scholarly journals Furegrelate, a Thromboxane Synthase Inhibitor, Blunts the Development of Pulmonary Arterial Hypertension in Neonatal Piglets

2012 ◽  
Vol 2 (2) ◽  
pp. 193-200 ◽  
Author(s):  
Dinesh K. Hirenallur-S ◽  
Neil D. Detweiler ◽  
Steven T. Haworth ◽  
Jeaninne T. Leming ◽  
John B. Gordon ◽  
...  

2013 ◽  
Vol 77 (8) ◽  
pp. 2127-2133 ◽  
Author(s):  
Atsuhiro Nakamura ◽  
Noritoshi Nagaya ◽  
Hiroaki Obata ◽  
Katsuya Sakai ◽  
Yoshiki Sakai ◽  
...  


1984 ◽  
Vol 51 (02) ◽  
pp. 257-260 ◽  
Author(s):  
A J Carter ◽  
J A Bevan ◽  
S P Hanley ◽  
W E Morgan ◽  
D R Turner

SummaryThe amounts of 6-keto-prostaglandin F1α (6-keto-PGF1α) and thromboxane B2 (TxB2) produced by the endothelial surfaces of paired samples of human pulmonary arteries and veins, obtained from patients undergoing thoracic surgery, were measured. The amounts of 6-keto-PGF1α and TxB2 produced by arteries compared with veins were not different. However, both arteries and veins produced more 6-keto-PGFlα than TxB2, the ratio being approximately 7.5:1 for both. 6-keto-PGFlα synthesis by arteries was significantly correlated with that produced by veins but the relative amounts of TxB2 were not correlated. 6-keto-PGFlα synthesis was correlated with TxB2 synthesis for veins but not for arteries. 8 of the 12 arterial samples exhibited some degree of intimal fibrosis.Incubation with the thromboxane synthase inhibitor, dazoxiben, caused a significant inhibition of vascular TxB2 synthesis and a significant increase in 6-keto-PGFlα synthesis. In 3 of the 5 cases the increase in 6-keto-PGFlα was too large to be explained by the fall in TxB2.



1991 ◽  
Vol 71 (4) ◽  
pp. 1376-1381 ◽  
Author(s):  
K. Fujioka ◽  
K. Sugi ◽  
T. Isago ◽  
J. T. Flynn ◽  
L. D. Traber ◽  
...  

We studied the cardiopulmonary response to endotoxin (lipopolysaccharide, LPS) in sheep with and without the administration of a thromboxane synthase inhibitor, OKY-046. The animals were instrumented for crystalographic dimension analysis of the left ventricle (LV) and for measurement of LV, aortic, left atrial, and pulmonary arterial pressures and cardiac index, as well as lung lymph flow. They received 1.0 micrograms/kg of Escherichia coli LPS with (n = 8) and without (n = 8) OKY-046 (10 mg/kg bolus, then 10 micrograms.kg-1.min-1). OKY-046 prevented the increase of pulmonary arterial pressure and the decrease of cardiac index that occurred during the early phase of endotoxemia. Between 8 and 12 h after LPS, cardiac index increased from 6.8 +/- 0.7 to 8.9 +/- 0.51.min-1.m-2. Concomitantly, the end-systolic pressure-diameter relationship (ESPDR, sensitive myocardial contractility index) significantly decreased from 14.7 +/- 0.6 to 7.7 +/- 0.7. Other indexes of the LV contractility (+dP/dtmax) were also reduced. OKY-046 prevented the decreases of ESPDR and +dP/dtmax. OKY-046 also attenuated the increased lung lymph flow changes seen with LPS.









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