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Daily treatment of female rats with medroxyprogesterone acetate in aqueous suspension resulted in adrenocortical atrophy. The doses given were those used for oestrus synchronisation. Intramuscular injections of 2-0 mg medroxyprogesterone acetate were used to investigate the atrophic process. Adrenocortical involution was associated with extensive single cell deletion (apoptosis). It is suggested that theses changes were due to suppression of pituitary ACTH secretion. The cytological changes support the concept that single cell death plays an important role in organ remodelling. Biochemical determinations of DNA, RNA, protein and dry matter, and histological examination, did not reveal significant changes in the liver.

In the liver of pregnant rats, fed ad libitum, there was an increase in acid phosphatase specific activity which occurred in two peaks, one at the 15th day and the other at the end of gestation. By light and electron microscopic histochemistry, the activity was found to be localized in parenchymal cell peribiliary dense bodies and also in phagosomes present in macrophages and parenchymal cells. There was an increase in liver wieght which reached a peak at the 17th day of gestation. Total DNA also rose to the 17th day; there was a high rate of cell division in the hepatic parenchyma at the 17th and 18th days of gestation. During this period single cell deletion by apoptosis was relatively frequent and in late pregnancy there was evidence of cell deletion by lysis. During pregnancy there was a slight increase in sinusoidal macrophages as a proportion of the total cell population but there did not appear to be significant changes in macrophage enzymic activity. It is suggested that the acid phosphatase activity present in macrophages makes a minor contribution to total liver activity, most of which is present in parenchymal cells. Acid phosphatase activity associated with single cell deletion appears to be quantitatively negligible. There was a direct relationship between total hepatic acid phosphatase activity and the numbers of peribiliary dense bodies, which were most numerous at the 15th day and at the end of gestation. It is suggested that these residual bodies contain products of detoxification processes and also cell structural elements resulting from enhanced liver metabolism and intracellular turnover during pregnancy.

Comparisons were made between specimens of intestinal mucosa from three young Friesian steers, killed when showing clinical signs associated with copper deficiency, and three controls that had received supplementary copper. Copper deficiency was associated with marked depiction of cytochrome oxidase in the epithelium of the duodenum, jejunum and ileum, and with partial villus atrophy in the duodenum and jejunum. Enterocytes from the duodenum, jejunum and ileum showed mitochondrial abnormalities ranging from slight swelling to marked localised dilation. Many of the mitochondria not affected by swelling had a distinctly condensed appearance. These changes are discussed in relation to the copper-responsive diarrhoea that affects a proportion of cattle suffering from copper deficiency.

Reproduction in Finnish Landrace × Polled Dorset Horn ewes was accompanied by thickening of the wall of the gall bladder. The thickening was caused by hypertrophy of the epithelium, the presence of cysts, proliferation of blood vessels, glands and fibrous tissue in the lamina propria and hypertrophy of smooth muscle. The changes appeared to be initiated during pregnancy but to persist in a modified and chronic form in post-parturient animals.

Lesions were found in the pancreas of clinically normal cattle of low copper status. In comparison with the pancreas of cattle with normal hepatic copper reserves, the abnormalities were an increase in the dry matter content and reduction in the concentrations of protein and copper in the wet tissue. Cytochrome oxidase activity and protein-to-RNA ratio were also reduced. Histologically, there were defects in acinar basement membranes, splitting and disorganization of acini, cellular atrophy and dissociation, and stromal proliferation. The pancreatic ductular system did not show atrophy or disorganization.

SummaryLactation in ewes is associated with hypertrophy of the liver, due to cell proliferation and enlargement. The mean diameter of hepatic parenchymal cell nuclei increased after parturition to reach a maximum at 6 weeks, after which there was a decline.The liver regressed in weight after weaning but total DNA declined less than liver weight and remained elevated in comparison with livers of unmated ewes, while DNA concentration increased. Total liver DNA remained relatively high for approximately 6 months. It is suggested that the final fall to control values was associated with cell death and disorganization of the hepatic parenchyma.These results imply that the life span of one type of liver parenchymal cell may be at least 6 months.

