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1.

001-es BibID:BIBFORM027565
Első szerző:Bak István (vegyész, analitikus, farmakológus)
Cím:Evaluation of systemic and dermal toxicity and dermal photoprotection by sour cherry kernels / Istvan Bak, Attila Czompa, Evelin Csepanyi, Bela Juhasz, Heibatullah Kalantari, Khadija Najm, Nasreen Aghel, Balazs Varga, David D. Haines, Arpad Tosaki
Dátum:2011
ISSN:0160-2446
Megjegyzések:The present report describes outcomes of animal studies conducted to determine the systemic and dermal toxicity of Prunus cerasus (sour cherry) seed kernel contents; and a separate evaluation of the photoprotective capacity of the kernel oil fraction. B6 mice and Hartley guinea-pigs were used for these experiments. Dosage groups of 6-8 animals were administered whole kernel meal in a dose range of 0-3000 mg/kg by gavage for 8 days, following which they were killed. The liver and kidney weights were recorded and histological examination performed on sections of these organs. Kidney function was assessed as blood urea nitrogen and creatinine and liver function by measurement of serum glutamic oxaloacetic transaminase, glutamic pyruvic transaminase and alkaline phosphatase. Dermal toxicity was evaluated in a Hartley guinea-pig model by comparing UVB-irradiated shaved skin to which the kernel oil had been applied with distilled water controls. In conclusion, no evidence of toxicity was observed to result from the consumption or dermal application of sour cherry seed kernel in the dose range at which it is likely to be used in foods or healthcare. Moreover, it was shown to have a powerful capacity to protect skin from UV damage. These results suggest it will prove to be a highly safe and effective addition to a wide range of products for general use. Copyright © 2011 John Wiley & Sons, Ltd.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
egyetemen (Magyarországon) készült közlemény
Megjelenés:Phytotherapy Research. - 25 : 11 (2011), p. 1714-1720. -
További szerzők:Czompa Attila (1985-) (gyógyszerész) Csépányi Evelin (1985-) (gyógyszerész) Juhász Béla (1978-) (kísérletes farmakológus) Kalantari, Heybatullah Najm, Khadija Aghel, Nasreen Varga Balázs (1984-) (kísérletes farmakológus) Haines, David Donald (1981-) (gyógyszerész) Tósaki Árpád (1958-) (kísérletes farmakológus, gyógyszerész)
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DOI
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2.

001-es BibID:BIBFORM041168
035-os BibID:PMID:12409985
Első szerző:Cui, Jianhua
Cím:Cardioprotection with grapes / Jianhua Cui, Bela Juhasz, Arpad Tosaki, Nilanjana Maulik, Dipak K. Das
Dátum:2002
Megjegyzések:Epidemiologic studies suggest that mild-to-moderate wine consumption is associated with a reduced incidence of mortality and morbidity from coronary heart disease. Because wines are produced from grapes, this study was done to determine whether the grapes were equally cardioprotective. Sprague-Dawley male rats were given (orally) standardized grape extract (SGE) (obtained from the California Table Grape Commission, Fresno, CA, U.S.A.) (50, 100, or 200 mg/kg body weight per day) for 3 weeks. Time-matched control experiments were performed by feeding the animals 45 microg/100 g of glucose plus 45 microg/100 g of fructose per day for 3 weeks. After 21 days, rats were killed and the hearts excised and perfused via working mode. Hearts were made ischemic for 30 min followed by 2 h of reperfusion. At 100 mg/kg and at 200 mg/kg, grapes provided significant cardioprotection as evidenced by improved postischemic ventricular recovery (aortic flow, developed pressure, the maximum first derivative of the developed pressure) and reduced amount of myocardial infarction. There were no differences in results between the two groups (100 mg/kg versus 200 mg/kg). No cardioprotection was apparent when rats were given grape samples at a dose of 50 mg/100 g/d. SGE reduced the malonaldehyde content of the heart, indicating reduction of oxidative stress during ischemia and reperfusion. In vitro studies demonstrated that the SGE could directly scavenge superoxide and hydroxyl radicals that are formed in the ischemic reperfused myocardium. The results demonstrate that the hearts of the rats fed SGE are resistant to myocardial ischemia reperfusion injury, suggesting a cardioprotective role of grapes.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
egyetemen (Magyarországon) készült közlemény
Megjelenés:Journal of Cardiovascular Pharmacology 40 : 5 (2002), p. 762-769. -
További szerzők:Juhász Béla (1978-) (kísérletes farmakológus) Tósaki Árpád (1958-) (kísérletes farmakológus, gyógyszerész) Maulik, Nilanjana Das, Dipak Kumar
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3.

