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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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001-es BibID:BIBFORM020462
Első szerző:Kovács Péter (belgyógyász, kardiológus, klinikai farmakológus)
Cím:Effect of transdermal nitroglycerin on glucose-stimulated insulin release in healthy male volunteers / P. Kovacs, Z. Szilvassy, P. Hegyi, J. Nemeth, P. Ferdinandy, Á. Tosaki
Dátum:2000
ISSN:0014-2972
Megjegyzések:Morpholinosydnonimine, a nitric oxide (NO) donor, has been reported to inhibit insulin release in isolated pancreatic islets. We studied whether transdermal application of nitroglycerin, another NO donor widely used for angina prophylaxis, influenced glucose-stimulated insulin release in healthy, young, male volunteers.METHODS AND RESULTS:Oral glucose tolerance tests [(OGTT) 75 g glucose in 200 mL of water) were performed in the presence of placebo patches or nitroglycerin-releasing 'active' patches (approx. 0.4 mg hour-1 nitroglycerin) in the same patients with a 2-week intertest interval. Venous blood samples were taken before and 15, 30, 60, 90, 120 and 180 min after the glucose load and evaluated for plasma glucose level and immunoreactive insulin responses (radioimmunoassay). Glucose-stimulated maximum increase in plasma insulin immunoreactivity were 36.3 +/- 5 and 78.8 +/- 6.1 mU mL-1 (P < 0.05) in the presence of active and placebo patches, respectively. Nevertheless, both fasting and postload blood glucose levels were the same at either patch. Active patches significantly decreased blood pressure with a marginal increase in heart rate.CONCLUSION:We conclude that inhibition of glucose-stimulated insulin release by transdermal nitroglycerin without causing hyperglycaemia may serve as a novel component of the antianginal mechanism of action of nitrates.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
transdermal nitroglycerin
glucose-stimulated insulin
Effect of transdermal nitroglycerin
Megjelenés:European Journal Of Clinical Investigation 30 : 1 (2000), p. 41-44. -
További szerzők:Szilvássy Zoltán (1957-) (belgyógyász, farmakológus, klinikai farmakológus) Hegyi Péter Jenő (belgyógyász) Németh József (Pécs) Ferdinándy Péter Tósaki Árpád (1958-) (kísérletes farmakológus, gyógyszerész)
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DOI
Intézményi repozitóriumban (DEA) tárolt változat
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