Protective Effects of the Thromboxane Receptor Antagonists BM 13.177 and BM 13.505 against U 46619-Induced Sudden Death in Rats

Pharmacology ◽  
1988 ◽  
Vol 36 (5) ◽  
pp. 340-347 ◽  
Author(s):  
E.F. Smith, III ◽  
J. McDonald
Keyword(s):  
Sudden Death ◽  
Protective Effects ◽  
Receptor Antagonists ◽  
Thromboxane Receptor

Anticoagulants of primary haemostasis

2009 ◽  
Vol 29 (03) ◽  
pp. 274-278 ◽  
Author(s):  
U. Steigerwald ◽  
U. Walter ◽  
J. Kössler
Keyword(s):  
Experimental Studies ◽  
Antiplatelet Agents ◽  
Bleeding Risk ◽  
Factor Xii ◽  
Receptor Antagonists ◽  
Thromboxane Receptor ◽  
Adenosine Uptake ◽  
Interaction Factor ◽  
Favorable Clinical Outcome ◽  
Adp Receptor Antagonists

SummaryInhibition of platelet function plays an important role in the treatment and secondary prevention of cardiovascular or cerebrovascular ischemic diseases. Established antiplatelet agents use different pharmacological targets for this role. Acetylic salicylic acid achieves a reduction of thromboxane A2 formation by inhibition of COX-1. Ticlopidin or clopidogrel are ADP-P2Y12 receptor antagonists. Tirofiban, abciximab or eptifibatid are used for the inhibition of the glycoprotein IIb/IIIa receptor which is activated at the surface of platelets preceding the final step of their aggregation. The mechanism of dipyridamole is based on the inhibition of adenosine uptake and of phosphodiesterase-5.Efforts are made to improve antiplatetelet therapy with the aim to find agents with favorable clinical outcome and lower bleeding risk. Current clinical studies focus on a new generation of ADP receptor antagonists (prasugrel, cangrelor and ticagrelor) as successors of ticlopidin and clopidogrel after coronary arterial interventions. Developments using platelet targets different from established drugs are thrombin receptor antagonists (like SCH530348) or thromboxane receptor antagonists (like S18886/terutroban) in patients with cerebrovascular events. Results from recent experimental studies could lead to new strategies for antiplatetelet therapy (like inhibition of GP Ib receptor, GP VI receptor, platelet-leukocyte interaction, factor XII and others) in the future.

Effect of thromboxane antagonists on ozone-induced airway responses in dogs

1990 ◽  
Vol 69 (3) ◽  
pp. 880-884 ◽  
Author(s):  
G. L. Jones ◽  
C. G. Lane ◽  
P. M. O'Byrne
Keyword(s):  
Airway Hyperresponsiveness ◽  
The Other ◽  
Receptor Antagonists ◽  
Thromboxane Receptor ◽  
Before And After ◽  
The Mean ◽  
Airway Responses ◽  
Control Infusion

Airway hyperresponsiveness after inhaled ozone in dogs may occur as a result of thromboxane release in the airway. In this study, two thromboxane receptor antagonists, L-655,240 and L-670,596, were used in doses that inhibit the response to an inhaled thromboxane mimetic, U-46619, to determine further the role of thromboxane in ozone-induced airway hyperresponsiveness. Dogs were studied on 2 days separated by 1 wk. On each day, the dogs inhaled ozone (3 ppm) for 30 min. On one randomly assigned day, 10 dogs received an infusion of L-655,240 (5 mg.kg-1.h-1) and 5 dogs received an infusion of L-670,596 (1 mg.kg-1.h-1); on the other day dogs received a control infusion. Airway responses to doubling doses of acetylcholine were measured before and after inhalation of ozone and were expressed as the concentration of acetylcholine giving a rise in resistance of 5 cmH2O.l-1.s from baseline (acetylcholine provocation concentration). The development of airway hyperresponsiveness after ozone was not inhibited by the thromboxane antagonists. The mean log difference in the acetylcholine provocative concentration before and after ozone on the L-655,240 treatment day was 0.62 +/- 0.12 (SE) and on the control day was 0.71 +/- 0.12 (P = 0.48); on the L-670,596 treatment day the mean log difference was 0.68 +/- 0.15 (SE) and on the control day it was 0.75 +/- 0.19 (P = 0.45). These results do not support an important role for thromboxane in causing ozone-induced airway hyperresponsiveness.

Synthesis of thromboxane receptor antagonists with the potential to radiolabel with 125I

1984 ◽  
Vol 25 (38) ◽  
pp. 4207-4210 ◽  
Author(s):  
D. Mais ◽  
D. Knapp ◽  
P. Halushka ◽  
K. Ballard ◽  
N. Hamanaka
Keyword(s):  
Receptor Antagonists ◽  
Thromboxane Receptor

Protective Effects of Endothelin Receptor Antagonists in Dogs with Aortic Cross-Clamping

1999 ◽  
Vol 34 (2) ◽  
pp. 199-205 ◽  
Author(s):  
Sébastien Roux ◽  
Changbin Qiu ◽  
Urs Sprecher ◽  
Rolf Osterwalder ◽  
Jean-Paul Clozel
Keyword(s):  
Endothelin Receptor Antagonists ◽  
Protective Effects ◽  
Endothelin Receptor ◽  
Receptor Antagonists

Ischemic brain injury in vitro: protective effects of NMDA receptor antagonists and calmidazolium

1990 ◽  
Vol 528 (1) ◽  
pp. 133-137 ◽  
Author(s):  
Roman Pohorecki ◽  
Gerald L. Becker ◽  
Pamela J. Reilly ◽  
Dennis F. Landers
Keyword(s):  
Brain Injury ◽  
Nmda Receptor ◽  
Ischemic Brain Injury ◽  
Nmda Receptor Antagonists ◽  
Protective Effects ◽  
Receptor Antagonists ◽  
Ischemic Brain

Antiaggregatory effects of thromboxane receptor antagonists in vivo

1985 ◽  
Vol 40 (5) ◽  
pp. 663-675 ◽  
Author(s):  
Harald Darius ◽  
Allan M. Lefer
Keyword(s):  
Receptor Antagonists ◽  
Thromboxane Receptor
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