No abstract

No abstract

For screening atopy risk in 6401 (84%) of all infants born during the year 1990 in six obstetric departments of five German cities, cord-blood IgE values were determined with CAP-RAST-FEIA. After cases with elevated IgA values had been excluded, 25% of the values were above the detection limit of 0.35 kU/l, and 8.5% were above 0.9 kU/l. Boys had significantly higher values than girls (P < 0.001). The distribution of values was significantly different for different nationalities of mothers (P < 0.001). The percentage of elevated values (> 0.9 kU/l) increased significantly with the number of close family members with atopic history (P < 0.001). Regarding the atopic history of the father, siblings, and mother separately, only the mother's history had a significant association with the cord-blood IgE class (P < 0.001). The IgE values of 81 twin pairs correlated significantly with a coefficient of r = 0.4909 (P < 0.001). The smoking history of the parents during pregnancy showed an association with cord-blood IgE values (P < 0.02). No significant association could be shown between cord-blood IgE distribution and other variables, i.e., gestational age, birth size, birth modus, Apgar score, cord-blood pH value, neonatal problems, parity, age of the mother, medication during pregnancy, educational level of mother or father, time of year, or obstetric department. It is hypothesized that, in addition to some postpartum contamination or placental transfer of maternal IgE, cord-blood IgE values are also determined by the fetal immunologic reaction to intrauterine exposure to allergens and trigger factors, and by genetic influences.

The method presented is based on whole-body plethysmography. The apparatus consisted of two chambers (a = respiratory, b = body chamber) separated by a tight water-filled rubber cuff which was fixed around the head of the animal. Experiments were performed under constant gas conditions: temperature 30 degrees C, 100% relative humidity, the volumes of the two chamber being identical. Volume changes in the chamber (delta Va, delta Vb) were recorded continuously by means of pressure transducers. Respiratory flow was calculated by differentiation of delta Va with respect to time. The three parameters delta Va, delta Vb and respiratory flow allowed the calculation of breathing frequency, inspiration/expiration ratio, (peak) expiratory flow and specific airway conductance. In addition we describe a new parameter indicating bronchial obstruction: a graphical plot of delta Vb against delta Va produces a closed loop, the area of which reflects the degree of airway obstruction, and we read off the parameter we term "compressed air" from this graph. In our hands this parameter was more than ten times as sensitive as other measures of bronchial obstruction. Using this new technique we have carried out pharmacological studies with eicosatetraynoic acid (ETYA), 2-aminomethyl 4-t-butyl-6-iodophenol (MK 447 = radical scavenger), the histamine antagonist clemastine and the histamine antagonist cimetidine. In allergen-tested animals we observed mild protective effects of ETYA when given as an aerosol (3 mg) and pronounced effects of MK 447 (4 mg i.p.). Combined H1 H2-antagonism was much more effective in preventing allergen-induced bronchial obstruction than H1-antagonism alone.

In the Ayurvedic medicine, Picrorhiza kurroa Royle ex Benth. is used for the treatment of liver and lung diseases. Using different chemical and pharmacological methods, we could identify the phenol glycoside androsin as active compound preventing allergen and platelet-activating factor induced bronchial obstruction in guinea pigs in vivo (10 mg/kg p.o.; 1 h prior to the inhalation challenge). Histamine release from human polymorphonuclear leukocytes in vitro was inhibited by other compounds yet to be identified.