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The possible role for adrenergic influences or prostaglandins in the effects of endotoxin to inhibit the glucocorticoid induction of hepatic tryptophan oxygenase (TO) activity, to decrease the hepatic microsomal cytochrome P--450-dependent drug-metabolizing activity, and to induce heme oxygenase activity was examined. Administration of the alpha-adrenergic locking agents phenoxybenzamine or phentolamine attenuated the inhibitory effect of the bacterial lipopolysaccharide on the induction of TO activity by dexamethasone. Injection of a beta-adrenergic blocker, propranolol, or of indomethacin, an inhibitor of prostaglandin biosynthesis, accentuated the effect of endotoxin to inhibit TO induction.
View Article and Find Full Text PDFThe experiment is aimed at establishing the consequences of the endotoxic stress (TAB) associated with alpha- or beta-adrenergic selective blocking drugs on the course of the acute irradiation disease in rats (700R, gamma rad Co60). TAB administered before or after irradiation, alone or associated with propranolol, increases the surviving rate at 30 and 60 days from exposure as compared to the controls (LD 95/30 days). Generally, dibenzyline has unfavourable effects on mortality and survival rate at the mentioned intervals.
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