Inhibition of rat kidney histamine-N-methyltransferase by biogenic amines.

Biogenic amines were found to inhibit the transfer of 3H-labelled methyl groups from S-adenosyl methionine to histamine by rat kidney histamine methyl transferase, the most potent being tyramine, tryptamine and their hydroxyl derivatives. There appeared to be no competition between histamine and other amines for methyl groups since methyl histamine was the only methylation product formed. The inhibition could not be explained by the formation of stable complexes between inhibitor and the methyl transferase. It is recommended that histamine determinations on biologic specimens by the radioenzymatic assay include a control with added authentic histamine.

Interference with the fluorometric histamine assay by biogenic amines and amino acids.

Naturally occurring low molecular weight biogenic amines and amino acids were analyzed for interference in the fluorometric histamine assay. Three mechanisms of interference were detected, mimicking of histamine, suppression of histamine fluorescence and generation of increasing histamine-like fluorescence during excitation or preirradiation of the o-phthaldialdehyde condensation product with daylight or UVA light. The latter effect was seen only with amino acids. Rat peritoneal lavage fluid contained no fluorescence-suppressing substances, but there were considerable amounts of histamine-mimicking compounds which could not be digested with a diamine oxidase, and of substances generating increasing histamine-like fluorescence when exposed to UV light after condensation with phthaldialdehyde. Although butanol extraction was highly effective in selecting histamine over interfering compounds, it was not sufficient to avoid interference. In contrast, Dowex 50 W-X8 ion exchange chromatography added little to separating histamine and interfering substances. Precautions are recommended to avoid the different types of interference when biological samples are analyzed for histamine content with the fluorometric assay.

[Neonatal chylothorax with trisomy 21]. / Neonataler Chylothorax bei Trisomie 21.

Neonatal chylothorax is an uncommon cause of respiratory distress in the newborn. It may result from anomalous lymph drainage with or without association with aneuploidy syndromes (trisomy, Turner's syndrome, Noonan's syndrome), from injury to the thoracic duct, and from obstruction of the superior vena cava. We report a term newborn and a premature infant with neonatal chylothorax, both associated with trisomy 21. In the case of the term infant, bilateral pleural effusions were diagnosed immediately before birth. The baby suffered from respiratory distress. The physical findings were characteristic of trisomy 21. In the premature infant (gestational age 24 weeks, 735 g) the ductus arteriosus was ligated on day nine after birth. Four days after surgery a central venous line was inserted via the left vena mediana cubiti into the left vena subclavia. Nine days after surgery a left-sided chylothorax occurred. The infant had subtle signs of a trisomy 21 (slightly enlarged tongue, brachycephalic head. questionable simian crease). In both children, cytogenetic studies were done and confirmed the diagnosis of trisomy 21. Infants with neonatal chylothorax should be carefully evaluated for dysmorphic signs of a trisomy or monosomy. Premature infants may present with only subtle clinical signs requiring cytogenetic studies to confirm an aneuploidy syndrome.

Preeclampsia is associated with loss of neuronal nitric oxide synthase expression in vascular smooth muscle cells of the human umbilical cord.

AIMS: Umbilical blood vessels are not innervated and regulation of blood flow to the placenta must depend on structural changes and the effect of vasoactive factors. Failure to achieve these adaptations may result in reduced fetoplacental perfusion. The purpose of this study was to determine whether neuronal nitric oxide synthase (nNOS) is expressed in human vascular smooth muscle cells (VSMCs) of the fetoplacental circulation. nNOS has been described as a non-endothelial NOS counterregulating vasoconstriction only in the VSMCs of animal models. Therefore, we investigated nNOS expression in the fetoplacental unit from preeclamptic and healthy pregnancies. METHODS AND RESULTS: We investigated nNOS regulation by immunohistochemistry, Western blotting and reverse transcriptase-polymerase chain reaction analysis. nNOS activity was determined by measuring the conversion of L-3H-arginine to L-3H-citrulline. nNOS expression was revealed only in VSMCs of the human umbilical veins, but not in umbilical arteries. A more direct assessment of nNOS activity showed that a small, but consistent amount of nNOS is present in the denuded media of the umbilical vein. In VSMCs of the umbilical veins during preeclampsia a total loss of nNOS protein expression and a significant decrease in mRNA expression were seen. CONCLUSIONS: Loss of nNOS expression is associated with preeclampsia. It may alter the regulation of blood flow in the fetal and maternal placental vasculature in preeclampsia. However, the impact of NO produced by nNOS on the vascular tone of umbilical veins remains to be elucidated.

[Management of premature rupture of fetal membranes in obstetrical departments in Germany]. / Management des frühen vorzeitigen Blasensprungs an geburtshilflichen Abteilungen in Deutschland.

Since the treatment of premature ruptures of membranes is not only controversial in the German but also in the international literature, we performed a survey of all obstetrics departments in Germany. From a total of 843 hospitals, 444 questionnaires were returned for evaluation (52.7%). The purpose was to determine which diagnostic and therapeutic regimes are used and how these agree with the literature. In addition to questions on the type of hospital, birth rates with a percentage of premature births and applied diagnostic parameters, our special interest focused on therapy, particularly with regard to prophylactic antibiotic application, tocolytic treatment and lung maturity induction. Prophylactic antibiotics are used in 36.7% and prophylactic tocolytic therapy in 41.7% of the departments. Interestingly, lung maturity induction was performed in 93.5%, in part even before the 28th week of pregnancy, although the effect of this therapy has not yet been proven at a very early stage of gestation. Due to the different views in the literature and, in part, a lack of basic scientific data, it seems there is a preference for the procedure, in which the best personal experience has been made. Because premature ruptures of the membranes is responsible for 30-40% of premature births, it is urgently necessary to clarify this controversial problem by large multicenter studies so that the treatment of early premature ruptures of the amnion can be founded on a rational basis.

Expression of inducible nitric oxide synthase in placenta of women with gestational diabetes.

Gestational diabetes is one of the most prevalent medical complications of pregnancy and causes increased fetal wastage. Investigation of placentas from diabetic mothers indicate chronic disturbances in intervillous, circulation, dilatation of capillaries, and a relatively immature villous structure. Abnormal levels of nitric oxide (NO) may contribute to maternal disorders such as the pathogenesis of diabetic vascular complications. In the normal placenta NO is generated only by endothelial NOS, which apparently serves to regulate vascular tone in the fetoplacental circulation. In contrast, studies have reported the absence of inducible nitric oxide synthase (iNOS) in human placentas under normal conditions. The aim of our study was to investigate whether iNOS is expressed in placentas from patients with gestational diabetes. Reverse transcription-polymerase chain reaction and Western blot analysis demonstrated iNOS mRNA and protein expression in placental tissue only from patients with gestational diabetes. Immunohistochemistry localized iNOS staining to endothelial cells and trophoblasts. We conclude that iNOS can be expressed in human placenta. Its expression might play an important role in placental pathophysiology.