001-es BibID:BIBFORM054296
Első szerző:Czompa Attila (gyógyszerész)
Cím:Cardioprotection afforded by sour cherry seed kernel : the role of heme oxygenase-1 / Attila Czompa, Alexandra Gyongyosi, Andras Czegledi, Evelin Csepanyi, Istvan Bak, David D. Haines, Arpad Tosaki, Istvan Lekli
Dátum:2014
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
Molekulatudomány
Doktori iskola
Megjelenés:Journal of Cardiovascular Pharmacology. - 64 : 5 (2014), p. 412-419. -
További szerzők:Gyöngyösi Alexandra (1990-) (táplálkozástudományi szakember) Czeglédi András Csépányi Evelin (1985-) (gyógyszerész) Bak István (1975-) (vegyész, analitikus, farmakológus) Haines, David Donald (1981-) (gyógyszerész) Tósaki Árpád (1958-) (kísérletes farmakológus, gyógyszerész) Lekli István (1981-) (gyógyszerész)
Pályázati támogatás:K-104017
OTKA
PD-83808
OTKA
TÁMOP-4.2.1/B-09/1/KONV-2010-0007
TÁMOP
Kardiovaszkuláris megbetegedések génterápiás befolyásolása
TÁMOP-4.2.2/B-10/1-2010-0024
TÁMOP
Gyógyszerészeti Tudományok Doktori Iskola
TÁMOP-4.2.2.A-11/1/KONV-2012-0045
TÁMOP
Gyógyszerhatástan Kutatócsoport
TÁMOP 4.2.4. A/2-11-1-2012-0001
TÁMOP
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DOI
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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: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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6.

001-es BibID:BIBFORM041636
Első szerző:Hearse, David J.
Cím:Reperfusion-Induced Arrhythmias and Free Radicals : studies in the Rat Heart with DMPO / David J. Hearse, Arpad Tosaki
Dátum:1987
Megjegyzések:We have shown that the free radical spin trap DMPO (5,5-dimethyl-1-pyrroline-N-oxide) reduces reperfusion-induced arrhythmias in a dose-dependent manner in the isolated perfused rat heart subjected to 10 min regional ischemia and 3 min reperfusion. At its optimal concentration (1,000 mumol/L) DMPO, added to the perfusate 5 min prior to ischemia, reduced (p less than 0.05) the incidence of reperfusion-induced irreversible ventricular fibrillation from 83 (10 of 12) to 33% (4 of 12). When hearts were subjected to ischemia (10 min) and reperfusion, with DMPO (1,000 mumol/L) added to the perfusion fluid only 2 min before reperfusion, comparable protection was observed. To ascertain whether or not DMPO achieved an absolute reduction in vulnerability to arrhythmias irrespective of the duration of ischemia, hearts (12 for each group) were also subjected to 5, 10, 20, 30, or 40 min of ischemia; DMPO (1,000 mumol/L) was added to the perfusate either 5 min before ischemia or 2 min before reperfusion. In each instance a bell-shaped time-response profile was obtained. In the DMPO-free controls this gave a maximal vulnerability to arrhythmias after 10 min of ischemia. In the DMPO-treated hearts this curve was shifted to the right, with a peak vulnerability at 20 min. These results indicate that the primary action of DMPO is to exert a delaying effect which extends the duration of ischemia that can be tolerated before the heart becomes vulnerable to reperfusion-induced arrhythmias. However, this effect is achieved during the reperfusion period and not during the preceding period of ischemia. The precise mechanism by which this free radical spin trapping agent achieves this unusual effect remains to be resolved, but in studies with light-inactivated DMPO, this protective effect was lost, indicating that its ability to be oxidized, possibly by superoxide or hydroxyl radicals, may be critical to its mechanism of action.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Journal of cardiovascular pharmacology. - 9 : 6 (1987), p. 641-650. -
További szerzők:Tósaki Árpád (1958-) (kísérletes farmakológus, gyógyszerész)
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7.

