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1.

001-es BibID:BIBFORM041643
035-os BibID:PMID:3398055
Első szerző:Hearse, David J.
Cím:Free radicals and calcium : simultaneous interacting triggers as determinants of vulnerability to reperfusion-induced arrhythmias in the rat heart / David J. Hearse, Arpad Tosaki
Dátum:1988
ISSN:0022-2828
Megjegyzések:Using the isolated perfused rat heart with regional ischemia and reperfusion, we have two antiarrhythmic interventions (the spin trap agent PBN [N-tert-butyl-alpha-phenylnitrone] and perfusate calcium reduction), administered just before reperfusion, to investigate mechanisms determining the vulnerability of the heart to reperfusion-induced ventricular fibrillation. Hearts were subjected to regional ischemia (5, 10, 20, 30 or 40 min) followed by reperfusion. Four groups were studied for each ischemic time: (i) control hearts with no antiarrhythmic intervention; (ii) hearts perfused with PBN (30 mumol/l) during the final 1 min of ischemia and throughout reperfusion, (iii) hearts perfused with low-calcium buffer (0.4 mmol/l) during the final 1 min of ischemia and throughout reperfusion and (iv) hearts perfused with PBN (30 mumol/l) and low-calcium (0.4 mmol/l) during the final 1 min of ischemia and throughout reperfusion. In control hearts, a bell-shaped time-vulnerability curve was obtained with 0, 91, 67, 33 and 17% of the hearts exhibiting irreversible fibrillation during reperfusion after 5, 10, 20, 30 and 40 min of ischemia, respectively. In the PBN group, the values were 8, 41 (P less than 0.05), 41, 33 and 8%, respectively. In the calcium reduction group the values were 17, 50, 8 (P less than 0.05), 8 and 0, respectively. Thus, PBN caused a significant reduction in reperfusion-induced ventricular fibrillation after 10 min of ischemia but had no significant effect with reperfusion after 20 min of ischemia. In contrast, calcium reduction had no significant effect after 10 min of ischemia but caused a significant reduction after 20 min of ischemia. When PBN treatment with calcium reduction were combined we obtained significant anti-arrhythmic effects after both 10 min (P less than 0.05) and 20 min (P less than 0.05) of ischemia. The additive effects of these two interventions, and the different ischemic-times after which they are most effective, has led us to propose that multiple triggers, each with different underlying mechanisms may be capable of initiating events which lead to ventricular fibrillation.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
külföldön készült közlemény
Megjelenés:Journal of Molecular and Cellular Cardiology. - 20 : 3 (1988), p. 213-223. -
További szerzők:Tósaki Árpád (1958-) (kísérletes farmakológus, gyógyszerész)
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
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2.

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)
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
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3.

001-es BibID:BIBFORM041635
Első szerző:Hearse, David J.
Cím:Free radicals and reperfusion-induced arrhytmias : protection by spin trap agent PBN in the rat heart / David J. Hearse, Arpad Tosaki
Dátum:1987
ISSN:0009-7330
Megjegyzések:Using the isolated perfused rat heart with transient (10-minute) regional ischemia induced by coronary artery ligation, we have shown that PBN (N-tert-butyl-alpha-phenylnitrone), an organic spin trap agent designed specifically to form "stable" adducts with free radicals in electron spin resonance studies, can dramatically reduce the vulnerability of the myocardium to reperfusion-induced ventricular fibrillation. Studied in the concentration range of 5-1,000 microM/L, PBN added to the perfusate 5 minutes prior to ischemia exerted a dose-dependent protective effect. At the optimum concentration of 30 microM/L PBN reduced the incidence of ventricular fibrillation to 50% (6 of 12) from its control value of 100% (12 of 12). The antiarrhythmic effect was achieved without any substantial effect on coronary flow or heart rate. Investigating whether this was a direct antiarrhythmic effect, operating during reperfusion, or an indirect effect arising from the action of PBN on the heart during ischemia, PBN (30 microM/L) was added to the perfusion fluid 2 minutes before reperfusion. In the control group, 100% of the hearts fibrillated whereas only 50% fibrillated in the PBN group. Additional studies were designed to ascertain whether the drug caused an absolute reduction in vulnerability to reperfusion-induced arrhythmias (irrespective of the duration of ischemia) or whether it only shifted the ischemic time-reperfusion vulnerability curve to the right (i.e., delayed the onset of vulnerability). Thus, studies were undertaken to define the relation between the duration of ischemia and the incidence of reperfusion-induced arrhythmias in control hearts and hearts treated with PBN
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Circulation Research. - 60 : 3 (1987), p. 375-383. -
További szerzők:Tósaki Árpád (1958-) (kísérletes farmakológus, gyógyszerész)
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
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4.

