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Prostaglandin inhibitors

W. R. Hanson, Prostaglandin Inhibitors in Tumor Immunology andimmunotherapj, CRC Press, Inc., Boca Raton, 1994, pp. 171—186. [Pg.502]

New substances of this family are in development, and we cannot exclude the possibility that oriented modifications of the molecules of SERMs, statins, or prostaglandin inhibitors will be able to enhance their effect on the breast or bone, maintaining equivalent power in their genuine indication. Knowing that a perfect multitasking molecule is unlikely, we can expect to obtain the maximal benefit from a single pharmacological intervention with substances with relevant added positive effects. [Pg.351]

Nonsteroidal anti-inflammatory drugs [P] Indomethacin reduces antihypertensive response other prostaglandin inhibitors probably also interact. [Pg.1388]

Buprofezin / A, / S (Cyclic urea) ) N NC(CH,j)3 N 0 CH(CHj)2 Probable chitin synthesis and prostaglandin inhibitor. Hormone disturbing effect, leading to suppression of ecdysis... [Pg.782]

Assignment of NSAIDs as cyclooxygenase inhibitors and thus prostaglandin inhibitors. [Pg.230]

White wiUow bark is a source of salicylate, a prostaglandin inhibitor. Prostaglandin inhibition may enhance adrenergic stimulation via inhibition of NE breakdown (see the earlier discussion of ephedrine). [Pg.2672]

Studies of the pathophysiology of acute renal failure has classically considered both tubular and vascular mechanisms [227,228]. In vitro techniques isolating either the vascular or tubular components have been developed. For example, the use of isolated proximal tubules in suspension or in culture allows the study of tubular mechanisms of injury in the absence of vascular factors [229] [230]. There are both in vitro and in vivo models to study vascular injury in the kidney. In vitro models include the study of vascular smooth muscle cells or endothelial cells in culture. In this section, the in vivo methods to evaluate the renal micro-circulation will be discussed. This is of relevance as many nephrotoxins exert their deleterious effects through pharmacologic actions on the resistance vasculature with parenchymal injury occurring as a consequence of ischemia. In clinical practice nephrotoxins may cause prerenal azotemia as a result of increased renal vascular resistance. Nephrotoxins that cause acute renal failure on a vascular basis include prostaglandin inhibitors e.g. aspirin, non-steroidal anti-... [Pg.95]


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See also in sourсe #XX -- [ Pg.85 , Pg.87 ]

See also in sourсe #XX -- [ Pg.129 ]




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