001-es BibID:BIBFORM020336
Első szerző:Karsai Dénes
Cím:Effect of nucleoside transport blockade on the Interstitial adenosine level characterized by a novel method in guinea pig atria / Karsai, Dénes, Zsuga, Judit, Juhász, Béla, Dér, Péter, Szentmiklósi, András József, Tósaki, Árpád, Gesztelyi, Rudolf
Dátum:2006
Megjegyzések:Several accepted methods are available to estimate theadenosine (Ado) concentration of interstitial fluid ([Ado]ISF) in functioningheart, providing results spanning over nano- to micromolarconcentrations. This extremely large range points to the necessity ofnovel approaches for estimating [Ado]ISF or at least the alterationfrom basal [Ado]ISF. In the present study, the change in [Ado]ISF wascharacterized following nucleoside transport (NT) blockade elicitedby 10 mmol/L dipyridamole or 10 mmol/L nitrobenzylthioinosine inisolated guinea pig atria, by means of our novel procedure referred toas receptorial responsiveness method (RRM). The RRM provided anindex of the change in [Ado]ISF under NT blockade, namely theconcentration of N6-cyclopentyladenosine (CPA; a relatively stableA1 Ado receptor agonist), which is equieffective with the change in[Ado]ISF regarding the contractility. Our results show that dipyridamoleor nitrobenzylthioinosine produced an elevation in [Ado]ISFat the cardiomyocyte A1 Ado receptors equivalent to about 16 or20 nmol/l CPA, respectively. In addition, nitrobenzylthioinosine wasfound more appropriate for selective NT blockade than dipyridamole.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
atrium
guinea pig
heart
interstitial adenosine
Megjelenés:Journal of Cardiovascular Pharmacology. - 47 : 1 (2006), p. 103-109. -
További szerzők:Zsuga Judit (1973-) (neurológus, pszichoterapeuta, egészségügyi szakmanager) Juhász Béla (1978-) (kísérletes farmakológus) Dér Péter Szentmiklósi József András (1948-) (farmakológus, klinikai laboratóriumi szakorvos) Tósaki Árpád (1958-) (kísérletes farmakológus, gyógyszerész) Gesztelyi Rudolf (1969-) (kísérletes farmakológus)
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8.

001-es BibID:BIBFORM041687
Első szerző:Liu, X. K.
Cím:Salicylate Reduces Ventricular Dysfunction and Arrhythmias During Reperfusion in Isolated Rat Hearts / Liu X. K., Tosaki A., Engleman R. M., Das D. K.
