CCL

Összesen 8 találat.
#/oldal:
Részletezés:
Rendezés:

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

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

3.

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

4.

001-es BibID:BIBFORM020462
Első szerző:Kovács Péter (belgyógyász, kardiológus, klinikai farmakológus)
Cím:Effect of transdermal nitroglycerin on glucose-stimulated insulin release in healthy male volunteers / P. Kovacs, Z. Szilvassy, P. Hegyi, J. Nemeth, P. Ferdinandy, Á. Tosaki
Dátum:2000
ISSN:0014-2972
Megjegyzések:Morpholinosydnonimine, a nitric oxide (NO) donor, has been reported to inhibit insulin release in isolated pancreatic islets. We studied whether transdermal application of nitroglycerin, another NO donor widely used for angina prophylaxis, influenced glucose-stimulated insulin release in healthy, young, male volunteers.METHODS AND RESULTS:Oral glucose tolerance tests [(OGTT) 75 g glucose in 200 mL of water) were performed in the presence of placebo patches or nitroglycerin-releasing 'active' patches (approx. 0.4 mg hour-1 nitroglycerin) in the same patients with a 2-week intertest interval. Venous blood samples were taken before and 15, 30, 60, 90, 120 and 180 min after the glucose load and evaluated for plasma glucose level and immunoreactive insulin responses (radioimmunoassay). Glucose-stimulated maximum increase in plasma insulin immunoreactivity were 36.3 +/- 5 and 78.8 +/- 6.1 mU mL-1 (P < 0.05) in the presence of active and placebo patches, respectively. Nevertheless, both fasting and postload blood glucose levels were the same at either patch. Active patches significantly decreased blood pressure with a marginal increase in heart rate.CONCLUSION:We conclude that inhibition of glucose-stimulated insulin release by transdermal nitroglycerin without causing hyperglycaemia may serve as a novel component of the antianginal mechanism of action of nitrates.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
transdermal nitroglycerin
glucose-stimulated insulin
Effect of transdermal nitroglycerin
Megjelenés:European Journal Of Clinical Investigation 30 : 1 (2000), p. 41-44. -
További szerzők:Szilvássy Zoltán (1957-) (belgyógyász, farmakológus, klinikai farmakológus) Hegyi Péter Jenő (belgyógyász) Németh József (Pécs) Ferdinándy Péter Tósaki Árpád (1958-) (kísérletes farmakológus, gyógyszerész)
Internet cím:Szerző által megadott URL
DOI
Intézményi repozitóriumban (DEA) tárolt változat
Borító:

5.

001-es BibID:BIBFORM042019
Első szerző:Oroszi Gábor (Pécs)
Cím:Interaction between capsaicin and nitrate tolerance in isolated guinea-pig heart / Oroszi Gabor, Szilvassy Zoltan, Nemeth Jozsef, Ferdinandy Peter, Szolcsanyi Janos, Tósaki Árpád
Dátum:1999
Megjegyzések:Capsaicin-induced increases in heart rate and coronary flow were blocked by N(G)-nitro-L-Arg-methyl ester (30 mM) in Langendorff-perfused guinea-pig hearts. Neither heart rate nor coronary flow changed by capsaicin in hearts from animals made tolerant to the hypotensive effect of 30 microg/kg nitroglycerin by the administration of 50 mg/kg nitroglycerin subcutaneously 4 times a day over 3 days. We conclude that the effector function of sensory nerves may deteriorate in nitrate tolerance.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
MSH
Megjelenés:European Journal of Pharmacology. - 368 : 2-3 (1999), p. R1-R3. -
További szerzők:Szilvássy Zoltán (1957-) (belgyógyász, farmakológus, klinikai farmakológus) Németh József (1954-) (vegyész, analitikus) Ferdinándy Péter Szolcsányi János (Pécs) Tósaki Árpád (1958-) (kísérletes farmakológus, gyógyszerész)
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
Borító:

6.

001-es BibID:BIBFORM020518
Első szerző:Oroszi Gábor (Pécs)
Cím:Interplay between nitric oxide and CGRP by capsaicin in isolated guinea-pig heart / Gabor Oroszi, Zoltan Szilvassy, Joseph Nemeth, Arpad Tosaki, Janos Szolcsanyi
Dátum:1999
ISSN:1043-6618
Megjegyzések:AbstractCapsaicin at a concentration of 10(-7)m induced a significant increase in heart rate and increased coronary flow in isolated Langendorff-perfused guinea-pig hearts. This effect was completely blocked by 30 microm of N(omega)-nitro-L-arginine methyl ester (L-NAME), an inhibitor of nitric oxide synthase. Additional incubation with 3 m m L-Arg antagonized the inhibitory effect of L-NAME. In the presence of 1 microm of a human calcitonin gene-related peptide fragment (hCGRP 8-37), a CGRP-receptor antagonist, L-Arg was without effect. We conclude that a capsaicin-induced increase in coronary flow and heart rate is dependent from an interplay between CGRP and NO in guinea-pig hearts. 1999 Academic Press.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
nitric oxide
CGRP
capsaicin
Megjelenés:Pharmacological Research 40 : 2 (1999), p. 125-128. -
További szerzők:Szilvássy Zoltán (1957-) (belgyógyász, farmakológus, klinikai farmakológus) Németh József (Pécs) Tósaki Árpád (1958-) (kísérletes farmakológus, gyógyszerész) Szolcsányi János (Pécs)
Internet cím:Szerző által megadott URL
DOI
Intézményi repozitóriumban (DEA) tárolt változat
Borító:

7.

