Thromboxane physiologic effects

PRIMARY PHYSIOLOGIC EFFECTS OF THE MAJOR CLASSES OF PROSTAGLANDINS, THROMBOXANES, AND LEUKOTRIENES ... 

The eicosanoids—prostaglandins (PGs), thromboxanes (TXs), prostacyclins (PGIs), and leukotrienes (LTs)—are derived from essential fatty acids and act similarly to hormones (Chapter 30). However, they are synthesized in almost all tissues (unlike hormones, which are synthesized in selected tissues) and are not stored to any significant extent their physiological effects on tissues occur near sites of synthesis rather than at a distance. They function as paracrine messengers and are sometimes referred to as autacoids. 

Fatty acids are saturated and unsaturated carboxylic acids containing between twelve and twenty-four carbon atoms. Fatty acids with even numbers of carbon atoms occur most frequently in nature. The reactions of fatty acids are identical to those of carboxylic acids. They include esterification, production by acid hydrolysis of esters, saponification, and addition at the double bond. Prostaglandins, thromboxanes, and leukotrienes are derivatives of twenty-carbon fatty acids that have a variety of physiological effects. 

The functional significance of thromboxane A2 inhibition by kava is not certain. More needs to be understood about the functions of prostaglandins in the CNS, but given the inhibition of GABAA by thromboxane A2, kava s suppression of thromboxane A2 synthesis could conceivably contribute to its anxiolytic and sedative effects. More research is needed to determine if this mechanism of action is physiologically significant at normal kavalactone concentrations. 

The prostaglandins, thromboxanes, and leukotrienes have been shown to have a variety of effects on virtually every major physiologic system. Studies have indicated that these compounds can influence cardio-... 

Summary - Many diverse novel compounds that inhibit different platelet functions show great promise, not only for potential anti-thrombotic agents, but also for more specific effects on prostaglandin and/or thromboxane A2 synthesis, and serotonin or calcium uptake and release. Many active compounds can be used as tools in the search toward a more complete understanding of the physiologic interactions of the hemostatic mechanisms. This better understanding would lead to the development and use of more potent and selective synthetic compounds in the inhibition of platelet aggregation and fibrin formation, and in the enhancement of fibrinolysis for the control of both arterial and venous thrombosis. It is hoped that some of these new compounds will be evaluated clinically in the near fu ture. 

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