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1.

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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2.

001-es BibID:BIBFORM041708
035-os BibID:PMID:7752071
Első szerző:Tósaki Árpád (kísérletes farmakológus, gyógyszerész)
Cím:Alpha-1 adrenergic receptor agonist-induced preconditioning in isolated working rat hearts / Arpad Tosaki, Nadeem S. Behjet, Daniel T. Engelman, Richard M. Engelman, Dipak K. Das
Dátum:1994
Megjegyzések:The aim of this study was to determine whether pharmacologic preconditioning, without a short episode of myocardial hypoxia or ischemia, could improve myocardial function after a prolonged period of ischemia. Isolated rat hearts were perfused with .01, .1 or 1 mg/L of phenylephrine for 5 min followed by a 10-min washout period (preconditioning) before the induction of 30 min of normothermic global ischemia and 30 min of reperfusion. Hearts preconditioned with increasing concentrations of phenylephrine (an alpha-1 adrenergic receptor agonist) produced a reduction in the incidence of reperfusion-induced ventricular fibrillation (VF) and ventricular tachycardia (VT). Preconditioning of the hearts with the highest dose of phenylephrine (1.0 mg/L), after 30 min of ischemia, reduced the incidence of reperfusion-induced VF and VT from their nonpreconditioned control values of 87% and 100% to 33% (P < .05) and 50% (P < .05), respectively. After 30 min of ischemia, the recovery of myocardial function was significantly improved in phenylephrine-preconditioned groups. Thus, .1 and 1.0 mg/L of phenylephrine increased aortic flow from its nonpreconditioned control value of 10.8 +/- .9 ml/min to 22.4 +/- 2.4 ml/min (P < .05) and 26.5 +/- 1.5 ml/min (P < .05), respectively. Phenylephrine (1.0 mg/L) preconditioning significantly reduced ischemia/reperfusion-induced tissue Na+ and Ca2+ gains and prevented K+ and Mg2+ loss measured by an atomic absorption spectro-photometer. Our results show that alpha-1 adrenergic stimulation (preconditioning) can prevent postischemic abnormalities in intracellular ions, reperfusion arrhythmias, and contractile function without the inhibition of O2 delivery.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
külföldön készült közlemény
Megjelenés:The Journal of Pharmacology and Experimental Therapeutics. - 273 : 2 (1994), p. 689-694. -
További szerzők:Behjet, Nadeem S. Engelman, Daniel T. Engelman, Richard M. Das, Dipak Kumar
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
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3.

001-es BibID:BIBFORM041707
035-os BibID:PMID:8531071
Első szerző:Tósaki Árpád (kísérletes farmakológus, gyógyszerész)
Cím:Diabetes and ATP-sensitive potassium channel openers and blockers in isolated ischemic/reperfused hearts / Arpad Tosaki, Daniel T. Engelman, Richard M. Engelman, Dipak K. Das
Dátum:1995
Megjegyzések:The incidence of reperfusion ventricular fibrillation (VF) and tachycardia (VT), heart function and the maldistribution of cardiac cations were studied in isolated ischemic/reperfused hearts obtained from streptozotocin-induced diabetic rats. Effects of an ATP-sensitive potassium (KATP) channel opener, cromakalim, and a KATP channel blocker, glibenclamide, also were studied. After 2 and 8 weeks of diabetes, hearts were isolated and subjected to 30 min of ischemia followed by reperfusion. After 2 weeks of diabetes, the incidence of VF and VT was reduced from their nondiabetic control values of 100 and 100 to 42% (P < .05) and 50% (P < .05), respectively. The reduction in VF and VT was not observed with progressive diabetes and after 8 weeks cardiac failure developed. In the 8-week diabetics, the development of cardiac failure was reflected in the aggravation of heart function (26, 16 and 17% reductions in aortic flow, left ventricular developed pressure and first derivative of developed pressure, respectively), and ion shifts (56 and 71% accumulation in cellular Na+ and Ca++, respectively, and 15% loss in cell K+) before the induction of ischemia. After ischemia/reperfusion, these changes were pronounced in diabetic groups. Cromakalim aggravated and glibenclamide attenuated the incidence of arrhythmias, contractile function and ion shifts induced by ischemia/reperfusion in diabetic hearts. The data show that the use of KATP channel openers as anti-ischemic agents may be of particular concern in the population of postinfarction diabetic patients who are known to be at high risk of sudden coronary death.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
külföldön készült közlemény
Megjelenés:The Journal of Pharmacology and Experimental Therapeutics. - 275 : 3 (1995), p. 1115-1123. -
További szerzők:Engelman, Daniel T. Engelman, Richard M. Das, Dipak Kumar
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
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4.

