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001-es BibID:BIBFORM041656
Első szerző:Szekeres László
Cím:Delayed protection by oxo-7-PGI2 against cardiac transmembrance ion shipfts and early morphological changes due to ischemia and reperfusion / Szekeres L., Bálint Zs., Karcsu S., Tósaki A.
Dátum:1990
Megjegyzések:In previous experiments on dogs subjected to local myocardial ischemia, we have shown a late and prolonged anti-ischemic and anti-arrhythmic effect of a single injection of the stable prostacyclin analogue, 7-oxo-PgI2. The protection was dependent on dose and time. Maximal effects were observed 48 hours after an optimal intramuscular dose of 50/micrograms/kg. To study the mechanism of this protective effect we have followed the time-dependent changes in transmembrane cation homeostasis induced by ischemia and reperfusion by measuring the intracellular potassium, sodium and calcium ion concentrations in Langendorff guinea pig heart preparations isolated from untreated control animals and from animals receiving a single intramuscular injection of 50/micrograms/kg 7-oxo-PgI2 48 hours before preparation. Global ischemia was produced by stopping perfusion for 25 minutes and was followed by reperfusion. In a second series, similarly treated and untreated hearts were fixed for electron microscopy after 25 minutes' global ischemia as well as after 15 minutes' reperfusion. Ischemia and reperfusion evoked a rapid loss of intracellular potassium and gain of sodium as well as an accumulation of calcium in the reperfusion phase. Pretreatment with 7-oxo-PgI2 prevented all these changes. It also prevented the shortening of the sarcomers and swelling of mitochondria induced by ischemia and the deposition of calcium-dense granules in mitochondria appearing after reperfusion. The findings support the hypothesis that 7-oxo-PgI2 has a delayed cytoprotective action which preserves normal transmembrane ion transport and normal structure of myocardial cells under conditions of ischemic and reperfusion injury.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Cardioscience 1 : 4 (1990), p. 279-286. -
További szerzők:Bálint Zsuzsa Karcsu Sarolta Tósaki Árpád (1958-) (kísérletes farmakológus, gyógyszerész)
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
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2.

001-es BibID:BIBFORM041633
Első szerző:Szekeres László
Cím:Ion shifts in myocardial cells during ischemia and reperfusion and the effect of membrane stabilizing agents on ischemic ion transport / Szekeres L., Bálint Z., Tósaki A.
Dátum:1987
Megjegyzések:Ischemia-and reperfusion-induced time dependent changes of the intracellular K+/K+i/, Na+/Na+i/ and Ca2+/Ca2+i/ concentrations were analyzed in isolated Langendorff guinea pig hearts. In the ischemic period evoked by complete perfusion stop of 25 min duration a rapid loss of K+ and gain of Na+ was found. Ca2+i concentration started to increase only after 15 min of global ischemia. Reperfusion did not evoke substantial changes during the first minutes however Ca2+i very rapidly increased after 7 minutes of reperfusion. K+i rapidly increased above initial values in the first 3 minutes of reperfusion but then suddenly declined to the lowest ischemic level and remained at this level. Na+i concentration elevated by ischemia was not further affected by reperfusion. The membrane stabilizing antiarrhythmic agents: quinidine and lidocaine proved to be effective in preventing or moderating ischemia induced shifts in K+i and Na+i concentrations however did not affect Ca2+i content. This latter was markedly reduced by verapamil, a substance which failed to influence ischemic shifts of K+i and Na+i content.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Biomedica Biochimica Acta. - 46 : 8-9 (1987), p. S527-S533. -
További szerzők:Bálint Zsuzsa Tósaki Árpád (1958-) (kísérletes farmakológus, gyógyszerész)
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
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3.

