Rectal methohexital sedation for computed tomography imaging of stable pediatric emergency department patients.

OBJECTIVE: Rapid onset of sleep, brief duration of action, and ease of administration are properties that make rectal methohexital (MXT) an attractive choice for sedating stable pediatric emergency department (ED) patients for computed tomography (CT) imaging. METHODOLOGY: One hundred stable patients between 3 and 60 months of age who presented to any of 3 participating EDs and required sedation to undergo CT scanning were given 25 mg/kg of rectal MXT approximately 15 minutes before their imaging. Vital signs and oxygen saturation were recorded at regular intervals. Data collected included indication for CT imaging, time to achieve sleep, time to reach discharge criteria, adequacy of sedation, adverse effects, and parental satisfaction. RESULTS: Ninety-five percent of the patients were adequately sedated with rectal MXT. It took an average of 8 minutes to achieve full sedation and the duration of action averaged 79.3 minutes. Ten percent had transient side effects, but all recovered completely. None required intubation. Parental satisfaction was 90%. CONCLUSION: Rectal MXT compares favorably to other methods of nonintravenous sedation for CT scanning of stable pediatric ED patients in terms of rapidity of onset and reliability but does cause a significant amount of transient respiratory depression. Its use requires careful monitoring of oxygen saturation and should be used only in a setting where physicians skilled in airway management are present. If these requirements are met, it may be a good choice for the relatively noninvasive sedation of pediatric ED patients undergoing painless but anxiety-provoking procedures.methohexital, pediatric procedure sedation, rectal administration, computerized tomography imaging.

Role of porcine endometrial estrogen sulfotransferase in progesterone mediated downregulation of estrogen receptor.

Estrogen sulfotransferase (EST) is a progesterone (Pg) induced secretory endometrial enzyme which may effect estrogen receptor levels by esterifying estradiol-17 beta (E2) to an inactive, sulfate form. The effects of this enzyme were studied using specific inhibitors of EST that do not bind to estrogen receptor (ER): 4-nitroestrone 3-methyl ether and 4-fluoroestrone 3-methyl ether. A 1 h pulse with 4 nM E2 caused ERn (i.e. E2-bound, chromatin-bound receptor) to increase 40% in incubations of proliferative gilt endometrium (no EST activity), while the same E2 treatment of secretory endometrium (high EST activity) caused no increase in ERn. ERn accumulation was completely restored in these experiments by preincubating secretory endometrium with 4 microM 4-fluoroestrone 3-methyl ether. Gilt endometrial explants cultured 7 days with 1 nM E2 plus 1 microM Pg (which induced EST activity) possessed half the ERn as explants devoid of EST activity which were cultured in E2 alone. The addition of 10 microM 4-nitroestrone 3-methyl ester to the cultures of secretory endometrium restored ERn to the levels seen in minces cultured with E2 alone. Furthermore, ovariectomized gilts injected daily with 250 micrograms E2 plus 25 mg Pg had much lower ERn (0.06 fmol/micrograms DNA) than gilts injected with E2 only (0.21 fmol/microgram DNA). ERn was restored completely by supplementing the E2 plus Pg injections with 0.5 g 4-nitroestrone 3-methyl ether administered by vaginal suppositories.(ABSTRACT TRUNCATED AT 250 WORDS)

Induction of porcine uterine estrogen sulfotransferase activity by progesterone.

Studies have been carried out which were designed to examine the hormonal requirement for the appearance of estrogen sulfotransferase activity in porcine uteri. Mature, ovariectomized (OVX) gilts were housed for 3 weeks before being treated with various regimens of estradiol-17 beta (E2) and progesterone (P). Uteri were then removed, minced, incubated for 2 h with [3H] E2 (10(-8) M) and Na2 35SO4 (10(-4) M) and the labeled metabolic products were extracted and analyzed. Endometrial samples were also taken for the determination of E2 and P cytoplasmic and nuclear receptors (R). It was found that 4 daily injections of 250 micrograms of E2 was sufficient to bring plasma E2 concentrations to that representative of a normal estrous cycle (approx. 30 pg/ml) and to induce cytoplasmic PR to high levels (7000--19000 fmol/mg DNA). Estrogen sulfotransferase activity, which was negligible in OVX and E2-treated pigs, increased to near normal secretory levels (4 pmol product/h per 0.4 g tissue) only in pigs primed with E2 and subsequently treated with E2 and P (25--250 mg/day, 3 days). This treatment also brought about the translocation of PR to the nuclear compartment. The steroid alcohol sulfotransferase activity in these tissues decreased upon ovariectomy and remained unaffected by the hormone treatments. Endometria from treated and untreated pigs were cultured for a period up to 7 days. During this time E2 (10(-8) M) induced and/or maintained PR and P (10(-6) M) was shown to stimulate estrogen sulfurylation concomitant with the translocation of PR to the nucleus. These studies have demonstrated that, in OVX pigs and endometrial cultures, P stimulated uterine estrogen sulfotransferase activity to a level normally found in secretory uteri. In order for P to bring about elevated levels of estrogen sulfurylation it was necessary that the endometrium contain adequate concentrations of cytoplasmic PR (which required E2 priming of the system) and the P receptor complex must display nuclear translocation.