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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: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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4.

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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5.

001-es BibID:BIBFORM115159
Első szerző:Ferdinándy Péter
Cím:Antihyperlipidaemiás szerek / Ferdinandy Péter, Szilvássy Zoltán
Dátum:2020
ISBN:978-963-226-738-8
Tárgyszavak:Orvostudományok Klinikai orvostudományok könyvfejezet
könyvrészlet
Megjelenés:Farmakológia és klinikai farmakológia: egyetemi tankönyv / Szerk. Pintér Erika, Szilvássy Zoltán, Varró Adrás. - p. 284-293. -
További szerzők:Szilvássy Zoltán (1957-) (belgyógyász, farmakológus, klinikai farmakológus)
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6.

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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7.

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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8.

001-es BibID:BIBFORM046511
035-os BibID:PMID:8595627
Első szerző:Ferdinándy Péter
Cím:KATP channel modulation in working rat hearts with coronary occlusion: effects of cromakalim, cicletanine, and glibenclamide / Péter Ferdinandy, Zoltán Szilvassy, Marie T. Droy-Lefaix, Thierry Tarrade, Matyas Koltai
Dátum:1995
ISSN:0008-6363
Megjegyzések:OBJECTIVES: We studied the effects of ATP-sensitive potassium channel (KATP) modulation on ischemic cardiac performance and reperfusion-induced ventricular fibrillation (VF), and assessed the contribution of KATP to the cardioprotective and anti-arrhythmic effect of the anti-hypertensive drug cicletanine. METHODS: Isolated working rat hearts, subjected to a 10-min coronary occlusion followed by reperfusion, were perfused in the presence of vehicle, 0.1-60 microM cromakalim, an opener of KATP; 3-60 microM cicletanine; and 0.1-10 microM glibenclamide, a blocker of KATP, respectively. RESULTS: All concentrations of cicletanine, similarly to 0.1-10 microM cromakalim, attenuated ischemia-induced deterioration of aortic flow, left ventricular developed pressure, and left ventricular end-diastolic pressure. In contrast to cromakalim, cicletanine did not increase coronary flow. Cicletanine (60 microM) and cromakalim (10 and 60 microM) significantly reduced the incidence of reperfusion-induced VF; however, 60 microM cromakalim triggered VF during ischemia. Lower concentrations of cromakalim and cicletanine did not produce an anti-arrhythmic effect. Cardiac functional parameters were concentration dependently worsened by glibenclamide, and the drug did not change the incidence of VF. Glibenclamide (0.1 microM) did not significantly affect cardiac performance, but it did abolish the anti-ischemic effect of cromakalim (1-10 microM) and cicletanine (60 microM). Glibenclamide suppressed the anti-arrhythmic effect of 10 and 60 microM cromakalim; however, it did not affect the anti-arrhythmic effect of cicletanine. CONCLUSIONS: (i) The anti-ischemic but not the anti-arrhythmic effect of cicletanine may involve opening of KATP. (ii) opening of KATP attenuates, inhibition of the channel exacerbates functional consequences of coronary occlusion, and (iii) KATP opening attenuates reperfusion-induced VF, but it triggers ischemia-induced VF. KATP blocking does not affect VF.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
cicletanine
myocardial ischemia
myocardial function
arrhythmias
reperfusion
potassium channel openers
sulphonylureas
Megjelenés:Cardiovascular Research. - 30 : 5 (1995), p. 781-787. -
További szerzők:Szilvássy Zoltán (1957-) (belgyógyász, farmakológus, klinikai farmakológus) Droy-Lefaix, Marie-Thérèse Tarrade, Thierry Koltai Mátyás
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9.

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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10.

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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11.

001-es BibID:BIBFORM020577
Első szerző:Ferdinándy Péter
Cím:Adaptation to myocardial stress in disease states: is preconditioning a healthy heart phenomenon? / P. Ferdinandy, Z. Szilvassy, G. F. Baxter
Dátum:1998
Megjegyzések:Szegedi Tudományegyetem - Biokémiai Tanszék; Szegedi Tudományegyetem - Belgyógyászati Klinika
AbstractEffective therapeutic strategies for protecting the ischaemic myocardium are much sought after. Ischaemic heart disease in humans is a complex disorder, often associated with other systemic diseases such as dyslipidaemia, hypertension and diabetes that exert multiple biochemical effects on the heart, independently of ischaemia. Ischaemic preconditioning of myocardium is a well-described adaptive response in which brief exposure to ischaemia markedly enhances the ability of the heart to withstand a subsequent ischaemic insult. The underlying molecular mechanisms of this phenomenon have been extensively investigated in the hope of identifying new rational approaches to therapeutic protection of the ischaemic myocardium. However, most studies have been undertaken in animal models in which ischaemia is imposed in the absence of other disease processes. In this article, Peter Ferdinandy, Zoltan Szilvassy and Gary Baxter review the ways in which systemic diseases might modify the preconditioning response and they emphasize the importance of further preclinical studies that specifically examine preconditioning in relation to complicating disease states.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
myocardial stress
preconditioning
adaptation
Megjelenés:Trends in Pharmacological Sciences. - 19 : 6 (1998), p. 223-229. -
További szerzők:Szilvássy Zoltán (1957-) (belgyógyász, farmakológus, klinikai farmakológus) Baxter, G. F.
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12.

001-es BibID:BIBFORM007758
Első szerző:Ferdinándy Péter
Cím:Antihiperlipidémiás szerek / Ferdinándy P., Szilvássy Z.
Dátum:2007
Tárgyszavak:Orvostudományok Elméleti orvostudományok könyvfejezet
Megjelenés:Farmakológia / szerk. Gyires Klára, Fürst Zsuzsanna. - p. 241-251.
További szerzők:Szilvássy Zoltán (1957-) (belgyógyász, farmakológus, klinikai farmakológus)
Internet cím:elektronikus változat
Borító:
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