001-es BibID:BIBFORM041681
Első szerző:Tósaki Árpád (kísérletes farmakológus, gyógyszerész)
Cím:Isoproterenol and the genesis of reperfusion-induced arrhythmias in isolated rat heart : adrenoceptor or free radical-mediated mechanisms? / Tosaki A., Woodward B., Yamamoto F., Hearse D. J.
Dátum:1990
ISSN:0160-2446
Megjegyzések:In the isolated rat heart, reperfusion-induced arrhythmias were exacerbated by isoproterenol (0.01-1.0 microM). The proarrhythmic action of isoproterenol was primarily the result of a beta 1-receptor-mediated tachycardia rather than via a free radical-mediated process, since it was prevented competitively by the beta 1-receptor antagonist metoprolol, but not by the free radical scavengers mannitol, superoxide dismutase, and catalase. If heart rate was maintained by electrical pacing, the protective action of metoprolol against the isoproterenol-induced arrhythmias was lost. At high concentrations (5 and 50 microM), metoprolol alone produced a bradycardia that was probably not related to beta 1 blockade, and this resulted in some nonspecific antiarrhythmic activity. The data provide evidence that, in this model, heart rate during ischaemia is an important determinant of reperfusion-induced arrhythmias, and that free radical formation from the oxidation of high levels of exogenous isoproterenol present at the time of reperfusion does not contribute in a major way to the detrimental action of isoproterenol.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Journal Of Cardiovascular Pharmacology 15 : 3 (1990), p. 398-407. -
További szerzők:Woodward, Brian Yamamoto, Fumio Hearse, David J.
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
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5.

001-es BibID:BIBFORM041640
Első szerző:Tósaki Árpád (kísérletes farmakológus, gyógyszerész)
Cím:Fluoro-fatty acids and the impairment of cardiac function in the rat in vivo and in vitro / A. Tosaki, D. J. Hearse
Dátum:1988
Megjegyzések:Dichapetalum toxicarium seeds contain long chain fluoro-fatty acids, particularly fluoro-oleic acid, which in doses as low as 10 mg/kg can cause death. We have used the rat heart both in vivo and in vitro to assess the cardiovascular effects of various doses of the fluoro-oleic acid extract of the seeds of Dichapetalum toxicarium. Intraperitoneal administration of 0.25 ml of seed extract solution/kg body weight (estimated to be equivalent to 10 mg fluoro-oleic acid/kg body weight) or 0.5 ml/kg body weight (equivalent to 20 mg fluoro-oleic acid/kg body weight) resulted in death in all animals (n = 6 in each group). The mean time from administration to death was 36.4 +/- 4 h and 21.0 +/- 2 h, respectively. Death was attributable to severe bradycardia which developed progressively throughout the experiment. Thus, during the first 6 h, heart rate fell by 32.2% from 450 +/- 7 beats/min to 305 +/- 36 beats/min (p less than 0.01) in the 0.25 ml/kg group and by 66 +/- 10% to 150 +/- 20 beats/min (p less than 0.001) in the 0.5 ml/kg group. Administration of the extract solution alone or oleic acid alone (equivalent to 0.5 ml/kg seed extract) to control rats had no effect. Investigating the effects of the seed extract in vitro, hearts (n = 6 in each group) were perfused with buffer containing 0.5 ml/l seed extract (equivalent to 20 mg fluoro-oleic acid/l) or with buffer containing extract solution alone
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
egyetemen (Magyarországon) készült közlemény
Megjelenés:Basic Research in Cardiology. - 83 : 2 (1988), p. 158-166. -
További szerzők:Hearse, David J.
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
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6.

001-es BibID:BIBFORM041639
Első szerző:Tósaki Árpád (kísérletes farmakológus, gyógyszerész)
Cím:Diltiazem and the reduction of reperfusion-induced arrhythmias in the rat : protection is secondary to modification of ischemic injury and heart rate / Tosaki A., Szekeres L., Hearse D. J.
Dátum:1987
Megjegyzések:We have used the isolated rat heart with transient coronary artery occlusion to investigate whether diltiazem has an anti-arrhythmic action against reperfusion-induced ventricular arrhythmias. In the first series of studies (early administration group) the drug was administered 5 min prior to the induction of regional ischemia, this resulted in a dose-dependent reduction in reperfusion-induced ventricular fibrillation. With 5 X 10(-8), 10(-7), 5 X 10(-7), 10(-6) and 5 X 10(-6) mols of diltiazem/l, total ventricular fibrillation (reversible plus irreversible) was reduced from its control incidence of 100% (12/12) to 91%, 58% (P = less than 0.05), 17% (P = less than 0.001), 0% (P = less than 0.001) and 0% (P = less than 0.001) respectively. Heart rate was also reduced in a dose-dependent manner, falling from its control value of 268 +/- 6 beats/min to less than 50% with the highest concentration of diltiazem. Coronary flow was increased in a dose-dependent manner in the diltiazem treated groups. In additional studies with an anti-arrhythmic dose of diltiazem (5 X 10(-7) mols/l), hearts were paced to their drug free control value; under these conditions the anti-arrhythmic effect of diltiazem was lost. In further studies, diltiazem (10(-7) and 5 X 10(-7) mols/l) was administered just prior to reperfusion (late administration group), no anti-arrhythmic effects were observed. In additional studies we determined whether, with early administration, diltiazem (5 X 10(-7) mols/l) exerted its anti-arrhythmic effect by altering the relationship between the vulnerability to reperfusion-induced arrhythmias and the duration of preceding ischemia. In diltiazem-free control hearts a bell-shaped profile was observed with a maximum vulnerability after 10 min of ischemia (100% incidence of reperfusion-induced ventricular fibrillation). In diltiazem-treated hearts, a bell-shaped curve was also observed, however, its optimum was shifted to the right and downwards (20 min of ischemia gave maximum vulnerability [41%] to reperfusion-induced arrhythmias). We conclude that the ability of diltiazem to protect the isolated rat heart against reperfusion-induced arrhythmias is secondary to its anti-ischemic effect and in particular to its negative chronotropic properties.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Journal of Molecular and Cellular Cardiology. - 19 : 5 (1987), p. 441-451. -
További szerzők:Szekeres László Hearse, David J.
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
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7.

