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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: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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4.

001-es BibID:BIBFORM042021
Első szerző:Ferdinándy Péter
Cím:Cicletanine improves myocardial function deteriorated by ischemia/reperfusion in isolated working rat hearts / Ferdinandy Péter, Koltai Mátyás, Tósaki Árpád, Berthet Philippe, Tarrade Thierry, Esanu André, Braquet Pierre
Dátum:1992
Megjegyzések:The effect of cicletanine, a novel furopyridine antihypertensive drug was compared with that of nitrendipine, a dihydropyridine slow calcium channel blocker, on cardiac function and reperfusion-induced ventricular arrhythmias in isolated working rat hearts subjected to 10-min ischemia induced by ligation of the left main coronary artery followed by 10-min reperfusion. Before ischemia, cicletanine and nitrendipine, perfused at concentrations of 3 x 10(-5), 6 x 10(-5), 10(-4), and 2 x 10(-4) or 10(-8) M, respectively, did not influence heart rate (HR), LV developed pressure (LVDP), its first derivative (LVdP/dtmax), and LV end-diastolic pressure (LVEDP), whereas aortic flow (AF) was decreased by 2 x 10(-4) M cicletanine only. Coronary flow (CF) remained unchanged by various cicletanine concentrations but was slightly increased by nitrendipine. In the concentration range of 3 x 10(-5)-10(-4) M, cicletanine improved AF either in ischemia or during reperfusion, whereas 2 x 10(-4) M had no such effect. Nitrendipine slightly attenuated ischemia/reperfusion-induced decrease in AF. Cicletanine and nitrendipine enhanced LVDP during ischemia. Ischemia-induced deterioration of LVdP/dtmax was reduced by cicletanine, during reperfusion, but this parameter was reduced by nitrendipine and the highest cicletanine concentration. Cicletanine decreased LVEDP significantly during ischemia and reperfusion, but nitrendipine had no such effect. All cicletanine concentrations reduced the incidence of irreversible ventricular fibrillation (VF) during reperfusion, an effect roughly concentration dependent in the range of 3 x 10(-5)-10(-4) M, whereas nitrendipine had no influence on arrhythmias.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
MSH
Megjelenés:Journal of Cardiovascular Pharmacology. - 19 : 2 (1992), p. 181-189. -
További szerzők:Koltai Mátyás Tósaki Árpád (1958-) (kísérletes farmakológus, gyógyszerész) Berthet, Philippe Tarrade, Thierry Esanu, Andre Braquet, Pierre
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5.

001-es BibID:BIBFORM041711
035-os BibID:PMID:9673419
Első szerző:Ferdinándy Péter
Cím:Role of nitric oxide and TPEN, a potent metal chelator, in ischaemic and reperfused rat isolated hearts / Peter Ferdinandy, Yori Appelbaum, Csaba Csonka, Ingolf Blasig, Arpad Tosaki
Dátum:1998
Megjegyzések:1. The role of nitric oxide (NO) was studied in the control of ischaemic/reperfused cardiac function and the effect of N,N,N',N'-tetrakis-[2-pyridylmethyl]-ethylenediamine (TPEN), a potent metal chelator, on the regulation of cardiac NO formation. 2. Rat isolated working hearts were subjected to 30 min ischaemia and reperfusion. The incidence of reperfusion-induced ventricular fibrillation (VF), ventricular tachycardia (VT) and the recovery of cardiac function were measured. Nitric oxide was detected by electron spin resonance (ESR) spectroscopy. 3. With 5.0, 7.5 and 10.0 mumol/L of TPEN administered prior to ischaemia, the drug produced a reduction in the incidence of VF from its control value of 100% to 25% (P < 0.05), 17% (P < 0.05) and 8% (P < 0.05), respectively. The incidence of VT followed the same pattern. 4. When TPEN was given at the moment of reperfusion, a reduction in the incidence of VF and VT was still observed. Reduction in the incidence of VF and VT was reflected in the improvement of cardiac function both in the pre- and post-ischaemic TPEN-treated groups. 5. TPEN reduced basal cardiac NO content and prevented the accumulation of NO during ischaemia/reperfusion. 6. The results show that TPEN exerts beneficial effects on postischaemic cardiac function and dysrhythmias in relation to inhibition of the accumulation of NO in ischaemic/reperfused myocardium.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
külföldön készült közlemény
Megjelenés:Clinical and Experimental Pharmacology and Physiology 25 : 7-8 (1998), p. 496-502. -
További szerzők:Appelbaum, Yori Csonka Csaba Blasig, Ingolf E. Tósaki Árpád (1958-) (kísérletes farmakológus, gyógyszerész)
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6.

