and cholesterol-enriched diet markedly decreased cardiac NO content assayedby electron spin resonance spectroscopy. We conclude that NO may be involved in the triggering mechanism ofpacing-induced preconditioning, the protective effect of which is blocked by sustained exposure to dietarycholesterol, possibly by influencing cardiac metabolism of NO.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Pacing-induced
Nitric Oxide
NO
LNNA
Megjelenés:Journal of Molecular and Cellular Cardiology. - 29 : 12 (1997), p. 3321-3333. -
További szerzők:Szilvássy Zoltán (1957-) (belgyógyász, farmakológus, klinikai farmakológus) Horváth László I. Csont Tamás Csonka Csaba Nagy Erzsébet (Szeged) Szentgyörgyi Réka Nagy István Koltai Mátyás Dux László
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4.

001-es BibID:BIBFORM046569
Első szerző:Ferdinándy Péter
Cím:Nitroglycerin-induced direct protection of the ischaemic myocardium in isolated working hearts of rats with vascular tolerance to nitroglycerin / P. Ferdinandy, Z. Szilvássy, T. Csont, C. Csonka, E. Nagy, M. Koltai, L. Dux
Dátum:1995
ISSN:0007-1188
Megjegyzések:We investigated whether nitroglycerin (NTG) was able to produce an anti-ischaemic effect in isolatedworking hearts of rats with vascular tolerance to NTG. Hearts isolated from tolerant and non-tolerantrats were subjected to 10 min coronary occlusion in the presence of 10r M NTG and/or its solvent. NTGalleviated ischaemia-induced deterioration of cardiac function and decreased lactate dehydrogenaserelease whilst having no effect on coronary flow nor the area of the ischaemic zone both in heartsisolated from NTG-tolerant and non-tolerant rats. The magnitude of the effect was similar in the twogroups. These results suggest that the anti-ischaemic effect of NTG involves direct myocardialmechanisms independent of its vascular action and that vascular tolerance to NTG does not affect thisdirect protective action.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Coronary occlusion
nitroglycerin
nitroglycerin tolerance
cardioprotection;
rat heart
Megjelenés:British Journal of Pharmacology. - 115 : 7 (1995), p. 1129-1131. -
További szerzők:Szilvássy Zoltán (1957-) (belgyógyász, farmakológus, klinikai farmakológus) Csont Tamás Csonka Csaba Nagy Erzsébet (Szeged) Koltai Mátyás Dux László
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5.

001-es BibID:BIBFORM020561
Első szerző:Ferdinándy Péter
Cím:Rapid pacing-induced preconditioning is recaptured by farnesol treatment in hearts of cholesterol-fed rats : role of polyprenyl derivatives and nitric oxide / Peter Ferdinandy, Csaba Csonka, Tamás Csont, Zoltán Szilvássy, László Dux
Dátum:1998
Megjegyzések:AbstractWe have previously shown that hypercholesterolemia leads to the loss of pacing-induced preconditioning (PC), possibly due to the impairment of cardiac nitric oxide (NO) synthesis. It has been shown that excess exogenous cholesterol inhibits formation of several polyprenyl derivatives involved in signal transduction. In the present study, we examined whether PC and cardiac NO synthesis are restored by treatment with the key polyprenyl product, farnesol, in cholesterol-fed rats. Rats fed 2% cholesterol-enriched/control diet for 24 weeks were given i.p. 5 microM/kg farnesol/vehicle, respectively. An hour later, hearts were isolated and prepared for 'working' perfusion, then subjected to PC/non-PC protocols of 3 intermittent periods of pacing of 5 min duration at 10 Hz, followed by a 10 min coronary occlusion to test the effect of PC. PC increased ischemic aortic flow (AF) from its control value of 15.6+/-1.5 to 27.3+/-1.7 mL/min (p < 0.05). PC was not observed in hearts obtained from hypercholesterolemic rats (AF: 15.7+/-1.2 mL/min), however, it reappeared in the farnesol-treated hypercholesterolemic group (AF: 31.8+/-3.4 mL/ min, p < 0.05). In tissue samples from the left ventricle, cholesterol-diet markedly decreased the intensity of the electron spin resonance spectra of NO obtained after in vivo spin trapping with Fe2+-diethyl-dithio-carbamate complex. Farnesol-treatment did not influence cardiac NO content in the cholesterol-fed or in the control group. These results show that the lost PC can be recaptured by farnesol-treatment in hypercholesterolemia, however, farnesol-treatment does not restore cardiac NO synthesis.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
Rapid pacing-induced
farnesol treatment
cholesterol-fed
polyprenyl derivatives
nitric oxide
Megjelenés:Molecular and Cellular Biochemistry. - 186 : 1-2 (1998), p. 27-34. -
További szerzők:Csonka Csaba Csont Tamás Dux László Szilvássy Zoltán (1957-) (belgyógyász, farmakológus, klinikai farmakológus)
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