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Blood levels of total Mg, ionized Mg and intracellular ionized Mg of platelet were lowered in the 2nd trimester of gestation and thereafter. Urinary excretion of Mg does not change during the whole period of pregnancy. According to our results of animal experiments, intestinal absorption of Mg does not increase during pregnancy compared with non-pregnant state. These data suggest pregnant women tend to become magnesium deficiency. This is reflected in the fact that Mg metabolic parameters of pregnant women with preeclampsia are relatively reduced compared with those of healthy gravidae. In the obstetrical practice Mg has other significance, because magnesium sulfate is frequently used as a drug of choice in the therapy of threatened premature delivery and eclampsia. Mg plays important roles in physiology and pharmacology during gestation.

To determine the intrauterine defensive role of urinary trypsin inhibitor (UTI), we studied the effects of UTI in amniotic fluid, fetal membranes and myometrium. The level of UTI was 94 +/- 34 U/ml in neonatal urine (compared to adult urine 8.0 +/- 6.0 U/ml) and 88 +/- 37 U/ml in amniotic fluid. This may indicate that the main source of UTI in the amniotic fluid is the fetal urine. UTI was found to be concentrated in vernix, fetal intestine, amniotic membranes and uterine myometrium. Immunostaining of term amnion revealed a dark staining for UTI, whereas in premature deliveries UTI staining was markedly decreased. In myometrium, the concentration of UTI was found to be increased during pregnancy compared to non pregnant myometrium. Also, placentas were well stained for UTI in term pregnancy. Thus UTI has an important role in amniotic fluid, fetal membranes, placenta and uterine muscles. UTI has an inhibitory effect on several enzymes and cytokines. UTI was found to inhibit neutrophil elastase activity as well as trypsin activity. Its inhibitory activity was increased in the presence of lipid. LPS stimulated amnion cells trapped more UTI than unstimulated amnion cells. UTI in amnion cells was released after addition of 1% meconium solution. UTI was also found to inhibit the effect of IL-1, TNF and interleukin-8 on amnion. These results indicate that UTI localized in amnion is important in the protection of fetal membrane especially against bacterial infections and cytokines. It is known that endothelin (ET), prostaglandin F2 alpha (PGF2 alpha) and oxytocin can induce uterine contraction. UTI could inhibit uterine contractions stimulated by ET, PGF2 alpha and oxytocin in isometric contraction test. UTI could also inhibit cervical maturation induced by interleukin-8. Therefore UTI is essential for maintenance of pregnancy. From the isometric contraction tests, we assumed that UTI might works through regulation of calcium entry or availability in the cells. Initial increase in intracellular calcium was also inhibited by UTI pre incubation dose dependantly. We examined the change in intracellular calcium at single cell level by digital image analysis with Fura 2AM as a calcium probe. At resting level UTI incubation did not produce any significant changes in intracellular free calcium. Thrombin, LPS, interleukin-8 and ET-1, known calcium agonists could increase intracellular calcium in fibroblasts, amnion and uterine myocytes. Whereas as the same doses of those known calcium agonists could not change the intracellular free Ca2+ concentrations in UTI pre incubated fibroblasts, amnion cells and uterine smooth muscle cells.(ABSTRACT TRUNCATED AT 400 WORDS)

The efficacy and safety of early therapy with imipenem/cilastatin sodium (IPM/CS) were studied in patients who had chorioamnionitis with preterm PROM or threatened abortion and premature delivery. The following results were obtained. 1. The clinical efficacy of IPM/CS administered by intravenous drip infusion at daily dosages of 1 to 2 g as concurrent treatment with antiuteronics (ritodrine hydrochloride or terbutaline sulfate) was studied in patients with threatened abortion and premature delivery in the 11th to 34th week of pregnancy (n = 9), or premature PROM in the 23rd to 36th week (n = 9). 2. Response to IPM/CS were good in all of the patients with threatened abortion and premature delivery. Latent periods were prolonged for more than 7 days in 44.4% (4/9) of the patients with preterm PROM. 3. Changes in elastase appeared to be significant as those in CRP for inflammatory markers. 4. These findings combined with our previous results indicate that treatment of preterm PROM before the 32nd of pregnancy prolongs the latent period.