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SUMMARY

1. Furazolidone (0·75 g/kg) will interrupt pregnancy in mice.

2. Foetal tissue is particularly sensitive to the drug at the time of or before implantation of the ovum.

3. Intra-amniotic injection of furazolidone in rabbits causes foetal death and resorption.

4. Furazolidone applied locally does not antagonize the proliferative effect of progesterone on rabbit endometrium.

5. The mode of action of furazolidone on pregnancy is discussed. It is suggested that it acts directly on the foetus.

Abstract

The factors that determine the circulating levels of relaxin during pregnancy have been investigated by comparing the plasma levels of relaxin throughout pregnancy in women who became pregnant spontaneously (singleton, n=240) or following superovulation (singleton and multifetal pregnancies (two to ten conceptuses), n=83). Some of the women with multifetal pregnancies underwent selective fetal reduction to twin pregnancies. Relaxin levels were higher at 7–34 weeks of gestation in singleton pregnancies achieved following superovulation when compared with levels in spontaneously conceived singleton pregnancies (P<0·05–0·001). In samples obtained between 10 and 12 weeks of gestation (before fetal reduction for the multifetal pregnancies), plasma relaxin levels correlated with fetal number (r=0·526, P=0·0001). Reduction in fetal number to a twin pregnancy did not alter relaxin levels. These data suggest that the circulating levels of relaxin throughout pregnancy are determined during the cycle of conception by gonadotrophin stimulation, and within the first 10 weeks of pregnancy by the luteotrophic stimulus from the conceptus. Furthermore, once corpus luteum synthesis of relaxin is established, then reduction in the luteotrophic stimulus does not appear to affect it.

Journal of Endocrinology (1994) 142, 261–265

SUMMARY

The adrenal glands from twenty-four cases of sudden death during pregnancy and immediately post partum have been examined. The mean combined adrenal weight in the pregnancy cases was slightly greater than in controls, but the difference was not statistically significant. There was, however, a significant increase in the width of the z. fasciculata in the pregnancy cases due toan increase in the width of the inner part of this zone. This change occurred early in pregnancy, and there was no progressive increase in width with the duration of the pregnancy. Histochemical tests showed that the only difference from the controls was in the inner part of the z. fasciculata where there was reduction in the amount of sudanophilia. The appearance of the cortex in pregnancy was quite unlike that found in glands stimulated by systemic disease or corticotrophin. These findings are discussed in relation to the chemical evidence of increased urinary steroid excretion in pregnancy.

In late pregnancy the coefficient of variation of urinary 5β-pregnane-3α, 20α-diol from day to day is 24% in the same subject (Klopper, 1964). This variability is one of the factors which detracts from the value of pregnanediol assay. In 1959 Klopper & Macnaughton identified pregnanediol in faeces and suggested that a variable alimentary loss of pregnanediol might contribute to the variation in urinary pregnanediol. Davis, Plotz, Le Roy, Gould & Werbin (1956) measured the radioactivity recovered in the faeces after injection of [4-¹⁴C]progesterone but very little is known about the amount excreted in the faeces.

This study compares the urinary and faecal pregnanediol excretion during a 6-day period. All 12 subjects were between 30 and 34 weeks pregnant and had normal pregnancies. Complete urine and faecal collections were made for 6 days in a metabolic unit. Urinary pregnanediol was measured by the method of Klopper, Michie & Brown

SUMMARY

A histological study was made of ovaries obtained from patients in the latter half of pregnancy; the duration of pregnancy ranged from 26 to 40 weeks. During the first 7 weeks of this period there was little evidence of follicular activity. From 33 weeks to term new Graafian follicles, rarely exceeding 4 mm in diameter, appeared in progressively increasing numbers. This may be a critical stage in follicular development when the follicle must either go on to complete maturity or suffer atresia. Luteinization of the granulosa layer occasionally occurred in these follicles but it was not accompanied by proliferation of granulosa cells; the surrounding thecal cells frequently showed no sign of luteinization and were sometimes atrophic. The factors responsible for granulosa luteinization seem not to be the same as those necessary for theca luteinization, nor are they identical with the mechanisms responsible for luteal proliferation.