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001-es BibID:	BIBFORM041207
035-os BibID:	PMID:9362254
Első szerző:	Tósaki Árpád (kísérletes farmakológus, gyógyszerész)
Cím:	Ischemic preconditioning triggers phospholipase D signaling in rat heart / Arpad Tosaki, Nilanjana Maulik, Gerald Cordis, Ovidiu C. Trifan, Laurentiu M. Popescu, Dipak K. Das
Dátum:	1997
ISSN:	0002-9513
Megjegyzések:	Recent studies have indicated that repeated brief episodes of ischemia and reperfusion render the myocardium more tolerant to subsequent lethal ischemic injury. In view of the previous observations that ischemia-reperfusion potentiates phospholipase D signaling and that such signaling is beneficial for the heart, we investigated whether a similar phospholipase D signaling is responsible for the beneficial effects associated with repeated ischemia and reperfusion. Using an isolated perfused working rat heart model, we demonstrated that four brief episodes of 5 min of ischemia and 10 min of reperfusion reduced the incidence of ventricular arrhythmias, enhanced the postischemic ventricular performance, and decreased the release of creatine kinase from the reperfused heart, with simultaneous activation of phospholipase D generating the second messengers diacylglycerol and phosphatidic acid and leading to the translocation and activation of protein kinase C. The specific antiphospholipase D antibody blocked the activation of phospholipase D and attenuated the generation of diacylglycerol and phosphatidic acid and activation of protein kinase C. In concert, phospholipase D inhibition increased the incidence of ventricular arrhythmias, blocked the beneficial effects of preconditioning on the ventricular performance, and increased the amount of creatine kinase release from the coronary effluent. The results of this study indicate that repeated brief episodes of ischemia and reperfusion exert beneficial effects on the intact rat heart by triggering the activation of a phospholipase D signaling mechanism.
Tárgyszavak:	Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban külföldön készült közlemény
Megjelenés:	American Journal of Physiology. - 273 : 4 Pt. 2 (1997), p. H1860-H1866. -
További szerzők:	Maulik, Nilanjana Cordis, Gerald A. Trifan, Ovidiu C. Popescu, Laurenciu M. Das, Dipak Kumar
Internet cím:	Intézményi repozitóriumban (DEA) tárolt változat Szerző által megadott URL
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001-es BibID:	BIBFORM041159
035-os BibID:	PMID:9618433
Első szerző:	Tósaki Árpád (kísérletes farmakológus, gyógyszerész)
Cím:	Preconditioning of rat heart with monophosphoryl lipid A : a role for nitric oxide / Arpad Tosaki, Nilanjana Maulik, Gerald Cordis Elliott, Ovidiu C. Trifan, Laurentiu M. Popescu, Dipak K. Das
Dátum:	1998
ISSN:	0022-3565
Megjegyzések:	Preconditioning with monophosphoryl lipid A (MLA) protects rabbit hearts from prolonged ischemic reperfusion injury by a mechanism involving inducible nitric oxide synthase (iNOS) activation. This study was undertaken to determine whether MLA also could precondition rat hearts in a similar manner. Rats were injected with two different doses of MLA (300 microg/kg or 450 microg/kg i.v.) or vehicle (control), and after 24 hr the animals were sacrificed for preparation of isolated perfused rat hearts. Hearts were then perfused by working mode, and then made ischemic for 30 min followed by 30 min of reperfusion. Another group of hearts were treated simultaneously with a nitric oxide (NO) blocker, L-nitro-arginine-methyl-ester (L-NAME) (10 mg/kg) and MLA (450 microg/kg). For arrhythmia studies, 12 hearts were used in each group (total, 48 hearts). Cardiac functions were examined in a separate group of 24 hearts (n = 6/group). MLA-treated hearts (either dose) were tolerant to ischemic reperfusion injury as evidenced by improved postischemic ventricular recovery [coronary flow (ml/min) 19.1 +/- 0.8 (300 microg/kg MLA), 22.6 +/- 1.0 (450 microg/kg MLA) vs. 15.9 +/- 0.7 (control); aortic flow (ml/min) 20.7 +/- 1.8 (300 microg/kg MLA), 25.8 +/- 1.4 (450 microg/kg MLA) vs. 11. 0 +/- 0.8 (control); left ventricular developed pressure (kPa) 13.3 +/- 0.6 (300 microg/kg MLA), 14.6 +/- 0.2 (450 microg/kg MLA) vs. 10. 3 +/- 0.7 (control)]. Incidences of ventricular fibrillation and ventricular tachycardia were decreased compared with the control group only in the 450 microg/kg dose of MLA-treated hearts (92% to 33%). Pretreatment of the hearts with L-NAME inhibited the preconditioning effect of MLA. To examine the induction of the iNOS expression, RNAs were extracted from the control and MLA-treated hearts (after 2, 4,6, 8, 12 and 24 hr of treatment) and Northern blot analyses were performed with a specific cDNA probe for iNOS. A single band of approximately 4.6 kb corresponding to iNOS mRNA was detected after 4 hr of MLA treatment, whereas the maximal iNOS expression was found between 6 and 8 hr of MLA treatment. The results of this study demonstrated that MLA induced the expression of iNOS and protected the myocardium from ischemic reperfusion injury which is blocked by an inhibitor of NO synthesis, which suggests a role of NO in MLA-mediated cardioprotection.
Tárgyszavak:	Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban külföldön készült közlemény
Megjelenés:	Journal of Pharmacology and Experimental Therapeutics 285 : 3 (1998), p. 1274-1279. -
További szerzők:	Maulik, Nilanjana Elliott, Gerald Cordis Trifan, Ovidiu C. Popescu, Laurenciu M. Das, Dipak Kumar
Internet cím:	Intézményi repozitóriumban (DEA) tárolt változat Szerző által megadott URL
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001-es BibID:	BIBFORM041710
Első szerző:	Trifan, Ovidiu C.
Cím:	Ischemic preconditioning involves phospholipase D / Ovidiu C. Trifan, Laurentiu M. Popescu, Arpad Tosaki, Gerald Cordis, Dipak K. Das
Dátum:	1996
Tárgyszavak:	Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban külföldön készült közlemény
Megjelenés:	Annals of the New York Academy of Sciences 793 (1996), p. 485-488. -
További szerzők:	Popescu, Laurenciu M. Tósaki Árpád (1958-) (kísérletes farmakológus, gyógyszerész) Cordis, Gerald A. Das, Dipak Kumar
Internet cím:	Intézményi repozitóriumban (DEA) tárolt változat DOI
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