Dátum:1992
Megjegyzések:Recent studies have shown the ability of salicylic acid (SA) to trap hydroxyl radicals (OH.) generated during reperfusion in ischemic myocardium. Since OH. is implicated in the pathogenesis of reperfusion injury, we examined the effect of SA on reperfusion-induced arrhythmias and postischemic ventricular dysfunction. Isolated rat hearts perfused by the Langendorff technique were preperfused with Krebs-Henseleit buffer containing SA for 10 min. Hearts were then made ischemic for 30 min, followed by 30 min of reperfusion. In a separate group, SA was administered only at the onset of reperfusion. The left ventricular contractile functions, left ventricular developed pressure (LVDP) and its first derivative (LV dP/dt), coronary flow (CF), and creatine kinase (CK) release were determined before and after ischemia. Epicardial electrocardiogram (ECG) was also recorded to analyze the incidence of ventricular tachycardia (VT) and ventricular fibrillation (VF). SA improved LVDP, LV dp/dt, and CF recovery and reduced CK release compared to the control group. The incidence of VT and VF during reperfusion was also significantly reduced by SA. Analysis of tissue thiobarbituric acid-reactive products indicates that SA decreased oxidative stress during reperfusion. In conclusion, these results suggest that SA reduces myocardial reperfusion injury and attenuates ventricular arrhythmias by trapping OH. radicals upon reperfusion in isolated rat hearts.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Journal of Cardiovascular Pharmacology. - 19 : 2 (1992), p. 209-215. -
További szerzők:Tósaki Árpád (1958-) (kísérletes farmakológus, gyógyszerész) Engleman, R. M. Das, Dipak Kumar
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9.

001-es BibID:BIBFORM042332
035-os BibID:PMID:7799644
Első szerző:Maulik, Nilanjana
Cím:Myocardial salvage by 1-O-hexadecyl-Sn-glycerol : possible role of peroxisomal dysfunction in ischemia reperfusion injury / Nilanjana Maulik, Arpad Tosaki, Richard M. Engelman, Gerald A. Cordis, Dipak K. Das
Dátum:1994
ISSN:0160-2446
Megjegyzések:A recent study demonstrated biochemical and structural alterations of peroxisomes in rat kidney after ischemia/reperfusion. We examined whether peroxisomes play any role in the pathophysiology of myocardial ischemia/reperfusion injury. Isolated perfused rat heart was made ischemic for 30 min by terminating coronary flow (CF), followed by 30-min reperfusion. Experiments were divided into two groups; the experimental group received 1-O-hexadecyl-Sn-glycerol (chimyl alcohol) (25, 50, and 100 microM) before ischemia, and the control group received an equivalent amount of saline. Two of the experimental groups (50 and 100 microM) demonstrated improved postischemic myocardial performance, as demonstrated by accelerated recovery in left ventricular developed pressure (LVDP) and CF, as well as reduction in the incidence of ventricular fibrillation (VF). However, because the heart rate (HR) was significantly reduced in the 100-microM chimyl alcohol group, subsequent studies were performed with 50 microM chimyl alcohol as the optimal dose. Chimyl alcohol (50 microM) also reduced cellular injury, as evidenced by reduced creatine kinase (CK) release, and decreased development of oxidative stress, as evidenced by reduced formation of malonaldehyde (MDA). Peroxisomal catalase activity was decreased in the control group after ischemia/reperfusion, and chimyl alcohol treatment restored the activity of the enzyme. Our results indicate that chimyl alcohol, a precursor of ether-linked phosphoglyceride biosynthesis, can reduce myocardial ischemia/reperfusion injury, possibly by restoring catalase activity and reducing oxidative stress through synthesis of ether lipids, suggesting a possible role of peroxisomal disorder in ischemia/reperfusion injury.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
külföldön készült közlemény
Megjelenés:Journal of Cardiovascular Pharmacology. - 24 : 3 (1994), p. 486-492. -
További szerzők:Tósaki Árpád (1958-) (kísérletes farmakológus, gyógyszerész) Engelman, Richard M. Cordis, Gerald A. Das, Dipak Kumar
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10.

001-es BibID:BIBFORM015109
Első szerző:Szilágyi Szabolcs (kardiológus)
Cím:Two inotropes with different mechanisms of action : contractile, PDE-inhibitory and direct myofibrillar effects of levosimendan and enoximone / Szilagyi S., Pollesello P., Levijoki J., Haikala H., Bak I., Tosaki A., Borbely A., Edes I., Papp Z.
