Aiming at testing the hypothesis that, in the foetus with gastroschisis (GX) peritoneal dialysis during antenatal bowel exposure to the amniotic fluid may induce some modifications of the internal environment, we have studied the composition of blood, amniotic fluid and allantoic fluid in a chick embryo model of GX. Intestinal loops were surgically eviscerated in 184 embryos on the 14th day of incubation and exposed to the mixture of both embryonal fluids until the 19th day (hatching expected at the 21th). Typical lesions of GX were present in half of the 94 survivors (n = 42). For comparison we used a control group of non-manipulated animals (n = 19) and a "sham" group of animals in which the operation was carried out only until umbilical manipulation but without bowel exposure (n = 22). Chicks with GX were smaller and slightly dehydrated as attested by clinical signs and had moderately increased hematocrit. They had significant hyperkaliaemia and slight decreases in serum Na and Cl. Urea, total protein and protein fractions were not modified. Taking into account the gradients for such substances existing between the dialysate (amino-allantoic mixture) and the embryonal blood, the changes observed, albeit slight, suggest that there was some evidence of dialysis through the peritoneum: lower Na and Cl concentrations in the dialysate than in blood, induced slight falls in serum Na and Cl whereas higher K concentration resulted in severe hyperkaliemia. The high levels of albumin in the chick amniotic fluid did not allow protein depletion and therefore total protein and its fractions remained unchanged.(ABSTRACT TRUNCATED AT 250 WORDS)

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This paper explores whether, in addition to the previously described lung hypoplasia with arteriolar hypermuscularization present in the nitrofen-induced foetal rat model of congenital diaphragmatic hernia (CDH), there are changes in the respiratory exchange epithelium, consistent with the hypothesis that abnormal surfactant production and/or release could account in part for the respiratory insufficiency in this condition. Foetal lungs from nitrofen-treated rats were obtained on the 21st day of gestation, weighed and processed for light and electron-microscopic studies and compared to controls of the same age. Tissues from 29 control and 26 CDH foetuses were examined. In addition, lungs from 19 foetuses born to nitrofen-treated dams but without CDH were also studied. The lungs from CDH animals were hypoplastic by weight in comparison with control ones and so were those from treated foetuses without CDH. Airway branching was arrested in CDH at the pseudo-glandular stage of development, corresponding to the 16th day of gestation and the very narrow air spaces were lined by generally mature type II pneumocytes rich in glycogen and lamellar bodies corresponding to the 19th day of gestation. This pattern was in contrast to that of the control foetuses which had a normal terminal sac pattern with flat type I pneumocyte lining corresponding to their gestational age. Nitrofentreated animals without CDH had intermediate patterns. These findings support the hypothesis that the surfactant-producing system has the same lesions in this experimental model as in other less-affordable ones, like the foetal lamb one. Further studies on the contribution of this factor to the altered respiratory physiology in CDH using this model are warranted.