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1.

001-es BibID:BIBFORM020555
Első szerző:Csont Tamás
Cím:Lack of correlation between myocardial nitric oxide and cyclic guanosine monophosphate content in both nitrate-tolerant and -nontolerant rats / Tamás Csont, Tibor Páli, Zoltán Szilvássy, Péter Ferdinandy
Dátum:2000
ISSN:0006-2952
Megjegyzések:AbstractWe studied the effect of nitroglycerin (NTG) on cardiac nitric oxide (NO) and cyclic guanosine monophosphate (cGMP) content in nitrate-tolerant/nontolerant rats in vivo. The effect of the pharmacological blockade of endogenous NO synthesis and the effect of exogenous NO on cardiac cGMP were also examined. Rats were treated with 100 mg/kg of NTG and corresponding vehicle s.c. three times a day for 2.5 days to induce NTG-tolerance/nontolerance. Rats were then administered a single dose of s.c. 100 mg/kg of NTG to test the effect of NTG in tolerant/nontolerant states, respectively. Nontolerant rats treated with vehicle were controls, and nontolerant rats treated with the NO synthesis inhibitor NG-nitro-L-arginine (LNNA, 20 mg/kg) were negative controls. Another group of nontolerant rats treated i.v. with the direct NO donor sodium nitroprusside (SNP, 3 mg/kg) were positive controls. Cardiac NO assessed by electron spin resonance after in vivo spin-trapping increased 100-fold (P < 0.05) in the positive control, 10-fold (P < 0.05) in the NTG-tolerant group, and 4-fold (P < 0.05) in the single NTG group, when compared to controls. In the negative control group, NO was reduced to near the detection limit (four-fold reduction, P < 0.05). Cardiac cGMP measured by radioimmunoassay was increased significantly (two-fold, P < 0.05) only in the positive control group, and there were no differences among the other groups. This shows that: 1) in vivo cardiac bioconversion of NTG to NO is not impaired in nitrate tolerance; and 2) changes in cardiac NO content are not reflected by changes in cGMP content in nitrate-tolerant and -nontolerant rats.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
myocardial nitric oxide
cyclic guanosine monophosphate
nitrate-tolerant
nitrate-nontolerant
Megjelenés:Biochemical Pharmacology. - 56 : 9 (2000), p. 1139-1144. -
További szerzők:Páli Tibor Ferdinándy Péter Szilvássy Zoltán (1957-) (belgyógyász, farmakológus, klinikai farmakológus)
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2.

001-es BibID:BIBFORM020469
Első szerző:Csont Tamás
Cím:Direct myocardial anti-ischaemic effect of GTN in both nitrate-tolerant and nontolerant rats : a cyclic GMP-independent activation of KATP / Tamás Csont, Zoltán Szilvássy, Ferenc Fülöp, Saviana Nedeianu, Tibor Páli, Árpád Tósaki, László Dux, Péter Ferdinandy
Dátum:1999
ISSN:0007-1188
Megjegyzések:Abstract1. We have recently demonstrated that glyceryl trinitrate (GTN) exerts a direct myocardial anti-ischaemic effect in both GTN-tolerant and nontolerant rats. Here we examined if this effect is mediated by GTN-derived nitric oxide (NO) and involves guanosine 3'5' cyclic monophosphate (cyclic GMP) and ATP-sensitive K+ channels (KATP). 2. Rats were treated with 100 mg kg-1 GTN or vehicle s.c. three times a day for 3 days to induce vascular GTN-tolerance or nontolerance. Isolated working hearts obtained from either GTN-tolerant or nontolerant rats were subjected to 10 min coronary occlusion in the presence of 10-7 M GTN or its solvent. 3. GTN improved myocardial function and reduced lactate dehydrogenase (LDH) release during coronary occlusion in both GTN-tolerant and nontolerant hearts. 4. Cardiac NO content significantly increased after GTN administration in both GTN-tolerant and nontolerant hearts as assessed by electron spin resonance. However, cardiac cyclic GMP content measured by radioimmunoassay was not changed by GTN administration. 5. When hearts from both GTN-tolerant and nontolerant rats were subjected to coronary occlusion in the presence of the KATP-blocker glibenclamide (10-7 M), the drug itself did not affect myocardial function and LDH release, however, it abolished the anti-ischaemic effect of GTN. 6. We conclude that GTN opens KATP via a cyclic GMP-independent mechanism, thereby leading to an anti-ischaemic effect in the heart in both GTN-tolerant and nontolerant rats.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
Direct myocardial
anti-ischaemic effect
Direct myocardial anti-ischaemic effect
effect of GTN
GTN
cyclic activation of K(ATP)
cyclic GMP-independent activation of K(ATP)
K(ATP)
Megjelenés:British Journal of Pharmacology 128 : 7 (1999), p. 1427-1434. -
További szerzők:Szilvássy Zoltán (1957-) (belgyógyász, farmakológus, klinikai farmakológus) Fülöp Ferenc (Szeged) Nedeianu, Saviana Páli Tibor Tósaki Árpád (1958-) (kísérletes farmakológus, gyógyszerész) Dux László 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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6.

