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It has been well established that undernutrition and low energy availability disturb female reproductive functions in humans and many animal species. These reproductive dysfunctions are mainly caused by alterations of some hypothalamic factors, and consequent reduction of gonadotrophin-releasing hormone (GnRH) secretion. Evidence from literature suggests that increased activity of orexigenic factors and decreased activity of anorexigenic/satiety-related factors in undernourished conditions attenuate GnRH secretion in an integrated manner. Likewise, the activity of kisspeptin neurons, which is a potent stimulator of GnRH, is also reduced in undernourished conditions. In addition, it has been suggested that gonadotrophin-inhibitory hormone, which has anti-GnRH and gonadotrophic effects, may be involved in reproductive dysfunctions under several kinds of stress conditions. It should be remembered that these alterations, i.e., promotion of feeding behavior and temporary suppression of reproductive functions, are induced to prioritize the survival of individual over that of species, and that improvements in metabolic and nutritional conditions should be considered with the highest priority.

Objective : To investigate whether the human mastcell chymase-endothelin-1(1–31) system was present in human myometrium, chorion and umbilical cord in normal pregnancy. Methods : Myometrium, placenta and umbilical cord were obtained from five normal pregnant women and 10 with preeclampsia. Each tissue was stained with antibodies against hMC and ET-1(1–31). Results : Routine cells were located mainly around vessels. The number of hMC-positive cells and production of ET-1(1–31) were significantly higher in myometrium from patients with severe preeclampsia compared to those from normal pregnant women. In contrast, their numbers were significantly lower in placenta and umbilical cord in patients with severe preeclampsia. Conclusions : These results suggest that the hMC-ET-1(1–31) system is active in normal pregnancy. Overproduction of hMC and ET-1(1–31) in the myometrium may be involved in the pathogenesis of severe preeclampsia, and in such cases some defense mechanism may operate in the fetus to cope with the pathological eftect of the hMC-ET-1(1–31) system.

To investigate the mechanism of human uterine smooth muscle relaxation, the activation of Ca2+-activated K+ channels in cultured myometrial cells obtained from human pregnant myometrium at term by nitric oxide was evaluated at the single cell level using the patch-clamp technique. The open probability of the K+ channel after the addition of 3 × 10–3 M isosorbide dinitrate, a nitric oxide donor (0.116 ± 0.048) was significantly higher than that before the addition (0.059 ± 0.032; n = 9, p < 0.01). In myometrial cells pretreated with lipopolysaccharide, activation of K+ channels was also noted after the addition of L-arginine (10–4 M; open probability increased from 0.179 ± 0.076 to 0.380 ± 0.105, n = 9, p < 0.01: 10–3 M; open probability increased from 0.073 ± 0.050 to 0.242 ± 0.098, n = 12, p < 0.01). Either 10–3 M N-nitro-L-arginine-methyl-ester, an inhibitor of nitric oxide synthase, or 10–6 M methylene blue, an inhibitor of guanylate cyclase, abolished activation of the K+ channel by 10–3 M L-arginine in pretreated myometrial cells with lipopolysaccharide. Application of 10–3 M L-arginine to the intracellular surface of an excised inside-out patch in the myometrial cells pretreated with lipopolysaccharide failed to increase Ca2+-activated K+ channel activity, suggesting that the activation was mediated by intracellular messengers. These results indicate that nitric oxide should control human myometrial relaxation during pregnancy via activation of Ca2+-activated K+ channels.

We describe a 24-year-old pregnant woman complicated by cyclic neutropenia (CN), who was successfully treated with granulocyte-colony stimulating factor (G-CSF). Her white blood cell (WBC) and neutrophil count fluctuated from 2,600 to 4,600/microl, and 26 to 2,530/microl, respectively. The peak neutrophil count gradually decreased as pregnancy advanced, resulting in the disappearance of its cyclicity. At 39 weeks of pregnancy when the neutrophil count became 84/microl, the patient was started on G-CSF and her neutrophil count increased to 1,550/microl on the fourth day after delivery. She delivered a healthy baby without any complications at 39 weeks of pregnancy.

Objective: To investigate physiologic blood-flow-velocity waveform patterns of the fetal cerebral venous system during normal pregnancies by transvaginal Doppler studies and to evaluate cases with abnormal venous-flow patterns. Methods: Internal cerebral veins and the three dural sinuses, those of the superior sagittal sinus, vein of Galen, and straight sinus, were examined in normal cephalic-presenting fetuses of 20–40 weeks’ gestation. For analysis, the venous index was defined as maximum minus minimum velocity divided by maximum velocity. Different cases with intracranial abnormalities were evaluated with emphasis on abnormal venous blood-flow patterns. Results: Internal cerebral veins had pulsatile patterns with a venous index of 0.22 in 47.6% of fetuses, whereas all fetuses had pulsations in the dural sinuses. The vein of Galen had a significantly lower venous index (0.31) than the superior sagittal sinus (0.39) and the straight sinus (0.36), indicating that the amplitude of the intracranial venous pulsation might increase as the flow runs from the periphery toward the proximal portion. Significant regression lines of venous index were obtained, indicating the stability of the pulsation during pregnancy. A flat pattern of superior sagittal sinus flow was found in three cases of hydrocephalus and one of craniosynostosis. Conclusion: We showed the normal patterns of fetal cerebral venous blood-flow velocity and the abnormal patterns which might be associated with increased intracranial pressure. Doppler assessment of the intracranial venous system enabled us to evaluate intracranial abnormalities accompanied by increased intracranial pressure that might have prognostic clinical importance.

Objective To examine endocrine states of mothers with normal 75-g oral glucose tolerance tests (GTTs) who gave birth to large for gestational age (LGA) neonates (group I) and to examine those neonates. Methods We examined plasma glucose levels and serum immunoreactive insulin responses after the 75-g oral GTT was given to group I mothers ( N = 34), mothers with an abnormal oral GTT who gave birth to LGA neonates (group II, N = 21), and those with normal oral GTTs having appropriate for gestational age neonates (group III, N = 173). We also examined the infants, checking neonatal birth weight, levels of immunoreactive insulin and C-peptide immunoreactivity in cord sera at birth and the lowest blood sugar level after birth to see if a correlation existed between them. Results Group I and II mothers showed higher titers in plasma glucose levels and remarkably enhanced ratios of 60 to 30-minute immunoreactive insulin values (immunoreactive insulin up-ratio) after load compared with those of group III mothers. Cord serum immunoreactive insulin and C-peptide immunoreactivity were significantly higher and the lowest blood sugar level was significantly reduced in group I and II neonates compared with those in group III. We observed a positive correlation between cord serum immunoreactive insulin, C-peptide immunoreactivity, and birth weight, but a negative correlation between cord serum immunoreactive insulin, birth weight, and the lowest blood sugar level in group I and II neonates (strongest tendency in group II), but not in group III neonates. Conculsion All of the abnormal carbohydrate metabolic responses in group I mothers and neonates may result in the promotion of growth in LGA fetuses similar to group II, but to a lesser extent. Identification of group I mothers by the immunoreactive insulin up-ratio after oral GTT will help predict the occurrence of LGA neonates and their possible hypoglycemia. (Obstet Gynecol 1995;85:242–9)