001-es BibID:BIBFORM041699
Első szerző:Ferdinándy Péter
Cím:Pacing-induced Ventricular Fibrillation Leading to Oxygen Free Radical Formation in Aerobically Perfused Rat Hearts / Ferdinandy P., Das D. K., Tosaki A.
Dátum:1993
Megjegyzések:The objective of this study was to determine whether electrically-induced ventricular fibrillation can elicit oxygen free radical formation, even in the absence of ischemia and reperfusion. Rat hearts (n = 8 in each group) were perfused aerobically at 37 degrees C and ventricular fibrillation was induced by pacing (20 Hz, 1200 beats/min) for 10 min, during which time no changes in coronary flow rates were observed. In this study, electron spin resonance (ESR) studies using the spin trap 5,5-dimethyl-1-pyrroline-N-oxide (DMPO) demonstrated the formation of oxygen free radicals consisting of 1:2:2:1 quartet with peak concentration at the 3rd min of fibrillation in non-ischemic electrically fibrillating hearts. Since there were no significant changes in coronary flow rates during ventricular fibrillating (22.3 +/- 1.3 ml/min in control vs 22.3 +/- 0.9 ml/min in pacing-induced fibrillating group), the formation of oxygen free radicals could not be attributed to a pacing-induced ischemic event. In additional studies, hearts were paced by 10 Hz (600 beats/min), to demonstrate whether ventricular tachycardia could elicit free radical formation. In these experiments the genesis of oxygen free radicals was not observable after 1 min, 5 min, and 10 min of tachycardia, but a small amount of OH. radicals was detected at the 3rd min of ventricular tachycardia. When DMPO was infused into the heart giving a final perfusate concentration of 2.5 mmoles/litre during the pacing-induced fibrillation period, myocardial function (aortic flow, cardiac output, left ventricular developed pressure, first derivative of left ventricular developed pressure, and end-diastolic pressure) was significantly improved after the postfibrillating period. In conclusion, our studies clearly show that electrically-induced ventricular fibrillation is capable of eliciting free radical formation even in the absence of ischemia and reperfusion, and the cardioprotective effect of the spin trap is directly originated from its free radical trapping property and not from the other pharmacological activities of DMPO.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Journal of Molecular and Cellular Cardiology. - 25 : 6 (1993), p. 683-692. -
További szerzők:Das, Dipak Kumar Tósaki Árpád (1958-) (kísérletes farmakológus, gyógyszerész)
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7.