In parous, seasonally-bred Finnish Landrace × Dorset Horn ewes, there was hypertrophy of fibres in the internal oblique abdominal muscle, and a tendency towards an increase in the proportional number, and total cross-sectional surface area, of slow-twitch, oxidative fibres. In older ewes which had been bred intensively, these tendencies were exaggerated and were associated with sub-division and splitting of slow-twitch, oxidative fibres. In the same tissues there was a high incidence of muscle fibre degeneration and necrosis, with replacement of necrotic fibres by fibrous and adipose tissue. It appears that there are cyclical changes of hypertrophy and atrophy, geared to reproductive cycles, and that the processes of degeneration are accelerated during atrophy post-partum. It is likely, but not proven, that in ewes bred intensively the reproductive cycles proceed faster than the cycles of reorganization and repair, so that the extent of pathological change is roughly proportional to the age and productivity of the ewe.

Summary In lambs fed on a semi-synthetic diet containing less than 1 μg Zn/g, deficiency of zinc was associated with parakeratosis of the tongue and with big increases in the numbers of viable aerobic and anaerobic bacteria present on the dorsum. The numbers of bacteria quickly reverted towards normal levels when the lambs were given supplementary zinc. When zinc-deficient sheep were slaughtered, histological lesions in the tongue included degeneration of striated muscle, interstitial fibrosis, thinning of myelin nerve sheaths, abnormal morphology of motor nerve endings and degeneration of arterio-venous shunts in the lamina propria of the tongue.

SUMMARY Ewes were kept for the lest 3 months of pregnancy on a diet of grass cubes supplemented with sodium sulphate and ammonium molybdate. The brains of their offspring which were clinically normal were found to be deficient in copper and by histochemical methods a deficiency in cytochrome oxidase was observed in the central nervous system of these lambs. The large motor neurones of the red nucleus and of the ventral horns of grey matter in the spinal cord appeared to be affected most severely. It is suggested that a low content of copper in the brain leads to a deficiency of cytochrome oxidase in the motor neurones and that this is probably the primary lesion in swayback.

Summary The role of silicaceous spicules in the aetiology of rumenitis in cattle was investigated by feeding diets of pearl barley and cotton fibres, with and without screened debris from barley pearlings. Spicules from barley grain appeared to cause only minor physical damage to the ruminai mucosa. Minor damage is not necessarily negligible, but it is suggested that the findings do not justify the allocation of high priority rating to barley breeding programmes aimed at the elimination of rachilla and lodicule spicules. Multiple inflammatory lesions of the rumen wall were found in sheep fed on a diet of barley to which cut cattle hair had been added, but not in sheep fed on barley alone.

Summary Investigations have been made of some of the changes occurring in the calf rumen during the transition from conventional feeding to a diet containing 90% barley. During the first 7 weeks of barley feeding, there was a rise in the concentration of total volatile fatty acids in the rumen contents, with a rise in the propionic and butyric acid fractions and a fall in the acetic acid fraction. The pH of the rumen contents fell, but no increase was found in the amount of lactic acid in the rumen. A characteristic clumping of ruminal papillae developed after the change to barley feeding, and the rumen wall became thickened and increasingly rigid. The floors of the anterior dorsal sacs of the rumens from slaughtered calves showed, histologically, that the lesions of acanthosis, hyperkeratosis and parakeratosis had developed within 4 weeks of the change in diet. Many hairs were present in the interpapillary spaces of the rumen wall, and there were numerous lesions due to the penetration of the tissues both by animal and by vegetable hairs. Inflammation due to this cause appeared to be an important factor in the pathogenesis of rumenitis in calves fed on barley, and the thickening of the rumen wall was appreciably reduced when the ingestion of calf hair was prevented.

A biochemical and histological study was made of the livers of 12 ewes in late pregnancy, 18 post-parturient ewes, and 4 non-breeding ewes. Liver weight did not change significantly during pregnancy, but it increased in relation to the carcase weight, and there was an increase in the concentration of RNA in the tissues. After parturition, there were both hyperplasia and hypertrophy of the parenchymal tissue, and there were significant absolute increases in liver weight, and in the total contents of dry matter, protein, lipid, RNA and DNA. Large seasonal hypertrophic changes occurred also in the livers of non-breeding sheep.

