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1.

001-es BibID:BIBFORM041657
Első szerző:Blasig, Ingolf E.
Cím:Inverse relationship between ESR spin trapping of oxyradicals and degree of functional recovery during myocardial reperfusion in isolated working rat heart / Blasig I. E., Ebert B., Hennig C., Pali T., Tosaki A.
Dátum:1990
Megjegyzések:STUDY OBJECTIVE: The aim of the study was to investigate the generation of free oxyradicals as factors in myocardial ischaemia-reperfusion pathology. DESIGN: Isolated perfused rat hearts were subjected to 30 min global ischaemia followed by reperfusion. The spin trap 5,5-dimethyl-1-pyrroline-1-oxide was added to the effluent of the heart to avoid pharmacological interaction with the heart. The effluent was then analysed by electron spin resonance spectroscopy. MATERIALS: Studies were performed on hearts of 51 male Sprague-Dawley rats, weight 300-350 g. MEASUREMENTS AND RESULTS: During reperfusion, the formation of hydroxyl radical adducts of the trap was observed, with a maximal value after 3 min. The initial amount of radicals trapped during the first 3 min of reperfusion showed an inverse correlation with the degree of heart function restored within 30 min of reperfusion. Spearman's rank correlation coefficients were calculated to be -0.734 for heart rate, -0.825 for left ventricular developed pressure, -0.787 for the maximum of its first derivative, -0.787 for coronary flow, and -0.796 for aortic flow (p less than 0.05, n = 10, in each instance). No statistically significant correlation was found between the cumulative amount of radicals trapped in the effluent during the initial phase of reperfusion and the duration of ventricular fibrillation, duration of ventricular tachycardia, or number of ventricular ectopic beats (registered during 30 min reperfusion). CONCLUSIONS: The application of spin trapping to the effluent of isolated perfused hearts allows the generation of oxyradicals to be characterised without interaction of the trap with the heart. It also allows the time course of radical production to be investigated, and can detect relative changes in their intensity. These are important factors in the study of the pathogenic role of free radicals generated during reperfusion of an ischaemic heart.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Cardioscular Research. - 24 : 4 (1990), p. 263-270. -
További szerzők:Ebert, Berndt Hennig, Christian Pali Tibor Tósaki Árpád (1958-) (kísérletes farmakológus, gyógyszerész)
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2.

001-es BibID:BIBFORM041630
035-os BibID:PMID:3557105
Első szerző:Blasig, Ingolf E.
Cím:Effect of activated oxygen species on mitochondria isolated from myocardium after reperfusion injury / I. E. Blasig, P. Bor, A. Tósaki, L. Szekeres, H. Löwe
Dátum:1986
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
egyetemen (Magyarországon) készült közlemény
Megjelenés:General Physiol biophys 5 : 6 (1986), p. 655-658. -
További szerzők:Bor P. Tósaki Árpád (1958-) (kísérletes farmakológus, gyógyszerész) Szekeres László Löwe, H.
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3.

001-es BibID:BIBFORM041210
035-os BibID:PMID:11033413
Első szerző:Csonka Csaba
Cím:Effects of oxidative stress on the expression of antioxidative defense enzymes in spontaneously hypertensive rat hearts / Csaba Csonka, Tunde Pataki, Peter Kovacs, Sebastian L. Müller, Matthias L. Schroeter, Arpad Tosaki, Ingolf E. Blasig
Dátum:2000
Megjegyzések:Little is known concerning the effect of oxidative stress on the expression of antioxidative enzymes in the decompensated cardiac hypertrophy of spontaneously hypertensive rats (SHR), considered as a model of dilative cardiomyopathy in man. Superoxide dismutase (SOD), catalase, and glutathione peroxidase (GPx) were characterized in isolated perfused hearts of 18 month old SHR and the age-matched normotensive control Wistar-Kyoto (WKY) rats, before and after 30 min infusion of 25 microM H(2)O(2). After infusion of H(2)O(2), aortic flow decreased in WKY from 26.2 +/- 2.2 to 16.0 +/- 0.8 ml/min (p <.05) but not in SHR (18.2 +/- 1.9 vs. 20.7 +/- 2.2 ml/min). This protection was related to the higher myocardial activities of GPx, MnSOD and CuZnSOD in SHR, compared with those of the WKY group. Although total SOD activity in the SHR fell after H(2)O(2) exposure (to 1.81 +/- 0.13 from 3.56 +/- 0.49 U/mg of protein), catalase activity increased (to 2.46 +/- 0.34 from 1.56 +/- 0.29 k min(-1)mg(-1)protein), compared with the pre-infusion period (p <.05 in each case). In additional studies, hearts were subjected to 30 min of global ischemia followed by 30 min of reperfusion. The results obtained in ischemic/reperfused hearts show the same changes in enzyme activities measured as it was observed in H(2)O(2) perfused hearts, indicating that oxidative stress is independent of the way it was induced. The higher catalase activity derived from elevated mRNA synthesis. The antioxidative system in dilative cardiomyopathic hearts of SHR is induced, probably due to episodes of oxidative stress, during the process of decompensation. This conditioning of the antioxidative potential may help overcome acute stress situations caused by reactive oxygen species in the failing myocardium.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
külföldön készült közlemény
Megjelenés:Free Radical Biology & Medicine 29 : 7 (2000), p. 612-619. -
További szerzők:Pataki Tünde (1971-) (farmakológus, klinikai farmakológus) Kovács Péter (1939-) (farmakológus) Müller, Sebastian L. Schroeter, Matthias L. Tósaki Árpád (1958-) (kísérletes farmakológus, gyógyszerész) Blasig, Ingolf E.
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4.

