Acceleration of fetal maturation with intra-amniotic administration of thyroxine was employed in eight patients in whom preterm delivery was necessary because of malignant disease of the mother. Thyroxine (200 mcg to 500 mcg) was given at weekly intervals starting at the 27th to 32nd week of gestation until the L-S ratio exceeded 2.0. The fetuses were delivered between the 29.4 and 34.0 week. None of the newborns suffered from respiratory distress syndrome, and three newborns were cared for in the regular nursery. Thyroxine-induced acceleration of fetal maturation and pre-term delivery permits earlier initiation of antineoplastic and radiation therapy without exposing the fetus to the hazards of maternal therapy and those of prematurity.

Milk yield fell in a single rabbit mammary gland within 24 h after the litter had been reduced from six to eight pups to one pup. The diminished secretion lasted 2\p=n-\3 days, then rebounded to the expected level over the next 1\p=n-\2 days and thereafter maintained this level. During early to mid-lactation the decrease in milk secretion after reduction of the litter to one pup was prevented either by s.c. injections of prolactin or by s.c. injections of the \g=b\-adrenergicblocking drug, propranolol. These results suggest that milk secretion was reduced in the single gland as the result of sympathetic activation, triggered possibly by the turgid state which developed in the remaining glands after the litter was reduced. The results suggest also that the depression of milk secretion by the sympathetic system was due to a reduction in the effective amount of prolactin and probably of other adenohypophysial hormones reaching the mammary secretory cells rather than to an impairment of their release from the anterior pituitary.The magnitude of the depression and rebound in milk secretion of a single rabbit mammary gland, and the effectiveness of the preventive action of either propranolol or prolactin, was considerably less during late as compared with early to mid-lactation. We postulate from these results that the mammary gland of the rabbit has a functional lability, i.e. responsiveness, which diminishes as lactation progresses and which dictates the extent to which local, neural and humoral factors may alter the milk secretory function of the mammary gland. Since suckling in the rabbit does not change from a once-a-day frequency throughout lactation, a diminishing lability may be an important factor in the decline and cessation of lactation in this species.

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SUMMARY The mechanism by which suckling affects the hypothalamo-pituitary-ovarian system was studied in lactating Wistar rats. Unilateral ovariectomy was carried out on day 4 post partum and the subsequent ovarian compensatory hypertrophy (OCH) was assessed on day 14 post partum. The weight of the corpora lutea (CL) of lactation, the CL of pregnancy and of the remainder of the ovary, here termed interstitial tissue, was determined for both ovaries. A clear OCH, mainly due to an increase in interstitial tissue, occurred in rats whose pups were removed on day 4 post partum. Suckling by two pups inhibited OCH, whereas suckling by six or ten pups produced significant ovarian atrophy, these effects being due to a decrease in weight of both interstitial tissue and CL of pregnancy which overcame an increase in weight of the CL of lactation. Inhibition of OCH occurred in spinal-cord transected rats suckling six pups. Suckling was suspended in unilaterally ovariectomized rats nursing ten pups on day 14 post partum, and the weight of the remaining ovary was determined 16, 32, 64 and 96 h later in four groups of rats. The weight of the remaining ovary returned to that of the control ovary 64 h after withdrawal of suckling. This effect was due to an increase in weight of interstitial tissue and of the CL of lactation. Maintenance of suckling for 64 h in rats with the galactophores ligated to prevent milk removal, inhibited OCH. By contrast, both oxytocin injections and exteroceptive stimulation provided by litters failed to block ovarian growth after suckling withdrawal. The results suggest that suckling itself is an important influence in the inhibition of OCH, but that other factors may contribute to the ovarian changes observed during lactation in the rat.

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