Summary The serum of breeding ewes was analysed by the micro-Kjeldahl method for total protein and by disc electrophoresis in polyacrylamide gels. The amount of serum albumin/unit volume did not change from the end of pregnancy into the post-weaning period, but the gamma globulin fraction rose during lactation from a level that was considerably below that found in non-breeding controls to a relatively high value at weaning. The gamma globulin fraction increased at the mean rate of 0.093 g. protein/100 ml. serum/week of lactation, and there was a corresponding rise in the total protein content of the serum. A considerable increase in the number of plasma cells present in the upper gastrointestinal tract was associated with the change in composition of the serum proteins. It is suggested that the rise in serum gamma globulin that occurs during lactation is the result of an increased production that compensates, and eventually over-compensates, for a fall that appears to take place during pregnancy. The histological evidence is that the proximal parts of the small intestine may be regarded as one of the sites of the excess gamma globulin production in the lactating ewe.

SUMMARY The half-life of 125I-albumin was measured in ewes during the first 6 weeks of lactation, and in non-breeding controls. In the lactating animals the half-life was shorter by 3.0 ± 1·07 days. The difference was statistically significant (P = 0·025). During this period there was a slight increase in live weight and a relatively greater increase in total serum volume, so that the serum volume per kg. body weight of the lactating ewes was between 18 and 33% greater than that of the controls. The implications are that the turnover rate of serum albumin is considerably accelerated in the first half of the lactational period, and post-parturient hypertrophy of the liver in sheep is associated with an increase in serum albumin production. Accurate and reproducible values for serum volume in sheep were obtained by measuring the intravascular dilution of radio-active macromolecules.

The wall of the alimentary canal of Scottish sheep from 2 hill farms was found to fluctuate in weight and total nitrogen content during pregnancy, but to increase rapidly and progressively in weight and total nitrogen content during lactation. The peak was reached at weaning, after which there was a rapid decline. The protein laid down in the wall of the abomasum, small intestine and caecum from the first third of pregnancy to the height of lactation is negligible when compared with the extra protein requirements for pregnancy and lactation. Histological observations agreed with these data, showing a hypertrophy of the alimentary canal during lactation followed by post-weaning atrophy and, in some instances, degeneration. There were differences in the data obtained from the 2 groups of ewes which we ascribe to the differing husbandry and conditions on the farms from which they came.

SUMMARY Between 76 and 88 per cent of ulnae and humeri from 136 pigs had radiological and histological lesions in the distal epiphyseal growth plates and in the metaphyses. The pigs were litter-mate groups of boars, gilts and barrows, derived from six sires, and in each sex group there were pigs of different growth rates and pigs that were slaughtered at different live-weights. Statistical analyses of the results showed that the incidence and severity of the lesions in the two bones were not appreciably influenced by the sex, growth rate, or live-weight at slaughter of the pigs, or by the sire.

Amounts of plasma protein up to 96 g. were removed from sheep by the application of selective plasmapheresis to blood flowing in an extracorporeal circulation. All the plasma proteins were represented in the fraction collected, but a significant selection of γ-globulin was achieved. This resulted in a depression of the level of circulating γ- globulins. Normal levels of plasma protein were restored within 3 to 4 days by marked increases in the normal rates of synthesis. The half-lives of plasma albumin and γ-globulin in sheep recovering from plasma protein depletion did not differ from those in control sheep.

SUMMARYA comparison was made of the development of acid and alkaline phosphatase, invertase, lactase and leucine aminopeptidase specific activities in the small intestines of two groups of neonatal pigs. The groups consisted of two litters of suckling pigs and two litters of pigs that were delivered by hysterectomy and reared in incubators on a diet based on cow's milk. In the unsuckled pigs there was retardation of the development of invertase and leucine aminopeptidase. The unsuckled animals grew slowly and were affected by diarrhoea, and it is possible that enteric disease may have affected the development of the brush border of the intestinal epithelial cells, or enzymes specifically associated with the microvilli.

