CRITICAL ISSUES IN THE USE OF VASOACTIVE SUBSTANCES TO ASSESS LUNG MICROVASCULAR INJURY

1982 ◽  
Vol 384 (1 Mechanisms of) ◽  
pp. 435-457 ◽  
Author(s):  
S. Alex Stalcup ◽  
G. M. Turino ◽  
Robert B. Mellins
Keyword(s):  
Microvascular Injury ◽  
Vasoactive Substances ◽  
Critical Issues

Exploring Critical Issues in Behavior Therapy

1978 ◽  
Vol 23 (11) ◽  
pp. 863-864
Author(s):  
DENNIS UPPER
Keyword(s):  
Behavior Therapy ◽  
Critical Issues

Review of Critical Issues in Behavioral Medicine.

1983 ◽  
Vol 28 (3) ◽  
pp. 241-242
Author(s):  
Norman Stephenson ◽  
Oakley Ray
Keyword(s):  
Behavioral Medicine ◽  
Critical Issues

Review of Critical Issues in Aging Policy: Linking Research and Values.

1988 ◽  
Vol 33 (9) ◽  
pp. 833-833
Author(s):  
No authorship indicated
Keyword(s):  
Aging Policy ◽  
Critical Issues

Current Critical Issues in Mental Health Law

1989 ◽  
Vol 34 (9) ◽  
pp. 872-873
Author(s):  
David L. Shapiro
Keyword(s):  
Mental Health ◽  
Health Law ◽  
Mental Health Law ◽  
Critical Issues

Effect of Ridogrel on Vascular Contractions Gaused by Vasoactive Substances Released during Platelet Activation

1990 ◽  
Vol 64 (01) ◽  
pp. 091-096 ◽  
Author(s):  
W J Janssens ◽  
F J S Cools ◽  
L A M Hoskens ◽  
J M Van Nueten
Keyword(s):  
Smooth Muscle ◽  
Blood Vessel ◽  
Platelet Activation ◽  
Prostaglandin F2α ◽  
Thromboxane A2 ◽  
Femoral Arteries ◽  
Vasoactive Substances ◽  
Caudal Artery ◽  
Isolated Rat ◽  
Rat Platelets

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.

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