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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5.

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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6.

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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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:BIBFORM027563
Első szerző:Kovács Péter (belgyógyász, kardiológus, klinikai farmakológus)
Cím:Non-specific caspase inhibition reduces infarct size and improves post-ischaemic recovery in isolated ischaemic/reperfused rat hearts / Peter Kovacs, Istvan Bak, Levente Szendrei, Miklos Vecsernyes, Edit Varga, Ingolf E. Blasig, Arpad Tosaki
Dátum:2001
Megjegyzések:Myocardial ischaemia and reperfusion lead to myocardial cell death due, at least in part, to apoptotic mechanisms. Although cysteinyl aspartate-specific proteinase (caspase) activation is a major event and the most-cited culprit in the development of apoptosis, its potential contribution to ischaemic myocardial cell death is largely unknown. To study the role of caspase activation, isolated rat hearts (n=6 per group) were subjected to 30 min coronary artery occlusion followed by 120 min reperfusion. A non-selective [0.1 or 0.5 microM acetyl-Tyr-Val-Ala-Asp chloromethylketone (YVAD-cmk)] or selective caspase inhibitors [0.07 or 0.2 microM acetyl-Asp-Glu-Val-Asp-cmk (Ac-DEVD-cmk, caspase-3 inhibitor); 0.07 or 0.2 microM benzoxycarbonyl-Leu-Glu-OMe-His-Asp(OMe)-fluoromethylketone (z-LEHD-fmk, caspase-9 inhibitor)] were added to the perfusate at the start of reperfusion. Non-selective caspase inhibition with 0.1 or 0.5 microM YVAD-cmk limited infarct size: (21 +/- 4%, P<0.05; 17 +/- 3%, P<0.05, respectively) compared with the ischaemic/reperfused control (32 +/- 5%). In hearts treated with 0.1 or 0.5 microM caspase II non-selective inhibitor, the fraction of terminal-deoxynucleotidyl-transferase deoxyuridine nick end labelling (TUNEL)-positive myocyte nuclei in the infarcted zone was reduced from the ischaemic/reperfused non-treated control of 11.2 +/- 2.1% to 6.2 +/- 1.6% (P<0.05) and 1.2 +/- 0.2% (P<0.05), respectively. The recovery of post-ischaemic cardiac function (coronary flow, aortic flow and left-ventricular developed pressure) improved significantly with the application of the non-selective caspase inhibitor as well. In hearts perfused with specific caspase inhibitors (caspase-3 and caspase-9) there was no significant reduction in the infarct size, no improvement in post-ischaemic cardiac function and no reduction of apoptotic cell death. We conclude that non-specific inhibition of caspases may be therapeutically beneficial in myocardial ischaemia/reperfusion-induced damage, while selective caspase inhibitors may fail to prevent such reperfusion-induced injury in our model system.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
egyetemen (Magyarországon) készült közlemény
Megjelenés:Naunyn-Schmiedeberg's archives of pharmacology 364 : 6 (2001), p. 501-507. -
További szerzők:Bak István (1975-) (vegyész, analitikus, farmakológus) Szendrei Levente Vecsernyés Miklós (1959-) (gyógyszertechnológus, endokrinológus) Varga Edit (gyógyszerész) Blasig, Ingolf E. Tósaki Árpád (1958-) (kísérletes farmakológus, gyógyszerész)
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9.

