Thromboxane cerebral

Tokiyoshi K, Ohnishi T, Nii Y. 1991. Efficacy and toxicity of thromboxane synthetase inhibitor for cerebral vasospasm after subarachnoid hemorrhage. Surg Neurol 36 112-118. 

Platelet aggregation increases like an avalanche because, once activated, platelets can activate other platelets. On the injured endothelial cell, a platelet thrombus is formed, which obstructs blood flow. Ultimately, the vascular lumen is occluded by the thrombus as the latter is solidified by a vasoconstriction produced by the release of serotonin and thromboxane A2 from the aggregated platelets. When these events occur in a larger coronary artery, the consequence is a myocardial infarction involvement of a cerebral artery leads to stroke. 

Arruzazabala, M. L., V. Molina, D. Carbajal, S. Valdes, and R. Mas. Effect of policosanol on cerebral ischemia in Mongolian gerbils role of prostacyclin and thromboxane A2. Prostaglandins Leuko Essent Fatty Acids 1993 49(3) 695-697. 

As discussed previously, aspirin inhibits platelet-induced thrombus formation through its ability to inhibit thromboxane biosynthesis. Aspirin has therefore been used to help prevent the onset or recurrence of heart attacks in some individuals by inhibiting thrombus formation in the coronary arteries.97,109 Similarly, daily aspirin use may help prevent transient ischemic attacks and stroke by preventing cerebral infarction in certain patients.97,109 The role of aspirin in treating coagulation disorders is discussed in more detail in Chapter 25... 

By virtue of its effects on both cyclo-oxygenase isoenzymes, aspirin inhibits platelet thromboxane A2 formation. This effect in the platelet is irreversible and will persist for the lifetime of the platelet (that is up to 10 days), since the platelet cannot synthesize new cyclo-oxygenase. It is of clinical significance that the dose of aspirin necessary to inhibit platelet thromboxane A2 (around 40 mg/day) is much lower than that needed to inactivate the subendothehal prostacychn (PGI2). Hence, platelet aggregation is inhibited, with some associated dilatation of coronary and cerebral arterioles, at doses that do not... 

Thromboxane A2 Vitamin D Dietary Extreme cerebral vasoconstriction Cerebrovascular ischemia... 

Class II drugs can be further subdivided into at least three subgroups (Figure 3). For example the effect of diltiazem on the slow channels is more marked in the smooth muscle cells of the coronary (51) than the peripheral vasculature. Nimodipine (52) acts preferentially on slow channel transport in the cerebral vessels, where it blocks thromboxane-induced contractions (53) ... 

Synthesis of prostaglandins (PGE2 and PGF2 ) and their release into cerebral ventricular fluid have been reported to occur in mammalian central nervous system tissue. Levels of prostaglandins tend to range from 0.1 to 2.5 pg/g tissue. Their presence has been reported in cerebral cortex, cerebellum, and hippocampus, and levels can be enhanced in the presence of norepinephrine and other catecholamines. Thromboxane synthesis has also been reported to occur. The trace amounts of prostacyclin are probably the result of contamination of brain preparations with vascular elements. 

Platelet aggregation plays a central role in the clotting process and is especially important in clots that form in the arterial circulation. Platelets are believed to be especially important in coronary and cerebral artery occlusion. Platelet aggregation is facilitated by thromboxane, adenosine diphosphate (ADP), fibrin, serotonin, and other substances. Prostacyclin and increased intracellular cAMP inhibit aggregation. 

Park SA, Park BL, Park JH, Lee TK, Sung KB, Lee YK, Chang HS, Park CS, Shin HD (2009) Association of polymorphisms in thromboxane A2 receptor and thromboxane A synthase 1 with cerebral infarction in a Korean population. BMB Rep 42 200-205... 

The a-hnolenic acid derivatives EPA and DHA are found as structural components of brain and retinal tissue phosphohpids and as precursors of the triene prostaglandins. DHA is a component of human cerebral cortex, retina, and muscle [23]. EPA is the immediate precursor of prostaglandin E3, thromboxan A3, and prostacyclin 13. Only a small amount of exogenously administered a-linolenic acid is metabolized to these two acids. In particular EPA is ingested for the most part preformed in dietary fish oils [13, 24]. TTie slow conversion of a-linolenic acid to the longer derivatives exhibits a specie importance of EPA and DHA supplementation. 

Prostaglandins, Thromboxane, Leukotrienes and the Cerebral Circulation in Health and Disease... 

Chan, R. C., Durity, F. A., Thompson, G. B., Nugent, R. A., Kendall, M., 1984 The role of the prostacyclin-thromboxane system in cerebral vasospasm following induced subarachnoid haemorrhage in the rabbit. N. Neurosurg. 61, 1120-1128. 

Fredriksson, K., Rosen, L, Johansson, B., Wieloch, T., 1983 The thromboxane synthetase inhibitor OKY-1581 prevents cerebral ischaemia and neural transmission failure induced by sodium arachidonate platelet aggregation. J. Cereb. Blood Flow Metab. (Suppl. 1) i, S293-S294. 

Fukumori, T., Tani, E., Maeda, Y., 1984 Effect of selective inhibitor of thromboxane A 2 synthetase on experimental cerebral vasospasm. Stroke 15, 306-311. 

Sasaki, T., Wakai, S., Asano, T., Takakura, K., Sano, K., 1982 Prevention of cerebral vasospasm after SAH with a thromboxane synthetase inhibitor OKY-1581. J. Neurosurg. 57, 74-82. 

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