Veterinary manpower, past and future.
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Biomedical subjects
Publications and source records attributed to A R Michell.
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Sodium preference was examined in three groups of sheep which had all sustained two consecutive pregnancies and lactations on either adequate sodium intakes (group C) or low sodium diets (B and C). Group B received a potassium supplement as well as a low sodium diet during the present experiment. No convincing or sustained increase in sodium preference resulted from the reduction in body sodium caused by pregnancy and lactation in group B or C, whether the sodium solutions offered were 40 or 300 mmol/l. In a second experiment, sodium preference (sodium bicarbonate, 40 mmol/l) was studied throughout pregnancy in sheep on low or adequate sodium diets, also non-pregnant controls on low sodium diets. Again, pregnancy on a low sodium intake failed to intensify salt appetite except for a transient (but significant) peak around d90, close to the peak of aldosterone secretion; a similar increase in preference occurred on the adequate sodium diet. However, salt appetite failed to intensify during the period of peak sodium demand (the last third of pregnancy) whereas renal and faecal sodium conservation are appropriately increased.
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A low-sodium diet was given to Blackface ewes over two reproductive seasons. This diet provided a total of 3-7 mmol/d except during lactation when the intake was about 11 mmol/d. Control ewes were given the same diet supplemented with sodium chloride to provide recommended levels which were about tenfold that of the experimental diet. The output of Na in urine and faeces from ewes given the low-Na diet was very low, about 3 mmol/d, from early in the experiment and continued at about this level throughout. Lambs born to low-Na ewes and given a low-Na diet similar to that of their dams during lactation, grew, after weaning, more slowly than corresponding lambs from control ewes, but at 6 months of age when six from each group were killed, tissue Na contents were only slightly lower in experimental than control lambs. Fluids and tissues obtained at the end of the second lactation from four ewes of each group that had suckled twin lambs, were analysed for Na and potassium. The Na concentration in saliva and rumen fluid of low-Na ewes was about half that of control ewes and there were corresponding increases in K: the differences were significant. Although Na concentrations for experimental ewes were generally lower than those for control ewes in the tissues analysed (liver, kidney, heart, brain and bone), the difference was significant only for the heart (P less than 0.05). Haemoglobin and packed cell volume were significantly elevated in low-Na ewes (P less than 0.01), indicating decreased body fluid volume.(ABSTRACT TRUNCATED AT 250 WORDS)
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The hypothesis that the toxic effects of imidocarb mediated by reduced cholinesterase activity might be intensified by hypomagnesaemia was tested in calves. Hypomagnesaemia was induced in 12 males (50 kg) using an artificial milk based on a commercial nondairy coffee creamer. Although plasma magnesium levels reached 0.33 mmol litre-1 in two weeks no clinical signs were detected. In 12 control calves a daily magnesium supplement of 0.6 g was inadequate although the published requirement is 0.45 g; it was raised to 1.2 g to keep plasma magnesium normal. Lighter calves developed hypomagnesaemia more readily and fast-growing calves had lower plasma urea concentrations. Plasma calcium, but not plasma magnesium, showed significant positive correlation with plasma albumin. The only statistically significant effects of hypomagnesaemia were slight elevations of white cell count and plasma sodium. The hypomagnesaemic and normomagnesaemic calves were divided into two equal groups and treated with 3.3 mg kg-1 of imidocarb dipropionate or a placebo. The drug produced the expected clinical signs of mild toxicity and depression of cholinesterase but no other adverse effects. Transient slight depressions of plasma calcium and potassium concentration, a transient rise of plasma sodium and elevation of creatine kinase occurred. None of the effects of imidocarb treatment was intensified by hypomagnesaemia except, perhaps, constriction of the pupils; generally, hypomagnesaemic animals were affected less.
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This review aims to illustrate the relationships between a number of basic and clinical aspects of sodium metabolism with special emphasis on herbivores, particularly ruminants. These animals provide a challenge to some traditional views based essentially on humans, dogs and laboratory rats reared on liberal sodium intakes. Detailed attention is focussed on two central issues; the magnitude of sodium requirement and the relative importance of the kidney and the gut in regulating body sodium. Both provide strong reasons to question accepted beliefs.
The effects of oestrogen and progesterone, injected alone or during successive periods, were studied in mature ovariectomised ewes on sodium intakes ranging from 1 to 4 mmol kg-1 d-1. Progesterone had no effect on fluid and electrolyte balance. Oestrogen (17 beta oestradiol) inhibited drinking but had little effect on water excretion whereas it reduced both food intake and urinary potassium concentration. Since the resulting changes in potassium intake and excretion were very similar, oestrogen had little net effect on potassium balance; neither change lasted beyond the treatment period. Oestrogen had a biphasic effect on urinary and faecal sodium excretion, an initial enhancement of salt loss being followed by sodium retention. Faecal sodium retention and the biphasic effect on renal sodium excretion were independent of changes in food intake. These observations are discussed in relation to the pattern of change of electrolyte balance during the reproductive cycle and the influence of changes in food intake and factors affecting sodium preference. The fact that a variety of responses is involved in a coordinated change of sodium balance is emphasised and its possible importance is considered.
Five matched pairs of horses were used to investigate the effects of phenylbutazone on a range of physiological, biochemical and haematological variables. The drug was given by mouth daily for 15 consecutive days at the manufacturer's recommended dose rates to one group of horses (Group A); the second group (Group B) received equivalent doses of a placebo. For some of the measured parameters, significant changes were recorded in both groups, indicating background instability. Significant decreases in serum total protein, albumin, plasma pH, viscosity and magnesium, and an increase in albumin: globulin ratio occurred in Group A, but not in Group B. These changes were, therefore, attributed to phenylbutazone or its metabolites. Toxicologically, the change in pH is probably unimportant but the decrease in protein concentration may have resulted from a protein losing enteropathy and/or from decreased synthesis in the liver. In one animal which received phenylbutazone, clinical signs of toxicity (lethargy, inappetence, oedema) were observed and evidence of hepatotoxicity and haematological changes were also noted in this horse. It is concluded that recommended dose rates of phenylbutazone should never be exceeded and that the period for which the highest dose (4.4 mg/kg body weight twice daily for four days) is administered should be reduced. In clinical cases, where phenylbutazone toxicity is suspected, measurement of serum or plasma protein concentration might provide an indication of the need to reduce dose levels or stop therapy.
Fluid therapy took nearly a century to gain acceptance in human medicine, despite excellent early work demonstrating its rationale and its effectiveness. Progress in veterinary fluid therapy lagged behind, partly because of skepticism and partly because of real practical difficulties. From the earliest to the most recent developments, human cholera has provided the impetus for much of the progress in fluid therapy. The challenge of treating such a severe diarrhoea in primitive surroundings with severe limits on cost and supervision has led to the emergence of oral fluid therapy as the prime technique. It is not simply an alternative to parenteral treatment but, in most cases, a superior approach relating more directly to the underlying problem--electrolyte malabsorption. Similar principles can be applied to other forms of diarrhoea and in various species. The example is clear for those concerned with veterinary fluid therapy. Repair of extracellular fluid volume is the key objective in all forms of fluid therapy; oral hydration offers not only a practicable way of achieving this in farm animals but one with the potential for outstanding clinical and economic success.