001-es BibID:BIBFORM027561
Első szerző:Pataki Tünde (farmakológus, klinikai farmakológus)
Cím:Regulation of ventricular fibrillation by heme oxygenase in ischemic/reperfused hearts / Tunde Pataki, Istvan Bak, Csaba Csonka, Peter Kovacs, Edit Varga, Ingolf E. Blasig, Arpad Tosaki
Dátum:2001
Megjegyzések:We have assessed the relationship between reperfusion-induced ventricular fibrillation (VF) and heme oxygenase (HO) mRNA expression using northern blotting, reverse transcription-polymerase chain reaction (RT-PCR), and enzyme activity in isolated working ischemic/reperfused rat hearts. Isolated hearts were subjected to 30 min of global ischemia followed by 120 min of reperfusion. Upon reperfusion with VF, cardiac function was registered (n = 6 in each group), and HO mRNAs and enzyme activities were measured at the end of reperfusion in hearts that showed VF or did not develop VF. The expression of HO-1 mRNA (about fourfold) was observed in ischemic/reperfused nonfibrillated myocardium in comparison with the nonischemic control hearts. In those hearts when VF was developed, the expression of HO-1 mRNA was not observed in comparison with the nonischemic control myocardium. The results measured by RT-PCR and enzyme analysis support the data obtained by northern blotting. In additional studies, we decided to approach the question from a different angle. Thus, the purpose of our work was also to study the role of HO expression and enzyme activity in electrically fibrillated hearts without the ischemic/reperfused protocol. To simulate the period of 10 min of reperfusion-induced VF, hearts were electrically fibrillated, then defibrillated, and perfused for an additional 110 min, and HO-1 mRNA expression and enzyme activities were determined. Thus, electrically induced VF resulted in about 60%, 60%, and 70% reduction in HO-1 mRNA expression, RT-PCR signal intensity, and enzyme activity, respectively, compared with the nonfibrillated ischemic/reperfused group. In conclusion, our data provide evidence that the development of reperfusion-induced VF inhibits HO-1 mRNA expression and enzyme activity in both electrically fibrillated myocardium and ischemic/reperfused fibrillated hearts. The results clearly show that HO-1 mRNA expression and enzyme activity were increased in ischemic/reperfused nonfibrillated myocardium, suggesting that interventions that are able to increase HO-1 mRNA expression and enzyme activity may prevent the development of VF.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
egyetemen (Magyarországon) készült közlemény
Megjelenés:Antioxidants & redox signaling 3 : 1 (2001), p. 125-134. -
További szerzők:Bak István (1975-) (vegyész, analitikus, farmakológus) Csonka Csaba Kovács Péter (1947-) (belgyógyász, kardiológus, klinikai farmakológus) Varga Edit (gyógyszerész) Blasig, Ingolf E. Tósaki Árpád (1958-) (kísérletes farmakológus, gyógyszerész)
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10.

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)
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11.