Summary Ayrshire calves were fed for 6 weeks on pelleted diets of barley that contained 7.5%of sodium bicarbonate or sodium acetate. The fall in pH of the rumen contents was less in these animals than in control calves fed on a similar diet to which neither bicarbonate nor acetate had been added. At slaughter the lesions of hyperkeratosis, papillary clumping and rumenitis that occurred in the controls were reduced to negligible proportions in the calves fed on the experimental diet containing bicarbonate. The barley-acetate diet gave intermediate results with regard both to the pH of the rumen contents and to the severity of the ruminal lesions. The essential differences between the rumens from calves fed on the 3 diets appeared to lie in the extent of mucosal thickening and folding. It is suggested that the pathological changes in the rumen wall, characteristically found in animals fed on barley, may begin with a thickening of the epithelium and lamina propria, and that this is a reaction to the fall in pH of the rumen contents. It is probable that the formation of mucosal rugae, due to epithelial and stromal proliferation, leads to the trapping of debris, and that the thickening shows further progression as the trapped hairs penetrate the epithelium and cause inflammatory reactions.

Summary Deficiency of zinc in the rat was associated with parakeratosis of the oesophageal epithelium, atrophy of the epidermis and degenerative changes in the pancreatic acinar tissue. Many of the degenerating pancreatic acinar cells had the characteristic features of shrinkage necrosis. Lesions were not found in the liver. In deficient rats the mitotic indices of the oesophagus and pancreas were higher than in pair-fed controls; in the epidermis the mitotic index was lower, and in the liver it was not different from control values. When Zn-deficient rats were given a single oral dose of Zn the mitotic index in the oesophagus was reduced; in the epidermis, liver and pancreas it was increased. In the oesophagus, epidermis and liver the effects of colchicine in the Zn-deficient rats were limited to the arrest of mitosis in metaphase, but in the pancreas of Zn-deficient rats injected with colchicine there was mitotic arrest, and in addition a marked increase in the incidence of acinar cells affected by degenerative changes. Colchicine also had marked cytotoxic effects in the pancreas of rats fed on the Zn-deficient diet but given a single oral dose of Zn.

SUMMARYThe 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.All of the alimentary organs became hypertrophied during lactation, and regressed after weaning. Maximum values for the liver and ruminal mucosa occurred in the sixth week of lactation, and were maintained until weaning. The small intestine reached maximum weight after 4 weeks of lactation.

SUMMARY The distribution of activity of carbonic anhydrase (EC 4.2.1.1) per mg N within the mucosa of the sheep’s abomasum was similar to that of parietal cells. The histochemical localization of activity was mainly in parietal cells and in the walls of blood vessels. Lactation was associated with an increase in weight of stripped abomasal mucosa, with parietal cell hyperplasia and hypertrophy and with an increase in total carbonic anhydrase activity.

Copper deficiency had a differential effect between tissues in the rat pancreas. There was marked loss and atrophy of acinar cells, in which both hypertrophied and degenerating mitochondria were present. Cytochrome oxidase activity in acini was greatly depleted while monoamine oxidase activity was enhanced. Atrophy of acinar cells was accompanied by extensive degeneration of the rough endoplasmic reticulum, and by a failure of zymogen granule synthesis. These changes contrasted strongly with the appearance of non-acinar tissues, in which hypertrophy and degeneration of mitochondria were rarely observed. Islet tissue, pancreatic ducts and blood vessels showed no atrophic changes. Cytochrome oxidase activity in islet tissue, and in the epithelium of the main pancreatic ducts, appeared unaffected.

Pathological changes occurred in the alimentary canal of rats fed a diet containing 3 mg per kg Cu and 6 mg per kg Mo as tetrathiomolybdate. Mitochondrial abnormalities in the duodenum and jejunum and single cell deletion by apoptosis and necrosis in the caecum and colon were present from the first day of treatment until the end of the investigation which terminated on the 21st day. These were accompanied by cell proliferation, presumably compensatory in character. When the rats had been given thiomolybdate for 11 days or more, there was a marked increase in the incidence of apoptosis in the small intestine, and gross disorganization and oedema of the caecal mucosa. There were also changes in the bacterial population of the caecal contents, where the Gram negative population became more complex and was dominated by species with the morphological characteristics of Bacteroides. These changes, with the exception of the mitochondrial lesions, could not be attributed to secondary hypocuprosis; it is suggested that the aetiology of the cell toxicity may involve a block in sulphur metabolism, possibly complicated in the caecum by absorption of endotoxins.