001-es BibID:BIBFORM041704
035-os BibID:PMID:7921376
Első szerző:Tósaki Árpád (kísérletes farmakológus, gyógyszerész)
Cím:Ginkgo biloba extract (EGb 761) improves postischemic function in isolated preconditioned working rat hearts / Arpad Tosaki, Daniel T. Engelman, Tibor Pali, Richard M. Engelman, Marie-Therese Droy-Lefaix
Dátum:1994
ISSN:0954-6928
Megjegyzések:We studied the effect of preconditioning and Gikgo biloba extract (EGb 761) in relation to the recovery of contractile function after global ischemia in the isolated working rat heart. METHODS: Hearts (n = 12 in each group) were randomly divided into five groups: In group I, hearts were subjected to 30 min of normothermic global ischemia followed by 30 min of reperfusion; in group II, they were subjected to one cycle of preconditioning consisting of 5 min ischemia and 10 min reperfusion before the induction of 30 min of ischemia and 30 min of reperfusion; group III hearts underwent two cycles of preconditioning; group IV hearts underwent three cycles of preconditioning; and group hearts underwent four cycles of preconditioning before the onset of 30 min ischemia followed by 30 min of reperfusion. RESULTS: Ventricular fibrillation (total) and ventricular tachycardia (no preconditioning) both fell from 100% to 50% (P < 0.05) after four cycles of preconditioning. In relation to ventricular fibrillation, preconditioning significantly reduced the formation of oxygen free radicals, measured by electron spin resonance spectroscopy (ESR), but recovery of cardiac function was low in all preconditioned groups. Because of the relatively low incidence of arrhythmias (50% ventricular fibrillation and 50% ventricular tachycardia) and relatively low cardiac function in Group V, EGb 761, a free-radical scavenger, was chosen to improve myocardial contractile function in preconditioned hearts. Fifty and 100 mg/kg of EGb 761 (per os) significantly improved coronary flow, aortic flow, left ventricular developed pressure (LVDP), and the first derivative of LVDP (LVDdP/dtmax) in the four-cycle preconditioned group. Thus, after 30 min of reperfusion, aortic flow was improved from 11.6 +/- 0.9 ml/min to 19.7 +/- 1.2 ml/min (P < 0.05) with a dose of 50 mg/kg of EGb 761 and to 22.0 +/- 1.5 ml/min (P < 0.05) with a dose 100 mg/kg of EGb 761, in the four-cycle preconditioned group. During reperfusion, the formation of free radicals was reduced by approximately 50 and 60% using 50 mg/kg and 100 mg/kg of EGb 761, respectively, when compared with the four-cycle preconditioned drug-free control group. CONCLUSION: We have demonstrated that EGb 761 can improve contractile function after global ischemia in the isolated working rat heart by reducing the formation of oxygen free radicals, and we have shown that this protection is additive to that of ischemia-induced preconditioning.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
külföldön készült közlemény
Megjelenés:Coronary Artery Disease 5 : 5 (1994), p. 443-450. -
További szerzők:Engelman, Daniel T. Pali Tibor Engelman, Richard M. Droy-Lefaix, Marie-Thérèse
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
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5.

001-es BibID:BIBFORM041156
035-os BibID:PMID:8689644
Első szerző:Tósaki Árpád (kísérletes farmakológus, gyógyszerész)
Cím:The evolution of diabetic response to ischemia/reperfusion and preconditioning in isolated working rat hearts / Árpád Tosaki, Daniel T. Engelman, Richard M. Engelman, Dipak K. Das
Dátum:1996
ISSN:0008-6363
Megjegyzések:OBJECTIVE: Studies have shown that the diabetic heart exhibits abnormalities in cellular ion transport, which can affect susceptibility to reperfusion-induced ventricular fibrillation (VF), tachycardia (VT) and functional derangements. It has been shown that "preconditioning" renders the heart very resistant to a subsequent prolonged ischemic episode. This phenomenon has been extensively studied in healthy myocardium, but such a study has not been previously done in diseased (hypertrophic or myopathic) hearts. METHODS: We studied the incidence of reperfusion-induced VF, VT, cardiac function, and ion shifts (Na+, K+, Ca2+, and Mg2+) induced by ischemia/reperfusion in isolated hearts from rats with streptozotocin-induced diabetes. Following 2, 4, 6, and 8 weeks of diabetes, hearts were isolated and subjected to 30 min global ischemia followed by reperfusion. RESULTS: In the 2-week diabetic group the total incidence of VF and VT was reduced from their non-diabetic age-matched control value of 100 and 100% to 42 (P < 0.05) and 42% (P < 0.05), respectively. Such a reduction in the incidence of VF and VT was not observed with progressive diabetes (4, 6, and 8 weeks). In the 2-week diabetics, the reduction in the VF and VT was reflected in the improvement of postischemic function, the reduction of ischemia and reperfusion-induced Na+ and Ca2+ gains, and the prevention in K+ and Mg2+ loss. This diabetes-induced initial protection was not seen in the 4- and 6-week diabetics, and a deterioration of postischemic function was observed in the 8-week diabetics. Four cycles of preconditioning, each consisting of 5 min ischemia followed by 10 min reperfusion, failed to reduce the incidence of VF and VT, improve cardiac function, and prevent ion shifts induced by 30 min ischemia followed by 30 min reperfusion in 4- and 8-week diabetics. CONCLUSIONS: In the early phase of diabetes the heart is more resistant to ischemia/reperfusion than the non-diabetic heart. Preconditioning does not afford protection against a prolonged period of ischemia in diabetics, indicating that preconditioning may be a "healthy heart phenomenon".
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
külföldön készült közlemény
Megjelenés:Cardiovascular Research. - 31 : 4 (1996), p. 526-536. -
További szerzők:Engelman, Daniel T. Engelman, Richard M. Das, Dipak Kumar
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
DOI
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