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Notes: The diurnal uterine activity in four normal women in the secretory phase of their menstrual cycles and one woman suffering from dysmenorrhea were studied in relation to concomitant hormone levels in blood (progesterone, hGH, prolactin, cortisol, vasopressin, and 15-keto-13, 14-dihydro-PGF2α). In the four normal women uterine activity decreased after midnight, unrelated to circulating levels of 15-keto-13,14-dihydro-PGF2α. But during a dysmenorrheic episode the uterine hyper-contractility pattern correlated well with levels of the PGF2α-metabolite, indicating a role of endogenous-produced PGF2α in this condition. The results demonstrate a diurnal rhythm, possibly related to the wake-sleep cycle. No simple associations were seen between vasopressin, cortisol, prolactin, hGH, the PGF2α-metabolite, and uterine activity.

Notes: A series of tests for the supervision of pregnancy was evaluated in a prospective study of 93 randomly chosen women. Sixteen of these women (index group) had previously defined complications of pregnancy and/or infants of low birth weight due to preterm delivery or intrauterine growth retardation; the rest provided a normal control group. From the 17th week, fetal cephalometry ultrasound and maternal blood sampling were done every three weeks throughout pregnancy, an average of 9.4 times in every woman. Determinations of the plasma concentrations of alpha-fetoprotein (AFP), total oestriol, human placental lactogen (hPL), and human chorionic gonadotrophin (hCG) were later made radioimmunoassays. Deviation of the fetal biparietal diameter more than 3 mm from the expected value was considered abnormal; the normal distributions of plasma levels of the fetal protein and the hormones were established in the local population. The five test parameters remained normal during gestation in the entire control group. Twelve women of the index group had an abnormal level of one or more tests on at least one occasion. Eight fetuses had an impaired growth of the biparietal diameter. AFP levels were above normal in nine women, oestriol values were below normal in three, hPL fell below the normal range in one, and hCG remained normal in the entire index group. AFP levels in maternal plasma and fetal cephalometry seemed to have the highest predictive value for pregnancy complications and the well-being of the newborn; the lag times from the first positive test result to the onset of clinical signs were 6.6 and 6.1 weeks, respectively. For the prediction of low birth weight, measurement of the AFP concentration in maternal plasma, when done serially during pregnancy, can be substituted for fetal cephalometry.

Notes: The retroplacental compartment in which maternal blood is in direct and continuous contact with trophoblasts derived from the fetus seems to be the place where maternal and fetal cells regulate each others' activities. To assess the role of the retroplacental compartment in the immune regulation of pregnancy, 10 healthy pregnant women were selected for evaluation of the immune activity of their lymphocytes and plasma from the retroplacental blood. The results showed that the proliferation and cytotoxic capacity of these lymphocytes, but not of maternal peripheral lymphocytes, against fetal cells were significantly inhibited in unidirect mixed lymphocyte culture and direct cell-mediated cytotoxic assay, respectively. The plasma from retroplacental blood showed significant immunosuppressive properties and depressed the proliferation of maternal peripheral lymphocytes stimulated by fetal HLA as well as the cytotoxic activity of these cells against the fetal lymphocytes. The present data suggest that the retroplacental compartment seems to be an immunosuppressive barrier, protecting the fetus from maternal rejection.

Notes: Research on the neuroendocrine control of maternal behaviour has concentrated on the role of ovarian and pituitary hormones (1). It is known that the gastrointestinal tract plays an important role in synchronizing mother-young interactions (2), but the possible contribution of gastrointestinal secretions to maternal behaviour has not been investigated. We show here that treatment with oestradiol benzoate (OB) in combination with cholecystokinin octapeptide (CCK-8), a duodenal peptide (3), stimulates maternal behaviour within 4 h of exposure to newborn pups in ovariectomized rats. The elevated concentrations of CCK-8 which are found in the plasma of lactating rats may, therefore, contribute to the development and maintenance of mother-young interactions during lactation.

Notes: Methionine- and leucine-enkephalin were measured in the cerebrospinal fluid of lactating rats by high-performance liquid chromatography and electrochemical detection. The concentration of both peptides was high while the rats were nursing their litter. The concentration of methionine-enkephalin decreased rapidly when the mother left her litter and increased equally rapidly after mother-young reunion, provided the pups were allowed direct contact with the nipples of the mother. The level of leucine-enkephalin did not change during the period of time the lactating rat normally stayed away from its litter but decreased after prolonged (12 h) mother-pup separation. These results show that the concentration of methionine-, but not leucine-enkephalin in the cerebrospinal fluid fluctuates as the lactating rat interacts with its litter and is directly dependent upon the suckling stimulus. Although methionine-enkephalin may contribute to the inhibition of sexual behaviour which occurs during lactation, the role of the enkephalins in the other behavioural and endocrine adaptations of lactation is unknown.