001-es BibID:BIBFORM020523
Első szerző:Ferdinándy Péter
Cím:Cardioprotective effect of enantiomers of cicletanine (BN50417, BN50418) in ischaemic/reperfused isolated working rat hearts : interaction with glibenclamide / P. Ferdinandy, Z. Szilvássy, T. Csont, M. Koltai, M. T. Droy-lefaix
Dátum:2000
ISSN:1043-6618
Megjegyzések:AbstractIn the present study, interaction of the ATP-sensitive K+-channel blocker glibenclamide with enantiomers of the antihypertensive drug, cicletanine, was studied on ischaemic myocardial function, lactate-dehydrogenase (LDH) release, and early reperfusion-induced ventricular fibrillation (VF). Isolated working rat hearts subjected to 10-min coronary artery occlusion followed by 2-min reperfusion were perfused with 1.5x10(-5)-6.0x10(-5)M D-cicletanine[+] (BN50417) and L-cicletanine[-] (BN50418), respectively. Their interaction with 10(-7) M glibenclamide was also studied. The most effective concentration of BN50418 (3x10(-5) M) increased ischaemic aortic flow (AF) from its non-treated control value of 20.3+/-1.16 to 30.3+/-2.6 ml min-1(P<0.01), decreased left ventricular end-diastolic pressure (LVEDP) from 1.81+/-0.05 to 0.97+/-0.08 kPa (P<0.001), attenuated ischaemia-induced increase in LDH leakage from 164+/-41 to 14.8+/-20 mU min-1g-1 wet wt. (P<0.01) at the 10th-min of coronary occlusion, and reduced VF upon reperfusion. Glibenclamide did not considerably affect cardiac performance, however, it inhibited the anti-ischaemic but not the antiarrhythmic effect of BN50418. BN50417 (3x10(-5) M) tended to improve ischaemic AF to 24.2+/-1.1 ml min-1, and significantly attenuated ischaemia-induced increase in LVEDP to 1.3+/-0.08 kPa (P<0.01), relative increase in LDH release to 29.4+/-44 mU min-1g-1(P<0.05), and alleviated reperfusion-induced VF. Glibenclamide abolished the anti-ischaemic and antiarrhythmic effect of BN50417. The cardioprotective effect of both enantiomers of cicletanine involves a glibenclamide-sensitive mechanism, however, the antiarrhythmic effect of BN50418 is not glibenclamide sensitive. BN50418 is the more potent enantiomer of cicletanine in terms of its cardioprotective effect.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
cardioprotective effect
enantiomers of cicletanine
enantiomers
cicletanine
BN50417
BN50418
glibenclamide
Megjelenés:Pharmacological Research. - 39 : 3 (1999), p. 225-231. -
További szerzők:Csont Tamás Koltai M. Droy-Lefaix, Marie-Thérèse Szilvássy Zoltán (1957-) (belgyógyász, farmakológus, klinikai farmakológus)
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7.

001-es BibID:BIBFORM020451
Első szerző:Szilvássy Zoltán (belgyógyász, farmakológus, klinikai farmakológus)
Cím:Nitric oxide, peroxynitrite and cGMP in atherosclerosis-induced hypertension in rabbits : beneficial effects of cicletanine / Zoltán Szilvássy, Tamás Csont, Tibor Páli, Marie-Thérèse Droy-Lefaix, Péter Ferdinandy
Dátum:2001
ISSN:1018-1172
Megjegyzések:AbstractWe studied the effect of the furopyridine derivative antihypertensive drug, cicletanine, on blood pressure, vascular nitric oxide (NO) and cyclic guanosine 3':5'-monophosphate (cGMP) content in the aorta and the renal and carotid arteries, aortic superoxide production, and serum nitrotyrosine level in hypertensive/atherosclerotic rabbits. The effect of cicletanine was compared to that of furosemide. Rabbits were fed a normal or a cholesterol-enriched (1.5%) diet over 8 weeks. On the 8th week, the rabbits were treated per os with 2 x 50 mg/kg daily doses of cicletanine, furosemide, or vehicle for 5 days (n = 5-6 in each groups). The cholesterol diet increased mean arterial blood pressure (MABP) from 86 +/- 1 to 94 +/- 2 mm Hg (p < 0.05). Cicletanine decreased MABP in atherosclerotic rabbits to 85 +/- 1 mm Hg (p < 0.05), but it did not affect MABP in normal animals. Furosemide was without effect in both groups. In normal animals, NO content (assessed by electron spin resonance after in vivo spin trapping) in the aorta and the renal and carotid arteries was increased by cicletanine, and the drug increased cGMP in the renal artery as measured by radioimmunoassay. The cholesterol-enriched diet decreased both vascular NO and cGMP and increased aortic superoxide production assessed by lucigenin-enhanced chemiluminescence and serum nitrotyrosine determined by ELISA. In atherosclerotic animals, cicletanine increased NO and cGMP content in the aorta and the renal and carotid arteries and decreased aortic superoxide production and serum nitrotyrosine. Furosemide did not influence these parameters. We conclude that cicletanine lowers blood pressure in hypertensive/atherosclerotic rabbits. The antihypertensive effect of the drug in atherosclerosis may be based on its beneficial effects on the vascular NO-cGMP system and on the formation of reactive oxygen species.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
nitric oxide
peroxynitrite
cGMP
atherosclerosis-induced
atherosclerosis-induced hypertension
cicletanine
Megjelenés:Journal of Vascular Research. - 38 : 1 (2001), p. 39-46. -
További szerzők:Csont Tamás Páli Tibor Droy-Lefaix, Marie-Thérèse Ferdinándy Péter
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