001-es BibID:BIBFORM041690
Első szerző:Tósaki Árpád (kísérletes farmakológus, gyógyszerész)
Cím:Does the antiarrhythmic effect of DMPO originate from its oxygen radical trapping property or the structure of the molecule itself? / Tosaki A., Haseloff R. F., Hellegouarch A., Schoenheit K., Martin V. V., Das D. K., Blasig I. E.
Dátum:1992
Megjegyzések:Using the isolated perfused rat heart with transient (30 min) normothermic global ischemia, it was shown that DMPO (5,5-dimethyl-pyrroline-N-oxide), an organic spin trap agent designed specifically to trap free radicals, dramatically reduced the vulnerability of the myocardium to reperfusion-induced ventricular fibrillation (VF) and ventricular tachycardia (VT). DMPO (concentration range 30-500 mumol/l) infused in the heart at the moment and during the first 10 min of reperfusion exerted a dose-dependent antiarrhythmic effect. Thus, the doses of 30, 100, and 500 mumol/l of DMPO reduced the incidence of reperfusion-induced VF and VT from their control values of 100% and 100% to 83% and 91%, 50% (p < 0.05) and 67%, 25% (p < 0.01) and 50% (p < 0.05), respectively. Furthermore, the recovery of myocardial function was improved during postischemic reperfusion. A modification in the molecular structure of DMPO leading to HMIO (1,2,2,4,5,5-hexamethyl-3-imidazoline-oxide), so-called inactive DMPO which does not trap free radicals in the presence of a radical generating system or in the effluent of reperfused hearts, failed to reduce the incidence of reperfusion-induced arrhythmias or improve the recovery of postischemic reperfused myocardium. These findings suggest that the free radical trapping properties of DMPO or the effects of the formed DMPO-OH, a stable nitroxyl radical adduct, are responsible for the reduction of reperfusion-induced arrhythmias, and not the molecular structure of DMPO itself. Finally, it is of interest to note that the detection of free radicals was observed in fibrillating hearts, but not in nonfibrillating hearts. This consideration should be taken into account when making therapeutic interventions and risk assessments of a radical scavenger in this setting.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Basic Research in Cardiology. - 87 : 6 (1992), p. 536-547. -
További szerzők:Haseloff, R. F. Hellegouarch, Anne Schoenheit, K. Martin, V. V. Das, Dipak Kumar Blasig, Ingolf E.
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
DOI
Borító:

12.

001-es BibID:BIBFORM041658
Első szerző:Tósaki Árpád (kísérletes farmakológus, gyógyszerész)
Cím:Heart protection and radical trapping by DMPO during reperfusion in isolated working rat hearts / Tosaki A., Blasig I. E., Pali T., Ebert B.
Dátum:1990
Megjegyzések:The purpose of this study was to use a direct method, that of electron spin resonance (ESR) spectroscopy, to demonstrate that reperfusion after a period of ischemia results in a sudden increase in the production of free radicals in the myocardium. Furthermore, the role of free radicals in the development of reperfusion arrhythmias and functional disturbances also was investigated using a 30-min period of global ischemia followed by 30 min of reperfusion in the isolated working rat heart. The spin trapping agent 5,5-dimethyl-1-pyrroline-1-oxide (DMPO) when it perfused the heart, 100 mumoles/liter, during the first 10 min of reperfusion attenuated the development of reperfusion arrhythmias and improved the functional recovery of the heart during reperfusion. Without treatment, 55% of hearts showed irreversible ventricular fibrillation, and this was completely prevented by DMPO. In DMPO-treated hearts, the recovery of heart function was improved; thus, coronary flow, aortic flow, left ventricular developed pressure, and first derivative of left ventricular developed pressure were significantly increased from their maximal control values of 16.2 +/- 1.9 ml/min, 12.7 +/- 0.9 ml/min, 11.1 +/- 0.5 kPa, and 426 +/- 31 kPa/s to 21.8 +/- 1.3 ml/min (p less than 0.05), 28.4 +/- 3.0 ml/min (p less than 0.001), 14.5 +/- 1.0 kPa (p less than 0.01), and 584 +/- 41 kPa/s (p less than 0.01), respectively. Left ventricular end-diastolic pressure was also significantly reduced from its control value of 2.8 +/- 0.2 kPa to 2.1 +/- 0.2 kPa (p less than 0.05), while the recovery of heart rate was not improved by DMPO treatment. Parallel ESR studies using DMPO as spin trap demonstrated the formation of .OH radicals in the effluent of the reperfused hearts. ESR signals of the formed DMPO-OH, alpha N = alpha beta H = 1.48 mT, were observed within the first seconds of reperfusion with peak concentrations after about 3 min. In the first series of ESR studies, DMPO (200 mmol/liter) was mixed up effluent and ESR signals were recorded, while in the second series of studies, DMPO was directly infused into the heart. Both methods were appropriate to demonstrate the radical formation that peaked at 3 min of reperfusion after 30 min of global ischemia. Cardiotoxic effects of DMPO can be excluded by using of the "mix-up" method (DMPO is added to effluent) because relatively high DMPO concentration (20-200 mmol/liter) is important for demonstration of free radical production
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Free Radical Biology and Medicine. - 8 : 4 (1990), p. 363-372. -
További szerzők:Blasig, Ingolf E. Pali Tibor Ebert, Berndt
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
DOI
Borító:
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