Dátum:2005
Megjegyzések:We characterized the Ca2+-sensitizing and phosphodiesterase (PDE)-inhibitory potentials of levosimendan and enoximone to assess their contributions to the positive inotropic effects of these drugs. In guinea pig hearts perfused in the working-heart mode, the maximal increase in cardiac output (55%, P<0.05) was attained at 50 nM levosimendan. The corresponding value for enoximone (36%) was significantly smaller (P<0.05) and was observed at a higher concentration (500 nM). In permeabilized myocyte-sized preparations levosimendan evoked a maximal increase of 55.8+/-8% (mean+/-SEM) in isometric force production via Ca2+ sensitization (pCa 6.2, EC50 8.4 nM). Enoximone up to a concentration of 10 microM failed to influence the isometric force. The PDE-inhibitory effects were probed on the PDE III and PDE IV isoforms. Levosimendan proved to be a 1300-fold more potent and a 90-fold more selective PDE III inhibitor (IC50 for PDE III 1.4 nM, and IC50 for PDE IV 11 microM, selectivity factor approximately 8000) than enoximone (IC50 for PDE III 1.8 microM, and IC50 for PDE IV 160 microM, selectivity factor approximately 90). Hence, our data support the hypothesis that levosimendan exerts positive inotropy via a Ca2+-sensitizing mechanism, whereas enoximone does so via PDE inhibition with a limited PDE III versus PDE IV selectivity.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
egyetemen (Magyarországon) készült közlemény
Megjelenés:Journal of Cardiovascular Pharmacology. - 46 : 3 (2005), p. 369-376. -
További szerzők:Pollesello, Piero Levijoki, Jouko Haikala, Heimo Bak István (1975-) (vegyész, analitikus, farmakológus) Tósaki Árpád (1958-) (kísérletes farmakológus, gyógyszerész) Borbély Attila (1978-) (kardiológus) Édes István (1952-) (kardiológus) Papp Zoltán (1965-) (kardiológus, élettanász)
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11.

001-es BibID:BIBFORM042022
Első szerző:Tósaki Árpád (kísérletes farmakológus, gyógyszerész)
Cím:Cicletanine and reperfusion injury : is there any correlation between arrhythmias, 6-keto-PGF1 alpha, thromboxane B2, and myocardial ion shifts (Na+, K+, Ca2+, and Mg2+) induced by ischemia/reperfusion in isolated rat heart / Tósaki Árpád, Hellegouarch Anne, Braquet Pierre
Dátum:1991
Megjegyzések:We studied the effects of cicletanine, an anti-hypertensive drug, on reperfusion arrhythmias in relation to 6-keto-PGF1 alpha, thromboxane B2 (TXB2), and ion shifts (Na+, K+, Ca2+, and Mg2+) induced by ischemia and reperfusion in hearts isolated from spontaneously hypertensive rats. Hearts were subjected to 30-min global ischemia followed by 10-min reperfusion. 6-keto-PGF1 alpha and TXB2 concentrations were determined by radioimmunoassay (RIA) from coronary effluents, and myocardial Na+, K+, Ca2+, and Mg2+ contents were measured by atomic absorption spectrophotometry from myocardial tissue. Two basic protocols were used: (a) acute administration when 3, 10, 30, or 100 mg/L cicletanine was included in the perfusion buffer; and (b) chronic application, in which rats received cicletanine 3, 10, 30, or 100 mg/kg/day orally for 14 days. Acute administration of the drug in low concentrations (3 or 10 mg/L), significantly increased endogenous 6-keto-PGF1 alpha production before ischemia and during reperfusion, whereas higher doses of cicletanine (30 or 100 mg/L) as well as chronic application of the drug failed to increase production of 6-keto-PGF1 alpha in the myocardium. TXB2 production was not influenced by either acute or chronic treatment with the drug. Neither treatment changed myocardial ion contents in comparison with control values (Na+ = 45 +/- 4, K+ = 252 +/- 7, Ca2+ = 1.4 +/- 0.1, and Mg2+ = 12.5 +/- 0.3 mmol/kg dry weight) in nonischemic hearts. Thirty-minute ischemia resulted in a two- and fourfold accumulation of myocardial Na+ and Ca2+ and a 50% decrease in both K+ and Mg2+
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
MSH
Megjelenés:Journal of Cardiovascular Pharmacology. - 17 : 4 (1991), p. 551-559. -
További szerzők:Hellegouarch, Anne Braquet, Pierre
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12.