Notes: There is evidence for involvement of vasoactive intestinal polypeptide (VIP) and peptide histidine isoleucine (PHI) in control of prolactin secretion. In fact VIP- and PHI-like immunoreactivities have been demonstrated in the hypotha/amic paraventricular nucleus and at the median eminence level. Using immunohistochemistry we have compared the distribution of immunoreactive VIP and PHI in the hypothalamus of male Sprague-Dawley rats and BS rats, a rat strain which has a deficient release of prolactin after stressful stimuli. Quantitative information was obtained by radioimmunoassay for VIP. VIP- and PHI-positive cell bodies were found in the parvocellular part of the paraventricular nucleus in colchicine-treated rats and in nerve fibres within the median eminence of untreated rats to the same extent in both strains. Furthermore, intravenous injection of VIP caused a significant increase in serum prolactin tevets in both strains. However, at the median eminence level in BS rats, the blood vessels located in the lateral aspects of the median eminence did not show the dense VIP/PHI innervation seen in Sprague-Dawley rats. Also, a thick VIP/PHI-positive nerve bundle present on the surface of the median eminence of Sprague-Dawley rats could not be seen in BS rats. Radioimmunoassay analysis revealed that VIP levels in the median eminence were twice as high in Sprague-Dawley as compared to BS rats. Taken together, these results suggest that the defect in the prolactin release mechanism present in BS rats is not confined to the paraventricular system or the pituitary, but could be due to a deficit in VIP/PHI in fibres associated with portal vessels at the median eminence level.

Notes: The present study provides evidence that the human natural killer (NK) cell effector mechanism causing target cytolysis has a requirement for L-arginine. In a deficient medium (DM) containing only salts, buffer system and glucose, NK cell-mediated cytotoxicity was found to decrease by 70% as compared to that obtained in a complete medium (CM). However, adding L-arginine to such DM could restore the activity of NK cells to the normal level. Many other components of CM, such as serum, glutamine and vitamins did not improve NK cell-mediated killing in DM. When all amino acids except L-arginine were added to DM only a partial recovery of NK cell functional cytolysis was seen. L-arginine enhanced the NK cell activity in a dose-dependent manner. Additionally, the inhibitor of both inducible and constitutive nitric oxide synthase, N-monomethyl-L-arginine (L-NMMA) inhibited NK cytolytic activity in DM supplemented with L-arginine indicating participation of nitric oxide (NO). The results also show that the stimulatory effect of L-arginine on human NK cell-mediated cytotoxicity was accompanied by an increase in NO formation as determined by accumulation of nitrite and citrulline. L-NMMA gave a dose-dependent reduction in NO generation as well. The nitrite and citrulline production dose-dependenlly correlated with not only the concentration of L-arginine in the cultivation medium, but also the enhanced NK cell-mediated cytolysis. Taken together, these findings could define a L-arginine/NO-linked effector mechanism in human NK cells. Nitrite and citrulline were not formed when NK cell-mediated target cell killing took place in a L-arginine-free DM supplemented with additives. Thus, it appears as if human NK cells may cause target cell killing via both NO-dependent and -independent processes.

Notes: Male and female Sprague-Dawley rats were treated with nicotine during the prenatal period and the first three postnatal weeks (the pregnant and lactating rats were given nicotine hydrogen (+) tartrate (165 mg/l) in the tap water). Catecholamine fluorescence was evaluated using quantitative histofluorometry on brain sections treated according to Falck-Hillarp methodology. In order to evaluate catecholamine utilization in discrete hypothalamic catecholamine nerve terminal networks, the αMT- (α-methyl-(±)-p-tyrosine methyl ester) induced catecholamine disappearance was studied 2 h following the tyrosine hydroxylase inhibition. The body weight was reduced in both the male and female rats from 3 weeks of age until 9 weeks of age following pre- and postnatal treatment with nicotine.Following one week of withdrawal from pre- and postnatal treatment with nicotine, an increased catecholamine utilization was observed in the medial and lateral palisade zones of the median eminence mainly in the female rat. In the female rat, reduced prolactin serum levels were found both in the presence and absence of αMT treatment as well as reduced luteinizing hormone concentration in the presence of αMT treatment.At 6 months of age indications of a maintained, weak activation of the catecholamine nerve terminal systems in the medial palisade zones of the median eminence were observed in male rats pre- and postnatally treated with nicotine. Furthermore, increased noradrenaline levels were found in the paraventricular hypothalamic nucleus. An increase in serum luteinizing hormone levels was also found in these rats. In the 7-month old diestrous rat, maintained marked increases in catecholamine utilization in the medial and lateral palisade zones of the median eminence were found following treatment with nicotine during the pre- and postnatal period. A significant reduction of nigral dopamine stores was also demonstrated. The serum levels of thyroid stimulating hormone, prolactin and luteinizing hormone were unchanged in these rats both in the presence and absence of tyrosine hydroxylase inhibition. Finally, pre- and postnatal treatment with nicotine did not alter [3H]nicotine binding (quantitative receptor autoradiography) in cortical, striatal and thalamic areas of the adult diestrous rat.The results demonstrate that pre- and postnatal treatment with nicotine in the drinking water produces permanent activations of the catecholamine nerve terminal networks of the external layer of the median eminence mainly in the female rat. These changes appear to be associated with reduced serum prolactin levels in the 4-week old female rat. Sex-specific changes occur in discrete noradrenaline nerve terminal systems. The observed changes may have functional consequences for neuroendocrine regulation and for the regulation of food and water intake as well as sex-specific responses to stress in the male versus the female rat. Nicotine-induced disturbances in brain cell replication and differentiation may underlie the permanent alteration found in discrete catecholamine neuron systems after pre- and postnatal exposure to this drug.