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"This study investigated the effects of smoking cessation with and without nicotine substitution on the excretion of major urinary metabolites of thromboxane A₂ and prostacyclin; 11-dehydrothromboxane B₂ and 2, 3-dinor-6ketoprostaglandin F1 alpha, respectively, as well as on the excretion of leukotriene E4 in man."

"The fact that eicosanoid production remains at pre-cessation levels in volunteers who quit smoking but use nicotine substitution may be involved in the risk of cardiovascular complications reported during nicotine replacement therapy."

"The aim of this study was to determine the extent of change in platelet and coagulation markers in the acute phase of ischemic stroke and to assess the utility of marker mesurement in stroke subtype classification.  Urinary 11-dehydro-thromboxane B₂ (11-deTXB₂), a marker of in vivo platelet activation, and markers of coagulation activation, including prothrombin fragment 1 +2 (F1 + 2), thrombin-antithrombin complex (TAT) and fibrinogen, were measured in 25 patients with ischemic stoke within 24 h of onset symptoms. Eight patients taking aspirin at the time of the stroke had signficantly lower 11-dTXB2 values than patients not taking aspirin (964 vs. 4,314 pg/mg of creatinine P=0.0007).  Stroke patients not taking aspirin had significantly higher 11-dTXB2 concentration than age-matched controls (4,314 vs. 1,788 pg/mg of creatinine; P= 0.0006)."

"An unstable intermediate between the prostaglandin endoperoxides and thromboxane B_2.  The compound has a bicyclic oxaneoxetane structure.  It is a potent inducer of platelet aggregation and causes vasoconstriction.  It is the principal component of rabbit aorta contracting substance ORCS)."

"These results suggest that bronchial asthma patients with high urinary 11-DHTXB₂ levels could markedly respond to Seratrodast treatment. ”

"Previous studies relating increased thromboxane (TX) biosynthesis to cardiovascular risk factors do not answer the question whether platelet activation is merely a consequence of more prevalent atherosclerotic lesions or reflects the influence of metabolic and hemodynamic disturbances on platelet biochemistry and function."

"The occurrence of large-vessel peripheral arterial disease per se is not a trigger of platelet activation in vivo.  Rather, the rate of TXA2 biosynthesis appears to reflect the influence of coexisting disorders such as diabetes mellitus, hypercholesterolemia, and hypertension on platelet biochemistry and function.  Enhanced TXA2 biosynthesis may represent a common link between such diverse risk factors and the thrombotic complications of peripheral arterial disease."

“The urinary excretion of 11-dehydro-TxB₂ was significantly higher in patients with COPD than in control subjects. Moreover, 11-dehydro-TxB₂ excretion was inversely related with arterial oxygen tension.”

"Thromboxane A2 (TXA2) biosynthesis is enhanced in the majority of patients with type lla hypercholesterolemia.  Because simbastatin (a 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor) was previously shown to reduce platelet aggregation and TXB2 production ex vivo, we investigated TXA2 biosynthesis and platelet function in 24 patients with type ll hypercholesterolemia randomized to receive in a double-blind fashion simvastatin (20mg/d) or placebo for 3 months.  The urinary excretion of 11-dehydro-TXb2, largely a reflection of platelet TXA2 production in vivo, was measured by a previously validated radioimmunoassay technique.  Blood lipid levels and urinary 11-dehydo-TXB2 excretion were significantly (p<.001) reduced by simvastatin.  In contrast, placebo-treated patients did not show any statistically signficant changes in either blood lipids or 11-dehydro-TXB2 excretion."

"In the 24 patients in whom the plaque score was measured, multivariate analysis indicated a significant positive correlation between urinary excretion of 11-dehydrothromboxane B₂ and plaque score, age, smoking and hypercholestermia.  Our results indicate the risk factors such as age, hypercholestermia, atherosclerosis and smoking activate platelets in vivo to develop carotid atherosclerosis."

"Multivariate analysis indicated a significant positive correlation between urinary excretion of 11-dehydrothromboxane B₂ and plaque score, age, smoking and hypercholesteremia."

“Cigarette smoking increased the urinary excretion of 11-dehydrothromboxane B₂ (reflecting thromboxane A₂ generation).”

“Cigarette smoking was also associated with higher levels of fibrinogen in plasma.”

“Cigarette smoking and transdermal nicotine treatment were both associated with a higher white blood cell count compared with the placebo patch.”

"High-dose supplements of fish oil reduce thromboxane synthesis in nonpregnant human subjects and were therefore proposed as a means of preventing various small-vessel disorders, including preeclampsia.  The effect of fish oil on thromboxane metabolism in pregnancy was investigated in our study."

"A decrease ranging from 32% to 71%, in 24-hour urinary 11-dehydro-thromboxane B₂ excretion (mean reduction from 1606 pg/mg creatinine to 779 pg/mg creatinine, p < 0.001) was found among the 11 fish oil-treated women. No change in excretion was found among the control women. No maternal, fetal, or neonatal bleeding disturbances occurred, and no laboratory changes in coagulation markers were observed.”

“An increase in the release of the vasoconstrictor thromboxane A₂, suggesting the activation of platelets, occurs in both the primary and secondary forms of pulmonary hypertension.” By contrast, the release of prostacyclin is depressed in these patients.   Whether the imbalance in the release of these mediators is a cause or a result of pulmonary hypertension is unknown, but it may play a part in the development and maintenance of both forms of the disorder."