001-es BibID:BIBFORM042024
Első szerző:Tósaki Árpád (kísérletes farmakológus, gyógyszerész)
Cím:The Role of Protein Kinase C in Ischemic/Reperfused Preconditioned Isolated Rat Hearts / Tósaki Árpád, Maulik Nilanjana, Engelman Daniel T., Engelman Richard M., Das K. Dipak
Dátum:1996
Megjegyzések:Protein kinase C (PKC) has been implicated in the preconditioning-induced cardiac protection in ischemic/reperfused myocardium. We studied the effect of PKC inhibition with calphostin C (25, 50, 100, 200, 400, and 800 nM), a potent and specific inhibitor of PKC, in isolated working nonpreconditioned and preconditioned ischemic/reperfused hearts. In the nonpreconditioned groups, all hearts underwent 30 min of normothermic global ischemia followed by 30 min of reperfusion. In the preconditioned groups, hearts were subjected to four cycles of ischemic preconditioning by using 5 min of ischemia followed by 10 min reperfusion, before the induction of 30 min ischemia and reperfusion. At low concentrations of calphostin C (25, 50, and 100 nM), the PKC inhibitor had no effect on the incidence or arrhythmias or postischemic cardiac function in the nonpreconditioned ischemic/reperfused groups. With 200 and 400 nM of calphostin C, a significant increase in postischemic function and a reduction in the incidence of arrhythmias were observed in the nonpreconditioned ischemic/reperfused groups. Increasing the concentration of calphostin C to 800 NM, the recovery of postischemic cardiac function was similar to that of the drug-free control group. In preconditioned hearts, lower concentrations (< 100 nM) of calphostin C did not change the response of the myocardium to ischemia and reperfusion in comparison to the preconditioned drug-free myocardium. Two hundred and 400 nM of the PKC inhibitor further reduced the incidence of ventricular fibrillation (VF) from the preconditioned drug-free value of 50% to 0 (p < 0.05) and 0 (p < 0.05), respectively, indicating that the combination of the two, preconditioning and calphostin C, affords significant additional protection. Increasing the concentration of calphostin C to 800 nM blocked the cardioprotective effect of preconditioning (100% incidence of VF). The recovery of cardiac function was similarly improved at calphostin C doses of 200 and 400 nM and was reduced at 800 nM (p < 0.05). With 200 and 400 nM of calphostin C, both cytosolic and particulate PKC activity were reduced by approximately 40 and 60%, respectively, in both preconditioned and preconditioned/ischemic/reperfused hearts. The highest concentration of calphostin C (800 nM) resulted in almost a complete inhibition of cytosolic (100%) and particulate (85%) PKC activity correlated with the abolition of preconditioning-induced cardiac protection. In conclusion, calphostin C protects the ischemic myocardium obtained from intact animals, provides significant additional protection to preconditioning at moderate doses, and blocks the protective effect of preconditioning at high concentrations. The dual effects of calphostin C appear to be strictly dose and "enzyme inhibition" related.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
MSH
Megjelenés:Journal of Cardiovascular Pharmacology. - 28 : 5 (1996), p. 723-731. -
További szerzők:Maulik, Nilanjana Engelman, Daniel T. Engelman, Richard M. Das, Dipak Kumar
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
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