Detail of "33125-97-2"

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Inhibition by etomidate of steroidogenesis in isolated bovine adrenal cells

Inhibition by etomidate of steroidogenesis in isolated bovine adrenal cells. Kenyon, C. J.; Young, J.; Gray, C. E.Chemicals with cas numbers 52-39-1 and 64-85-7 also play role.; Fraser, R. (Blood Pressure Unit, West. Infirm., Glasgow G11 6NT, UK). J. Clin. Endocrinol. Metab., 58(5), 947-9 (English) 1984. CODEN: JCEMAZ. ISSN: 0021-972X. DOCUMENT TYPE: Journal CA Section: 1 (Pharmacology) Section cross-reference(s): 2 Isolated bovine adrenocortical cells were incubated with and without 10-8M ACTH [9002-60-2] and with increasing doses of etomidate [33125-97-2] (0-625 ng/mL). ACTH-stimulated cortisol [50-23-7] synthesis was significantly inhibited by a concn. of etomidate (25 ng/mL) which is much less than therapeutic plasma levels (100-500 ng/mL). Both basal and ACTH-stimulated synthesis of cortisol, progesterone [57-83-0], 17a-hydroxyprogesterone [68-96-2], and corticosterone [50-22-6] were inhibited by 625 ng etomidate/mL, whereas deoxycorticosterone [64-85-7] output was more than doubled with this dose of anesthetic. These observations suggest that etomidate inhibits mitochondrial cytochrome P 450-dependent hydroxylation reactions in the adrenal steroidogenic pathway. Thus, the adverse side effects of the anesthetic etomidate are apparently linked with inhibition of adrenocorticoid synthesis. .

Diazepam, pentobarbital and D-etomidate produced increases in bicuculline seizure threshold; selective antagonism by RO15-1788, picrotoxin and (±)-DMBB

Diazepam, pentobarbital and D-etomidate produced increases in bicuculline seizure threshold; selective antagonism by RO15-1788, picrotoxin and (±)-DMBB. Ashton, David (Dep. Neuropharmacol., Janssen Pharm. Res. 16887-00-6 and 56-12-2 are also occured in this study. Lab., Beerse B-2340, Belg.). Eur. J. Pharmacol., 94(3-4), 319-25 (English) 1983. CODEN: EJPHAZ. ISSN: 0014-2999. DOCUMENT TYPE: Journal CA Section: 1 (Pharmacology) Section cross-reference(s): 14 The seizure threshold for different seizure components was measured after slow i.v. infusion of bicuculline [485-49-4] in the rat. Clear differences were seen in the seizure threshold for tremor (TRE) and clonic-forepaw (CLOF) as compared to clonic-hindpaw (CLOH) and tonic-forepaw (TONF). Seizure threshold was measured after treatment with different doses of diazepam [439-14-5], pentobarbital [76-74-4], d-etomidate [33125-97-2], picrotoxin [124-87-8], RO 15-1788 [78755-81-4] and 5-(1,3-dimethylbutyl)-5-ethylbarbituric acid (DMBB) [2964-06-9]. Direct and indirect antagonism between the agonists and antagonists was examd. The interactions between the drugs for TRE and CLOF resemble those described in in vitro receptor-binding assays using the GABA [56-12-2]-benzodiazepine-Cl ionophore complex (GBCI). The interactions for CLOH and TONF do not show this resemblance, suggesting less involvement of GABA in these phenomena. Diazepam was selectively antagonized by RO 15-1788. D-Etomidate and pentobarbital were directly antagonized by DMBB, suggesting shared activity at the barbiturate site. No evidence was found for an interaction between compds. acting at different sites within the GBCI. .