001-es BibID:BIBFORM041637
Első szerző:Tósaki Árpád (kísérletes farmakológus, gyógyszerész)
Cím:Metoprolol reduces reperfusion-induced fibrillation in the isolated rat heart : protection is secondary to bradycardia / A. Tosaki, L. Szekeres, D. J. Hearse,
Dátum:1987
Megjegyzések:We studied the effect of metoprolol on the incidence of reperfusion-induced ventricular fibrillation in the isolated rat heart with transient coronary artery occlusion and reperfusion. When administered prior to ischemia, metoprolol produced a dose-dependent reduction in reperfusion-induced ventricular fibrillation. Thus, with 1, 10, 30, 50, 100, and 200 mumol/L metoprolol, total ventricular fibrillation (reversible plus irreversible) was reduced from its control incidence of 100% to 91%, 83%, 58% (p less than 0.05), 25% (p less than 0.001), 25% (p less than 0.001), and 0% (p less than 0.001), respectively. Heart rate was also reduced in a dose-dependent manner from its control value of 268 +/- 6 beats/min to less than 75% at the highest concentration of metoprolol. Coronary flow was unaffected by metoprolol. Doses of metoprolol (1 and 10 mumol/L) that had no significant effect on heart rate had no antiarrhythmic effect. In additional experiments with a higher dose of metoprolol (50 mumol/L), hearts were paced to the rate of the drug-free control group and the antiarrhythmic effect of metoprolol was lost. When drug-free control hearts had their heart rate reduced to that of the metoprolol-treated hearts, a similar antiarrhythmic effect was observed. When metoprolol was administered just prior to reperfusion, no antiarrhythmic effects were observed. In further studies, we investigated the effect of the early administration of metoprolol (50 mumol/L) on the relationship between the vulnerability to reperfusion-induced arrhythmias and the duration of preceding ischemia
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Journal of Cardiovascular Pharmacology. - 10 : 5 (1987), p. 489-497. -
További szerzők:Szekeres László Hearse, David J.
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
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8.

001-es BibID:BIBFORM041634
Első szerző:Tósaki Árpád (kísérletes farmakológus, gyógyszerész)
Cím:Protective effect of transient calcium reduction against reperfusion-induced arrhythmias in rat hearts / Arpad Tosaki, David J. Hearse
Dátum:1987
ISSN:0002-9513
Megjegyzések:By using the isolated rat heart with regional ischemia and a perfusate Ca2+ of 2.4 mM, we have observed a bell-shaped relationship between the incidence of reperfusion-induced ventricular fibrillation (VF) and the duration of preceding ischemia. With 5, 10, 20, 30, and 40 min of ischemia, 8, 83, 58, 25, and 8% of the hearts (n = 12 per group) exhibited irreversible VF. In additional studies (10 min ischemia) perfusate Ca2+ was reduced (to 0.1, 0.4, 0.8, 1.2, 1.6, and 2.0 mM) for 1 min before coronary occlusion (to trap low Ca2+ in the ischemic zone) and for 1 min before and throughout reperfusion. VF fell in a dose-dependent manner from its control incidence of 83% (2.4 mM Ca2+) to 17 (P less than 0.01), 25 (P less than 0.01), 41, 58, 91, and 83%, respectively. In further studies Ca2+ was reduced to 0.4 mM just before ischemia and also just before and during reperfusion, and the ischemic time was varied (5, 10, 20, 30, or 40 min), VF was reduced from its time-matched control (2.4 mM Ca2+) values of 8, 83, 58, 25, and 8% to 0, 25 (P less than 0.01), 8 (P less than 0.05), 0, and 0%, respectively. In a final series of experiments, Ca2+ reduction (to 0.4 mM) was carried out only during reperfusion (1 min before and throughout reperfusion). When time-vulnerability curves were constructed some protection was observed after 20 min of ischemia (VF fell from its control incidence of 58 to 8%). We conclude that extracellular Ca2+ concentration can influence vulnerability to reperfusion-induced arrhythmias
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:American Journal Of Physiology 253 : 2PT2 (1987), p. H225-H233. -
További szerzők:Hearse, David J.
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
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