001-es BibID:BIBFORM041169
035-os BibID:PMID:11426844
Első szerző:Szolcsányi János (Pécs)
Cím:Functional and biochemical evidence for capsaicin-induced neural endothelin release in isolated working rat heart / Janos Szolcsanyi, Gabor Oroszi, Jozsef Nemeth, Zoltan Szilvassy, Ingolf E. Blasig, Arpad Tosaki
Dátum:2001
Megjegyzések:In isolated working rat heart, capsaicin elicited a concentration-dependent constriction of coronary arteries accompanied by decline of all cardiac parameters recorded (heart rate, coronary and aortic flow, left ventricular developed pressure, and first derivative of left ventricular developed pressure). The following evidence suggests that capsaicin-induced changes are mediated by endothelin of neural origin: (1) the capsaicin (10 nM)-evoked decrease in coronary flow resulting in deterioration of cardiac functions was mimicked by endothelin (0.1 nM); (2) the selective endothelin ET(A) receptor antagonist, cyclo (D-alpha-aspartyl-L-propyl-D-valyl-L-leucyl-D-tryptophyl) (1 microM), abolished the cardiac effects provoked by capsaicin (10 nM); (3) reduction of extracellular Ca2+ concentration from 2.4 to 1.2 or 0.6 mM inhibited the cardiac effects of capsaicin (10 nM) but not those induced by endothelin (0.1 nM); (4) perfusion of the heart with 0.1% (v/v) Triton X-100 damaged the endothelium and reversed the enhancement of coronary flow evoked by bethanechol (1 microM), decreased the basal flow, but was without effect on capsaicin-induced coronary constriction; (5) in response to capsaicin challenge (10-100 nM), the endothelin concentration measured in coronary effluent by means of radioimmunoassay increased up to sevenfold but remained unchanged in the presence of 0.6 mM Ca2+; (6) no reduction of coronary flow was induced by capsaicin (100 nM) applied to the heart of rats which were desensitised by capsaicin (150 mg/kg). It is concluded that, in the rat heart, capsaicin acting on VR1 capsaicin receptors elicits a release of endothelin from the sensory nerve terminals.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
egyetemen (Magyarországon) készült közlemény
Megjelenés:European Journal of Pharmacology. - 419 : 2-3 (2001), p. 215-221. -
További szerzők:Oroszi Gábor (Pécs) Németh József (Pécs) Szilvássy Zoltán (1957-) (belgyógyász, farmakológus, klinikai farmakológus) Blasig, Ingolf E. Tósaki Árpád (1958-) (kísérletes farmakológus, gyógyszerész)
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
DOI
Borító:

8.

001-es BibID:BIBFORM020476
Első szerző:Szolcsányi János (Pécs)
Cím:Endothelin release by capsaicin in isolated working rat heart / János Szolcsányi, Gábor Oroszi, József Németh, Zoltán Szilvássy, Árpád Tósaki
Dátum:1999
Megjegyzések:AbstractCapsaicin (1 nM-1 microM) induced a concentration-dependent decrease in heart rate, coronary flow, aortic flow, left ventricular developed pressure and its first derivative, dP/dt(max) in isolated working rat heart. The effect of 10 nM capsaicin was mimicked by 0.1 nM endothelin. PD142893 (200 nM), a non-selective endothelin receptor blocking agent antagonized the effect of either endothelin (0.1 nM) or capsaicin (10 nM). We conclude that the majority of the effects of capsaicin in the rat heart are mediated by neural endothelin release.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
endothelin
capsaicin
Megjelenés:European Journal of Pharmacology 376 : 3 (1999), p. 247-250. -
További szerzők:Oroszi Gábor (Pécs) Németh József (Pécs) Szilvássy Zoltán (1957-) (belgyógyász, farmakológus, klinikai farmakológus) Tósaki Árpád (1958-) (kísérletes farmakológus, gyógyszerész)
Internet cím:Szerző által megadott URL
DOI
Intézményi repozitóriumban (DEA) tárolt változat
Borító:
Rekordok letöltése1 
Corvina könyvtári katalógus v8.2.27 © 2023 Monguz kft. Minden jog fenntartva.