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001-es BibID:	BIBFORM028062
Első szerző:	Gesztelyi Rudolf (kísérletes farmakológus)
Cím:	Special sensitization pattern in adenosine-induced myocardial responses after thyroxine-treatment / Gesztelyi Rudolf, Zsuga Judit, Cseppentő Ágnes, Bajza Ágnes, Varga Angelika, Szabó Zs. Judit, Szentmiklósi József A.
Dátum:	2003
Megjegyzések:	Chronic thyroxine treatment reduces the susceptibility of atrial myocardium to adenosine. While the possible role of membrane adenosine receptors in this action is supported by several studies, the involvement of intracellular adenosine mechanisms has not been defined. The present experiments were carried out in electrically driven euthyroid and hyperthyroid guinea pig atrial myocardium. The extracellular and intracellular actions of adenosine were analyzed pharmacologically by the use of specific blockers of membrane adenosine transport and intracellular adenosine deaminase (ADA). The involvement of phosphoprotein phosphatase, phospholamban, and sarcoplasmic reticulum Ca2+ ATPase (SERCA) in the adenosine-induced responses was also studied. The major findings were as follows: i) pD(2)- and E(max)-values for adenosine-induced decrease of mechanical activity were significantly reduced after an 8-day thyroxine treatment in atrial tissues; ii) in atria of thyroxine-treated animals, membrane purine transport inhibitors (dipyridamole, NBTI) induced similar leftward shifts in concentration-response curves for adenosine in both euthyroid and hyperthyroid atrial myocardium without altering the depressed E(max) values; iii) the leftward displacement evoked by inhibitors of intracellularly located ADA (coformycin, EHNA) was more striking in hyperthyroid than euthyroid myocardia. ADA inhibitors induced a complete reversal of the maximum adenosine actions; iv) inhibition by cantharidin of phosphoprotein phosphatases (after inhibition of ADA) reduced the adenosine-induced responses. This inhibition was stronger in hyperthyroid atria; v) pharmacological elimination of sarcoplasmic reticulum Ca2+ ATPase by cyclopiazonic acid did not alter the cardiac responses to adenosine and this was independent of thyroid status. It is suggested that distinct modulation of the extra- and intracellular adenosine actions is present in eu- and hyperthyroid hearts. In the latter, a predominance of intracellular adenosine mechanisms can be proposed.
Tárgyszavak:	Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:	Journal of pharmacological sciences 91 : 4 (2003), p. 295-304. -
További szerzők:	Zsuga Judit (1973-) (neurológus, pszichoterapeuta, egészségügyi szakmanager) Cseppentő Ágnes (1953-) (orvos) Bajza Ágnes (1970-) (biológus) Varga Angelika (1977-) (biológus) Szabó Judit Zsuzsanna (farmakológus, klinikai laboratóriumi szakorvos) Szentmiklósi József András (1948-) (farmakológus, klinikai laboratóriumi szakorvos)
Internet cím:	DOI Intézményi repozitóriumban (DEA) tárolt változat
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001-es BibID:	BIBFORM020315
Első szerző:	Zsuga Judit (neurológus, pszichoterapeuta, egészségügyi szakmanager)
Cím:	Pre-clinical methods for the determination of insulin sensitivity / Zsuga Judit, Tory Kálmán, Jaszlits László, Bajza Ágnes, Németh József, Peitl Barna, Szilvássy Zoltán
Dátum:	2004
Megjegyzések:	AbstractWe compared the hyperinsulinaemic euglycaemic glucose clamping (HEGC) procedure and the rapid insulin sensitivity test (RIST) to characterize insulin sensitivity in anaesthetized rats. The changes in insulin sensitivity were then supplemented with the direct measurement of insulin-stimulated glucose uptake using tissue accumulation of radioactive 2-deoxyglucose in skeletal muscle samples obtained from animals undergone either procedure. Studies of the recently described endogenous insulin sensitizer mechanism termed hepatic insulin sensitizing (HISS) mechanism, by the two methods yielded data for evaluation. The HISS mechanism is defined as an increase in tissue insulin sensitivity in response to post-prandial hepatic release of an undefined substance through a nitrergic pathway. For the HEGC method, insulin was infused to attain a stable plasma insulin immunoreactivity of 100 microU/ml determined by radioimmunoassay, whereas with the RIST method the HISS mechanism was activated by a 50 mg/kg i.v. insulin bolus. Euglycaemia was kept constant by means of glucose infusion. With the HEGC and the RIST methods, insulin sensitivity was defined as the average rate of glucose infusion and the amount of glucose/kg body weight/40 min (RIST index) infused to maintain euglycaemia and preinvestigation blood glucose level, respectively. During HEGC 16+/-4.2 mg/kg/min glucose was able to maintain euglycaemia, which decreased to 8+/-2.9 (p<0.05) after administration of 10 mg/kg NG-nitro-L-arginine methyl ester (L-NAME) (i.p.), a NO synthase inhibitor. Conversely, the RIST index decreased by 55+/-6.9% (p<0.05) after L-NAME. Similarly, 2-deoxyglucose uptake by the gastrocnemius muscle was decreased by 49.9+/-5.8 (p<0.05) and 52.3+/-7.4% (p<0.05) with the HEGC and the RIST methods, respectively. The results show that both the HEGC and the RIST methods supplemented with tissue radioactive 2-deoxyglucose uptake determinations are appropriate methods to characterize the alteration of insulin sensitivity in context of the HISS mechanism.
Tárgyszavak:	Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban determination insulin sensitivity Pre-clinical methods
Megjelenés:	Journal of Biochemical and Biophysical Methods. - 61 : 1-2 (2004), p. 253-258. -
További szerzők:	Tory Kálmán Jaszlits László Bajza Ágnes (1970-) (biológus) Németh József (1954-) (vegyész, analitikus) Peitl Barna (1972-) (orvos, farmakológus) Szilvássy Zoltán (1957-) (belgyógyász, farmakológus, klinikai farmakológus)
Internet cím:	Szerző által megadott URL DOI Intézményi repozitóriumban (DEA) tárolt változat
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