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001-es BibID:BIBFORM020523
Első szerző:Ferdinándy Péter
Cím:Cardioprotective effect of enantiomers of cicletanine (BN50417, BN50418) in ischaemic/reperfused isolated working rat hearts : interaction with glibenclamide / P. Ferdinandy, Z. Szilvássy, T. Csont, M. Koltai, M. T. Droy-lefaix
Dátum:2000
ISSN:1043-6618
Megjegyzések:AbstractIn the present study, interaction of the ATP-sensitive K+-channel blocker glibenclamide with enantiomers of the antihypertensive drug, cicletanine, was studied on ischaemic myocardial function, lactate-dehydrogenase (LDH) release, and early reperfusion-induced ventricular fibrillation (VF). Isolated working rat hearts subjected to 10-min coronary artery occlusion followed by 2-min reperfusion were perfused with 1.5x10(-5)-6.0x10(-5)M D-cicletanine[+] (BN50417) and L-cicletanine[-] (BN50418), respectively. Their interaction with 10(-7) M glibenclamide was also studied. The most effective concentration of BN50418 (3x10(-5) M) increased ischaemic aortic flow (AF) from its non-treated control value of 20.3+/-1.16 to 30.3+/-2.6 ml min-1(P<0.01), decreased left ventricular end-diastolic pressure (LVEDP) from 1.81+/-0.05 to 0.97+/-0.08 kPa (P<0.001), attenuated ischaemia-induced increase in LDH leakage from 164+/-41 to 14.8+/-20 mU min-1g-1 wet wt. (P<0.01) at the 10th-min of coronary occlusion, and reduced VF upon reperfusion. Glibenclamide did not considerably affect cardiac performance, however, it inhibited the anti-ischaemic but not the antiarrhythmic effect of BN50418. BN50417 (3x10(-5) M) tended to improve ischaemic AF to 24.2+/-1.1 ml min-1, and significantly attenuated ischaemia-induced increase in LVEDP to 1.3+/-0.08 kPa (P<0.01), relative increase in LDH release to 29.4+/-44 mU min-1g-1(P<0.05), and alleviated reperfusion-induced VF. Glibenclamide abolished the anti-ischaemic and antiarrhythmic effect of BN50417. The cardioprotective effect of both enantiomers of cicletanine involves a glibenclamide-sensitive mechanism, however, the antiarrhythmic effect of BN50418 is not glibenclamide sensitive. BN50418 is the more potent enantiomer of cicletanine in terms of its cardioprotective effect.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
cardioprotective effect
enantiomers of cicletanine
enantiomers
cicletanine
BN50417
BN50418
glibenclamide
Megjelenés:Pharmacological Research. - 39 : 3 (1999), p. 225-231. -
További szerzők:Csont Tamás Koltai M. Droy-Lefaix, Marie-Thérèse Szilvássy Zoltán (1957-) (belgyógyász, farmakológus, klinikai farmakológus)
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001-es BibID:BIBFORM020368
Első szerző:Gellén B. (Szeged)
Cím:Vascular changes play a role in the pathogenesis of necrotizing enterocolitis in asphyxiated newborn pigs / B. Gellén, J. Kovács, L. Németh, P. Németh, J. Vágvölgyi, F. Bari, P. Megyeri, S. Pintér, P. Temesvári, M. A. Deli, M. Vecsernyés, Z. Szilvássy, M. Koltai, Cs. Abrahám
Dátum:2003
ISSN:0179-0358
Megjegyzések:Necrotizing enterocolitis (NEC) is the most common acquired gastrointestinal emergency in neonates. We have developed an animal model of NEC in asphyxiated newborn pigs and investigated the effects of asphyxia on blood flow in superior mesenteric artery and abdominal aorta, cardiovascular data, arterial acid-base and blood gas parameters, and endothelial cytoskeletal structure in mesenteric microvasculature. Anesthetized, mechanically ventilated newborn pigs were included in two groups: piglets underwent severe asphyxia, and sham-operated control animals. A cardiovascular and metabolic failure developed in asphyxiated piglets approximately 1 h after the induction: severe hypotension and bradyarrhythmia were seen and significant reductions of the blood flow were measured in the superior mesenteric artery and abdominal aorta during the critical phase. Rearrangement of cytoskeletal actin structure corresponding to enhanced vascular permeability was seen with bodipy phallacidin in mesenterial endothelium of asphyxiated piglets after a 24-h recovery period. In conclusion, severe vasomotor changes during asphyxia may result in mesenteric endothelial dysfunction implicated in increased vascular permeability, edema formation, and development of NEC in asphyxiated piglets.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
vascular changes
pathogenesis
enterocolitis
necrotizing enterocolitis
Megjelenés:Pediatric Surgery International 19 : 5 (2003), p. 380-384. -
További szerzők:Kovács J. Németh L. (Szeged) Németh Péter Vágvölgyi J. (Szeged) Bari Ferenc Megyeri Pál Pintér Sándor (Szeged) Temesvári P. (Kecskemét) Deli Mária A. Vecsernyés Miklós (1959-) (gyógyszertechnológus, endokrinológus) Szilvássy Zoltán (1957-) (belgyógyász, farmakológus, klinikai farmakológus) Koltai M. Abrahám Csongor
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