scholarly journals Aorto-Bilateral-Femoral-Bilateral-Popliteal Bypass for Leriche Syndrome With Occlusion of Both Superficial Femoral Arteries

2009 ◽  
Vol 88 (2) ◽  
pp. 683 ◽  
Author(s):  
Zan Mitrev ◽  
Lidija Veljanovska ◽  
Nikola Hristov
2009 ◽  
Vol 56 (S 01) ◽  
Author(s):  
H Krankenberg ◽  
H Reichenspurner ◽  
M Ismail ◽  
T Tübler

1990 ◽  
Vol 64 (01) ◽  
pp. 091-096 ◽  
Author(s):  
W J Janssens ◽  
F J S Cools ◽  
L A M Hoskens ◽  
J M Van Nueten

SummaryRidogrel (6.3 × 10−6 to 10−4 M) inhibited contractions of isolated rat caudal arteries and rabbit femoral arteries caused by U-46619. The slope of an Arunlakshana-Schild plot (pA2-value: 3.4 × 10−6 M) on the caudal artery was slightly higher than one (1.14). This effect was maximal within}D min of incubation of the blood vessel with the compound and easily reversible. Ridogrel antagonised contractions of isolated rabbit femoral arteries caused by prostaglandin Fzo2α in the same concentration range. Ridogrel also inhibited contractions induced by aggregating rat platelets on isolated rat caudal arteries (itt the presence of ketanserin 4 × 10−7 M) and on isolated rabbit pulmonary and femoral arteries (in the absence of ketanserin). Ridogrel had no effect on Ca2+-induced contractions in depolarised isolated rabbit femoral arteries, and at 10−4 M antagonised serotonin-induced contractions in this blood vessel. Its effect on serotonin-induced contractions was statistically significant but very small on isolated rat caudal arteries. These observations indicate that ridogrel is an antagonist of prostaglandin endoperoxide/thromboxane A2 and prostaglandin F2α raCeptors on vascular smooth muscle.


Circulation ◽  
1995 ◽  
Vol 91 (5) ◽  
pp. 1444-1449 ◽  
Author(s):  
Gerard Pasterkamp ◽  
Peter J. W. Wensing ◽  
Mark J. Post ◽  
Berend Hillen ◽  
Willem P. T. M. Mali ◽  
...  

1999 ◽  
Vol 277 (1) ◽  
pp. H399-H404 ◽  
Author(s):  
Pilar Nava ◽  
Verónica Guarner ◽  
Rosalinda Posadas ◽  
Israel Pérez ◽  
Guadalupe Baños

Insulin-elicited endothelin release in hypertriglyceridemic, hypertensive, hyperinsulinemic (HTG) rats was shown. Weanling male Wistar rats were given 30% sucrose in their drinking water for 20–24 wk. In vitro contractions of aorta and femoral arteries were elicited with 40 mM KCl. Endothelin release induced with KCl plus 50 μU/ml insulin resulted in increases in contractile responses: 41 ± 5.9 and 57 ± 6% for control and 65.5 ± 6 and 95 ± 9% for HTG aortas and femoral arteries, respectively. The endothelin ETB-receptor blocker BQ-788 decreased responses to KCl + insulin by 39 ± 8 and 53 ± 5% in control and 48 ± 13 and 79 ± 3.5% in HTG aortas and femoral arteries, respectively. The ETA-receptor antagonist PD-151242 inhibited these responses by 12 ± 10 and 1 ± 9% in control and by 51.5 ± 9 and 58.5 ± 1% in HTG aortas and femoral arteries, respectively. These results suggest that endothelin may contribute to the hypertension in this model.


Pharmacology ◽  
1988 ◽  
Vol 37 (5) ◽  
pp. 293-304
Author(s):  
Mikio Ito ◽  
Nobuhiro Satake ◽  
Takafumi Anno ◽  
Itsuo Kodama ◽  
Shoji Shibata

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