GESTATION 



979 



The mechanism whereby labor induces 

 a marked stimulation of the adrenal cortex 

 is still obscure. It is possible that labor is 

 a stressful state and the stress induced by 

 both the pain and the muscular work act to 

 stimulate the increased release of ACTH 

 resulting in increased adrenocortical ac- 

 tivity. Some confirmation of this may be 

 obtained from the fact that significant in- 

 (■i'eas(> in }ilasma 17a-hydroxycorticoids is 

 noted only if the labor lasts more than 6 

 hours. 



Analysis of the rise in plasma levels of 

 hydrocortisone during pregnancy has sug- 

 gested that the phenomenon is not simply 

 the result of an increased rate of secretion 

 from the adrenal cortex, but rather the re- 

 sult of an increased retention and an altera- 

 tion in the metabolism of the hormone 

 < Cohen, Stiefel, Redely and Laidlaw, 1958). 



2. Aldosterone 



The isolation for aldosterone by Simi)son, 

 Tait, Wettstein, Neher, von Euw, Schindler 

 and Reichstein (1954) and its identification 

 as the hormone regulating fluid and mineral 

 metal)olism stimulated marked interest in 

 the role of this hormone. Among the items 

 of interest was its significance in pregnancy 

 and in the toxemia of pregnancy. Early 

 studies by Chart, Shipley and Gordon 

 ( 1951 1 revealed the presence of a sodium 

 retention factor in the urine that increased 

 from a normal pregnancy value of 36 to 106 

 fxg. equivalent of desoxycorticosterone ace- 

 tate (DOCA) per 24 hours to a maximum of 

 1008 |U.g. equivalent in pregnancy toxemia. 

 These results were confirmed by Venning, 

 Simpson and Singer (1954) and by Gordon, 

 Chart, Hagedorn and Shipley (1954). In 

 addition a slight increase in the sodium re- 

 taining factor was observed in gravid wo- 

 men as compared to nongravid women. 



The discovery that the greater part of 

 the aldosterone in urine is present in the 

 conjugated fraction led to a repetition of 

 the above work using both acid hydrolysis 

 and incubation with /3-glucuronidase (Ven- 

 ning and Dyrenfurth, 1956; Venning, Prim- 

 rose, Caligaris and Dyrenfurth, 1957). The 

 results show little change in the excretion 

 of free aldosterone throughout pregnancy, 

 but the glucuronidase and acid-liydrolyzed 



fractions increased markedly (Fig. 16.17). 

 The urinary excretion values increased 

 from a prepregnancy normal of 1 to 6 /xg. 

 aldosterone (average for women was 3.8 ± 

 14 fig. per 24 hours; Venning, Dyrenfurth 

 and Giroud, 1956) to approximately 25 /xg. 

 per 24 hours. The first significant rise oc- 

 curred about the third month of gestation 

 and an increased concentration was ob- 

 tained until after parturition, when there 

 was a rapid fall to the nonpregnant values. 



G. THYROID GLAND 



Clinical data have long indicated a pos- 

 sible involvement of the thyroid gland in 

 gestation (Salter, 1940). In regions where 

 the iodine supply is low this is demon- 

 strated by an enlargement of the thyroid 

 during pregnancy. The formation of a 

 goiter has been interpreted as evidence for 

 an increased need for iodine during gesta- 

 tion. Scheringer (1930) and Bokelmann and 

 Scheringer ( 1930) reported a rise in the 

 iodine content of the blood of pregnant 

 women during the first trimester of preg- 

 nancy with a peak at the seventh month. 

 The increased concentration is maintained 

 until shortly after parurition. In the goat, 

 however, Leitch (1927) reported no change 

 in serum iodine during gestation until just 

 before parturition. Analysis of umbilical 

 vein blood revealed values that were nor- 

 mal, i.e., lower than in the mother (Leipert, 

 1934). Increased thyroid secretion (Scherin- 

 ger, 1931 ) and increased urinary excretion 

 of iodine have been reported in pregnant 

 women (Nakamura, 1932; 1933). However, 

 Salter (1940) concluded in his review that 

 no reliable evidence of increased thyroid 

 hormone levels in the blood during jireg- 

 nancy is available. 



Peters, Man and Heinemann (1948) re- 

 ported a range of 4 to 8 fig. per cent of 

 serum-precipitable iodine in the normal, 

 nonpregnant woman with a rise to 8.3 fig. 

 per cent (range 6 to 11.2 fig. per cent) in the 

 pregnant woman (Fig. 16.18). It is of in- 

 terest that the elevation in the protein- 

 bound iodine (PBI) does not follow the 

 course of changes in the basal metabolic 

 rate. Whereas the former is already high by 

 the second month of pregnancy the basal 

 metabolic rate rises gradually after approx- 



