CLAkA M. SZEGO 



157 



seen both 4 and 20 hours after estrogen administration, was completely in- 

 hibited by Cortisol and unchanged by desoxycorticosterone. 



A number of conclusions may be drawn from these studies. It is apparent 

 that the early changes in permeability and in electrolyte and water metabolism 

 in the estrogen-stimulated uterus were accompanied by evidences of shifts in 

 energy-yielding processes. It does not seem, however, that there was a marked 

 increase in energy requirements at this time, since total oxidative metabolism 

 was relatively unchanged 4 hours after the intravenous administration of 

 estradiol. The increase in glucose utilization at this time must, therefore, be 

 associated with a diminished utilization of endogenous substrate, and may be 

 a result of the increased permeability of the uterine cell to glucose. In like 

 manner, the antagonistic effect of Cortisol on glucose disappearance at the 

 4-hour period may be accomplished by preventing these permeability changes 



Fig. 4. Influence of steroids 

 injected 4-20 hours earlier on 

 uterine respiration in vitro. Each 

 point is the mean ± the standard 

 error of 6-55 experiments. Open 

 circles, uninjected castrate; solid 

 circles, estradiol-injected; squares, 

 estradiol })lus Cortisol acetate 

 (F.\); triangles, estradiol plus des- 

 oxycorticosterone acetate (DC.\). 



Dosage of steroids: estradiol, 

 0.5 /ig/ioo gm body weight; F.\ 

 and DCA, 2.5 mg/ioo gm body 

 weight. (Reprinted from ref. 25 

 l)y permission of the editors.) 



$20 



3. 



10 5 



uj - 



4 HOURS 



20 HOURS 



2 3 



HOURS OF INCUBATION 



after estrogen administration. The possibility that a significant portion of 

 estrogen-adrenocortical antagonism may be ascribed to counteractive influences 

 on permeability is certainly consistent with the experimental evidence as 

 earlier reviewed from this laboratory (cf. 24). However, a number of other 

 explanations is possible. These have been discussed at length elsewhere (24, 

 36). What portion of the later (20-hr.) inhibitory influence of Cortisol on the 

 metabolism and growth of the estrogen-stimulated uterus may be a reflection 

 of earlier (4-hr.) antagonistic effects cannot at present be decided. This dis- 

 sociability of the primary and secondary effects of the estrogenic hormones 

 on the uterus, under the influence of the adrenal steroids, appears to provide 

 a valuable tool for the study of steroid action and interaction. 



From the data thus far presented it would appear that reopening of the issue 

 of modification of selective permeability by certain biocatalytic substances, 

 advanced many years ago on the basis of classical pharmacological studies as a 



