Abstract
Vascular tissue synthesizes prostanoids (PGs) that modulate contractility, myocyte and fibroblast proliferation, platelet aggregation and leucocyte function, all of which are key components in the pathophysiology of atherogenesis. Furthermore, platelet and leucocyte release substances have been shown to stimulate the synthesis and release of PGs from vascular cells. It is possible, therefore, that vascular PGs are part of a protective response against atherogenic events. Consequently, any disruption of PG synthesis (viz. as a result of smoking) may accelerate the atherogenic state. Although smoking is a major risk factor in the development of atherosclerosis, the combination of smoking with other risk factor (e.g., diabetes, hypertension, hypercholesterolaemia) markedly increases the likelihood of death from atherosclerotic disease. The present paper therefore discusses the following:
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1)
How PGs relate to pathophysiology of atherosclerosis
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2)
Experimental findings on the effects of cigarette smoking on vascular and platelet prostanoid synthesis.
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3)
How other risk factors may interact with smoking to influence vascular permeability
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4)
Future directions and emphases on research into eicosanoids and smoking.
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© 1990 Plenum Press, New York
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Jeremy, J.Y., Mikhailidis, D.P. (1990). Vascular and Platelet Eicosanoids, Smoking and Atherosclerosis. In: Diana, J.N. (eds) Tobacco Smoking and Atherosclerosis. Advances in Experimental Medicine and Biology, vol 273. Springer, Boston, MA. https://doi.org/10.1007/978-1-4684-5829-9_14
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DOI: https://doi.org/10.1007/978-1-4684-5829-9_14
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