001-es BibID:BIBFORM041641
035-os BibID:PMID:3256423
Első szerző:Tósaki Árpád (kísérletes farmakológus, gyógyszerész)
Cím:Pacing and reperfusion induced arrhythmias : protection by slow heart rate in the rat heart / Arpad Tosaki, Susan Balint, Laszlo Szekeres
Dátum:1988
ISSN:0008-6363
Megjegyzések:Using the isolated perfused rat heart with transient (10 min) regional ischaemia induced by coronary artery ligation, we have shown that slow heart rate can dramatically reduce the vulnerability of the myocardium to reperfusion induced ventricular fibrillation and ventricular tachycardia. In the heart rate range of 200-400 beats.min-1, slower heart rates exerted a frequency dependent protective effect against reperfusion induced arrhythmias. At the optimal rate of 200 beats.min-1, the incidence of total ventricular fibrillation (irreversible plus reversible) and ventricular tachycardia fell to 33% and 50% of their control values (100%). The anti-arrhythmic effect was achieved with only a minor (less than 20%) effect on coronary flow. To ascertain whether or not slow heart rate achieved an absolute reduction in vulnerability to arrhythmias irrespective of the duration of ischaemia, hearts were also subjected to 5, 10, 20, 30 or 40 min of ischaemia followed by 30 min of reperfusion with and without pacing at 200 beats.min-1. A bellshaped time-response profile was obtained in both groups. In unpaced controls (n = 12) this gave a maximal vulnerability to arrhythmias after 10 min of ischaemia. In the paced hearts (n = 12) the curve was shifted to the right, with a peak vulnerability at 20 min. These results show that the action of pacing is to exert a delaying effect which extends the duration of ischaemia that can be tolerated before the heart becomes vulnerable to reperfusion induced arrhythmias. Heart rate can have a substantial effect on reperfusion induced arrhythmias and should be considered when making therapeutic interventions and risk assessments in this setting.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
egyetemen (Magyarországon) készült közlemény
Megjelenés:Cardiovascular Research. - 22 : 11 (1988), p. 818-825. -
További szerzők:Bálint Zsuzsa Szekeres László
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
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4.

001-es BibID:BIBFORM041625
035-os BibID:PMID: 2467078
Első szerző:Tósaki Árpád (kísérletes farmakológus, gyógyszerész)
Cím:Protective effect of lidocaine against ischemia and reperfusion-induced arrhythmias and shifts of myocardial sodium, potassium, and calcium content / Arpad Tosaki, Susan Balint, Laszlo Szekeres
Dátum:1988
ISSN:0160-2446
Megjegyzések:Isolated guinea pig hearts subjected to global ischemia, were used to investigate whether lidocaine exerts an antiarrhythmic action against reperfusion-induced arrhythmias, and the effects of this drug upon myocardial ion contents during ischemia and reperfusion were studied. In the first series of experiments, the drug was administered 5 min prior to the induction of global ischemia and maintained during reperfusion. With 3.6 X 10(-6), 7.2 X 10(-6), 14.7 X 10(-6), and 29.5 X 10(-6) mol/L lidocaine, reperfusion-induced ventricular fibrillation and tachycardia were reduced from their control incidence of 83% and 100% to 41% and 58%, 33% (p less than 0.05) and 25% (p less than 0.001), 8% (p less than 0.01) and 8% (p less than 0.001), 0% (p less than 0.001) and 0% (p less than 0.001), respectively. The ion contents of myocardium were determined by atomic absorption spectrophotometer after washout of the ions from vasculature. Ischemia induced a marked accumulation of sodium and loss of potassium in the myocardial tissue. Both ischemia-induced sodium gain and potassium loss were significantly inhibited by lidocaine treatment. During reperfusion, sodium was further increased in the control group and this value was significantly lower in the lidocaine-treated group after 1 min of reperfusion. Sodium content remained at nearly constant level for the rest of reperfusion period. Potassium was suddenly increased during the first 5 min of reperfusion then continuously decreased until the end of reperfusion
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
egyetemen (Magyarországon) készült közlemény
Megjelenés:Journal of Cardiovascular Pharmacology. - 12 : 6 (1988), p. 621-628. -
További szerzők:Bálint Zsuzsa Szekeres László
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
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