DURING lactation in the rat the alimentary canal shows an increase in weight and nitrogen content compared with that of unmated controls (Poo, Lew and Addis, 1939), or pregnant rats (Boyne, Chalmers and Cuthbertson, 1953; Souders and Morgan, 1957). Po0 et al. included with the alimentary canal the entire contents of the abdomen and pelvis except for the liver, kidneys and uterus, whereas Boyne et al. examined the cleaned and empty gut and Souders and Morgan studied only the small intestine. The determinations were made on the loth day of lactation by Po0 et al., on the 16th day by Boyne et al. and immediately after weaning by Souders and Morgan.We felt that the increase in nitrogen content of the alimentary canal during lactation was suilicient to justify a more detailed study, the results of which are presented in this paper. MATERIALS AND METHODSAnimals and diet. Adult virgin or lactating, prirniparous Hooded Lister female rats were used in these experiments. The food was '' Diet 86 ", compounded as cubes by the North-Eastern Agricultural Coop. Soc. Ltd, Aberdeen. It contained: wheat 50 per cent.; barley 25; white fish meal 7; meat and bone meal 6 ; dried brewers' yeast 5 ; dried grass meal 5 ; sodium chloride 1; and cod liver oil or equivalent stabdised vitamins A and D, 1 per cent. Analysis gave: dry matter 85.7 per cent.; protein 20.0; fat 3.8; soluble carbohydrate (by difference) 53.4; fibre 3.3; and ash 5.2 per cent.Food and water were freely available to dam and litter in all experiments. In some experiments the cubes were milled to facilitate the recording of food consumption. All the lactating rats ate an unrecorded amount of wood-wool litter.Usually the litters were reduced to 8 young per rat on the day of birth, but since the results were apparently not influenced by litter size we have included some early data obtained from rats with litter size greater than 8.Weight of ufimentury d. Lactating rats were killed with ether vapour at daily intervals from the first day postpartum up to the early post-weaning period, at which dates their average body weight was 280 g. They were eviscerated and the omentum, mesentery and fat were removed from the viscera. The length of the small intestine was recorded and Peyer's patch= were counted. The small inhtine was then divided into three equal lengths, which for the purposes of this paper were regarded as corresponding approximately to duodenum, jejunum and ileum; the stomach, caecum and colon were treated separately. The parts were cut open, washed in water, blotted and weighed. Twelve virgin female controls of average body weight 260 g. were treated similarly. In the final experiment the young of primiparous rats were killed on the day I. PA-BMX.--VOL 85 (1963) 179 Acta anat., 43,264. This J o u d , 81,251.

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The food intake, the apparent digestibilities of dry matter, and of nitrogen were measured in housed Blackface ewes during late pregnancy, lactation, and after the lambs were weaned. The ewes were slaughtered serially together with non-breeding controls, and the liver, ruminal mucosa, intestines, CNS and carcass were weighed. In association with differing reproductive status marked changes occurred in the content of dry matter and protein in the alimentary organs, but not in the CNS, and the mean weight of DNA in the CNS for all the animals was 130 + 20 (S.D.) mg.

There have been several reports on weight and total nitrogen gains in the alimentary canal of the lactating rat (Poo, presented a more detailed study of these changes, describing progressive increases in weight, size and total nitrogen content of the alimentary canal of the rat from parturition to weaning, with histological observations on hypertrophic changes in the wall of the stomach, small intestine and caecum. All parts of the alimentary canal were involved but the mucosa of the lower small intestine showed the greatest relative enlargement. One possible explanation of the hypertrophy was that it was due to a direct effect of increased food consumption on the gut wall, but for several reasons we suggested that the alimentary enlargement in lactation was due to an adaptive response of the mucosa to the increased bodily demands, independent of the level of food intake. This hypothesis involved the assumption that the hypertrophy and associated increase in surface area would be accompanied by an increased efficiency of digestion and absorption. The possibility of a direct action of lactogenic hormone on the alimen-tary canal was also considered. In this paper we describe experiments on rats and mice to investigate the role of lactogenic hormone in alimentary hypertrophy, the effects of restricting the food intake, and the efficiency of digestion in the hypertrophied and normal intestine. METHODS Studies on lactating mice. Twenty-four individually-caged T.O. strain mice of 21-6 g average body weight were divided into mated and virgin control groups. On the 18th day post-partum the lactating and control mice were killed by a blow on the head and rapidly eviscerated, the alimentary canal was perfused with and washed in 10 % formol-saline, divided into stomach, small intestine and caecum, blotted and weighed. Experiment8 with lactogenic hormone. Forty virgin female T.O. strain mice of 22-0 g average body weight were caged separately and their food consumption and body weight were recorded daily. The amount of food offered each day was restricted to the average

Fibrin deposition and removal is a feature common to major pathological processes such as wound healing, chronic inflammation and tumour invasion: processes involving the ingrowth of new blood vessels. Low molecular weight fibrin degradation products (MW less than 50,000) are now shown to induce angiogenesis in the chick chorioallantoic membrane (CAM). This effect has also been shown by new quantitative assays to be associated with stimulation of both DNA and protein synthesis. Autoradiography indicates that all cell types in the CAM are stimulated to divide, and it is proposed that fibrin degradation products are a pathological growth factor.