001-es BibID:BIBFORM027564
Első szerző:Haines, David Donald (gyógyszerész)
Cím:Cardioprotective effects of the calcineurin inhibitor FK506 and the PAF receptor antagonist and free radical scavenger, EGb 761, in isolated ischemic/reperfused rat hearts / David D. Haines, Istvan Bak, Peter Ferdinandy, Fadia F. Mahmoud, Saleh A. Al-Harbi, Ingolf E. Blasig, Arpad Tosaki
Dátum:2000
ISSN:0160-2446
Megjegyzések:Effects of the calcineurin inhibitor FK506, the platelet-activating factor (PAF) antagonist, and free radical scavenger Ginkgo biloba extract, EGb 761, and their combination on reperfusion-induced ventricular fibrillation (VF), ventricular tachycardia (VT), and recovery of cardiac function were studied after 30 min of global ischemia followed by 2 h of reperfusion in isolated rat hearts. In the first series of studies, rats received a daily (oral) dose of 0, 1, 5, 10, 20, or 40 mg/kg/day FK506 for 10 days. FK506 dose-dependently reduced the incidence of reperfusion-induced total (irreversible plus reversible) VF from a value of 92% for untreated animals to 92% (NS), 83% (NS), 67% (NS), 33% (p<0.05), and 25% (p<0.05), for doses of 1-40 mg/kg/day, respectively, with effects on incidence of VT showing the same pattern. FK506, between 20 and 40 mg/kg/day, also resulted in significant recovery of postischemic cardiac function. In the second series of studies, rats were treated with EGb 761 alone or in combination with FK506. Whereas no significant reduction in arrhythmias or improvement in cardiac function resulted from a single intervention of EGb 761 at 25 mg/kg/day, combined treatment of rats with 25 mg/kg/day of EGb 761 and 1 or 5 mg/kg/day of FK506 resulted in a reduction in total and irreversible VF of 92% and 92% to 42% (p<0.05) and 33% (p<0.05), 25% (p<0.05) and 8% (p<0.05), respectively, versus untreated control animals, paralleled by similar effects on the incidence of VT and accompanied by significant improvements in postischemic cardiac function. Our results demonstrate a novel cardioprotective characteristic of FK506 and suggest that combination therapy by using FK506 plus EGb 761 synergistically improves postischemic cardiac function, while reducing the incidence of reperfusion-induced VF and VT, which may expand the clinical utility of FK506 and allow therapy with FK506 at lower doses than are currently useful.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
egyetemen (Magyarországon) készült közlemény
Megjelenés:Journal Of Cardiovascular Pharmacology 35 : 1 (2000), p. 37-44. -
További szerzők:Bak István (1975-) (vegyész, analitikus, farmakológus) Ferdinándy Péter Mahmoud, Fadia F. Al-Harbi, Saleh A. Blasig, Ingolf E. Tósaki Árpád (1958-) (kísérletes farmakológus, gyógyszerész)
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8.

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)
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9.

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)
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10.

001-es BibID:BIBFORM042023
Első szerző:Varga Edit (gyógyszerész)
Cím:The protective effect of EGb 761 in isolated ischemic/reperfused rat hearts : a link between cardiac function and nitric oxide production / Varga Edit, Bódi Annamária, Ferdinandy Péter, Droy-Lefaix Marie-Therese, Blasig Ingolf E., Tósaki Árpád
Dátum:1999
Megjegyzések:This study was conducted to evaluate the effect of Ginkgo biloba extract (EGb 761) on the nitric oxide (NO) production in relation to the recovery of postischemic cardiac function in isolated working rat hearts. Rats were orally treated with various doses (25, 50, 75, and 100 mg/kg/day) of EGb 761 for 10 days. Hearts were isolated in "working mode" and subjected to 30-min ischemia followed by 120 min of reperfusion. EGb 761 inhibited NO production measured by electron spin-resonance spectroscopy (ESR), and improved the recovery of postischemic cardiac function (coronary flow, aortic flow, left ventricular developed pressure and its first derivative) in the ischemic/reperfused myocardium. Thus in rats treated with 25, 50, 75, and 100 mg/kg/day of EGb 761 and in hearts subjected to 30-min ischemia followed by 120 min of reperfusion, aortic flow was increased from its postischemic drug-free control value of 8.0+/-0.4 to 8.6+/-0.4 ml/min (NS), 17.3+/-0.9 ml/min (p<0.05), 21.5+/-1.1 ml/min (p<0.05), and 23.6+/-1.2 ml/min, respectively. The same recovery in postischemic coronary flow, left ventricular developed pressure, and its first derivative also was observed. In the initial phase of reperfusion, NO production measured by ESR was reduced by 85% in the 75 mg/ kg/day of EGb 761-treated group in comparison with the drug-free ischemic/reperfused hearts. Inducible NO synthase (iNOS) messenger RNA (mRNA) measured by reverse transcription-polymerase chain reaction (RT-PCR) also was reduced by 41 and 58% in the groups treated with 75 and 100 mg/kg/day of EGb 761, respectively. Our findings show that EGb 761 directly acts as an NO scavenger and concomitantly inhibits the expression of iNOS mRNA. Thus, EGb 761 may act as a potent inhibitor of NO production under the condition of ischemia/reperfusion, improving the recovery of postischemic cardiac function.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
MSH
Megjelenés:Journal of Cardiovascular Pharmacology. - 34 : 5 (1999), p. 711-717. -
További szerzők:Bódi Annamária (1957-) (kardiológus) Ferdinándy Péter Droy-Lefaix, Marie-Thérèse Blasig, Ingolf E. Tósaki Árpád (1958-) (kísérletes farmakológus, gyógyszerész)
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