Prenatal development of the human Brunner's glands.

The prenatal development of the human Brunner's glands has been investigated in 23 fetuses from the 10th week of gestation to full-term. At 12 weeks, a few cords of epithelial cells were seen budding from the duodenal mucosa immediately beyond the pyloric sphincter. They represent the initial stage of the development of Brunner's glands. At 16 weeks, Brunner's glands originated as simple tubular downgrowths from the bottoms of the most proximal crypts of the duodenum. The secretory products of the component cells of these primitive tubules contained periodic acid schiff (PAS) positive material which was largely supranuclear in position and resisted digestion by diastase. From 20 weeks to full term, the Brunner's glands developed in a progressive fashion starting in the proximal part of the duodenum near the pyloroduodenal junction. Further tubular downgrowths were added distally, leading to an increase in length of the glandular tissue. The gland showed an increase in size proximally due to elongation and branching of the tubules. At birth, the glandular cells of Brunner's glands resembled those of normal adult in structure and staining reactions. The PAS staining of the cells of the early developed glands (at 12 weeks) was as intense as those of the full-term. The secretory materials of the developed Brunner's glands showed negative reaction with Alcian blue (AB) at pH 2.5 at any stage of development. These results suggest that the mucin secreted by the developed Brunner's glands of human is neutral mucopolysaccharide in nature.

Histopathological changes in pregnant rat's liver following repeated halothane exposure.

Adult white rats were divided into 3 groups; 6 rats each, (two males and four females). Group I was exposed to 1.5% halothane for 20 minutes every other day for 6 exposures. The rats were mated and exposed another 10 exposures. Group II was given 0.1% phenobarbitone in milk one week before, and during the period of exposure to halothane which was similar to the first group. Group III was kept as a control. At the suspected date of delivery, the rats were sacrificed, and specimens were taken from the liver for hematoxylin and eosin stain, PAS reaction and Sudan black stain. Repeated exposure to halothane did not affect the pregnancy rate, but it resulted in hepatic focal and centrilobular necrosis with glycogen poverty and moderate lipid content. The portal spaces showed thick connective tissue and lymphocytic infiltration. Phenobarbitone reduced the pregnancy rate and resulted in 16.5% fetal mortality with more hepatic necrosis and increase in glycogen and lipid content.

Histochemical changes in pregnant rat's liver following repeated halothane exposure.

Eighteen adult white rats were divided into 3 groups, 6 rats each (two males and four females). The first group was exposed to 1.5% halothane for 20 minutes, every other day for 6 exposures. The rats were mated and exposed for another 10 exposures. The second group was given 0.1% phenobarbitone in milk starting one week before and during the period of exposure, which was similar to the first group. The third group was kept as a control. At the suspected date of delivery, the rats were sacrificed and specimens were taken from the mother's liver for estimation of the activities of the enzymes succinate dehydrogenase, acid phosphatase and alkaline phosphatase. Repeated halothane exposure decreased the activity of the enzymes succinate dehydrogenase, acid phosphatase and alkaline phosphatase. Treatment with phenobarbitone has the same effect on succinate dehydrogenase, but partially spared the activities of acid and alkaline phosphatases.