Summary This paper describes a collaborative project, conducted under the auspices of the British Equine Veterinary Association's survey section and financed by the Horserace Betting Levy Board, with the objective of collecting relevant data from breeding and racing statistics and evaluating losses (areas of wastage) that occur in the Thoroughbred racing industry. The investigation, which was carried out between 1977 and 1980, was divided into 2 parts. In Phase 1 the available statistics showed that considerable wastage existed from the time of covering to the appearance of the progeny on the flat, but that losses were closely consistent each year. Of the active mares in the General Stud Book for the seasons 1973 to 1979, 11.8 per cent were eliminated because no covering return was received and a further 10.1 per cent were either not covered, were covered by halfbreds or foaled abroad. The remaining mares, which were confirmed to have been covered (ie, applicable covered returned mares) were used to base the estimates of wastage. These were failure to conceive, 22.5 per cent, aborted or had a non‐surviving foal, 10.1 per cent, live progeny not named, 13.9 per cent, named animals not trained (2 to 4) years), 20.1 per cent and trained animals that did not run at 2 to 4 years, 6.2 per cent. This gave an overall figure for wastage of 72.8 per cent. Data on the numbers of outings as well as the numbers of animals imported and exported are quoted. An estimate of the cost of these losses was made under the following categories: lost stallion fees, keep of mares, keep of unnamed foals and keep of named animals that did not run. The cumulative losses for the 1974 season and its progeny was calculated to be at least £15.2 million. Phase 2 examined more specifically some of the areas of wastage caused by breeding losses and the reasons for an unsatisfactory number of racing appearances. The most substantial reason for not competing or competing less than the average number of times was horses showing little or no ability to race. In a survey of 762 horses, 26.5 per cent did not race up to the age of 4 years; of these just over one third were being kept as “store” animals for National Hunt racing. The final part of the survey examined the veterinary reasons for wastage. In 314 horses in Newmarket, lameness was the most significant factor. There was an incidence of lameness of 53 per cent at some periods during the season and in 20 per cent of cases the lameness was sufficient to prevent racing afterwards. Résumé Cet article produit les résultats d'une étude menée sous les auspices de la commission d'enquète de la BEVA, étude financée par le British Horserace Betting Levy Board. L'objectif de cette étude était de réunir des informations utilisables à partir des statistiques des courses et de l'elevage afin d'évaluer les pertes et les points faibles de l'industrie des courses de pur sang. Les recherches ont été conduites entre 1977 et 1980. Les résultats sont exposés en deux parties. Dans la première, les statistiques disponib...

Summary Nine Thoroughbred horses were assessed to determine the normal response of insulin, glucose, Cortisol, plasma potassium (K) and erythrocyte K through conditioning and to exercise over 400 and 1,000 m. In addition, adrenaline, noradrenaline, Cortisol, plasma K, erythrocyte K and L‐lactate concentrations were evaluated in response to maximal exercise with and without the administration of acepromazine. Conditioning caused no obvious trends in plasma K, erythrocyte K, insulin or glucose concentration. Serum Cortisol increased (P < 0.05) from the initial sample at Week 1 to Weeks 4 and 5 (attributed to a response to training), and then decreased. During conditioning, three horses had low erythrocyte K concentrations (< 89.3 mmol/litre). Further work is needed to define the significance of low erythrocyte K concentrations in the performance horse. In all tests maximal exercise increased plasma K, glucose and Cortisol concentrations, whereas insulin and erythrocyte K concentrations decreased. Thirty minutes following exercise, plasma K and erythrocyte K concentrations returned to resting values, whereas glucose and Cortisol concentrations continued to increase and the insulin concentration also was increased. The magnitude of the changes varied for pre‐conditioned vs post‐conditioned exercise tests and the duration of exercise. The administration of acepromazine prior to exercise over 1,000 m failed to alter the circulating noradrenaline and adrenaline concentrations in anticipation of exercise or 2 mins following exercise. Acepromazine administration, however, did cause lower L‐lactate concentration 2 mins (P < 0.03) and 30 mins (P ≤ 0.005) following exercise. Also, erythrocyte K showed a delayed return to baseline levels at 30 mins post exercise. Further evaluation of these trends may help explain the beneficial role acepromazine plays in limiting signs of exertional rhabdomyolysis when administered prior to exercise.

Summary Ten hyperinsulinaemic ponies divided into conditioned (N = 5) and rested (N = 5) groups were evaluated for their insulin and glucose response following oral glucose administration at Weeks 0, 2, 4, and 6. All ponies received a controlled intake of a pelleted ration during the study. In both groups body weight had decreased from baseline by Week 4 and remained low. After 2 weeks of exercise, ponies in the conditioned group had significantly decreased insulin and glucose indices, including peak insulin response, area under the insulin curve from 0 to 210 min (TIS), and the TIS value: area under the glucose curve from 0 to 210 min. By Week 4 of conditioning, although the insulin and glucose indices continued to decrease in the exercised ponies, there was no significant difference between the groups. Over the first 6 weeks of the study all ponies improved their insulin sensitivity accompanied by a loss of body weight. The conditioned ponies were further evaluated during deconditioning at Weeks 8, 10 and 12. The improved insulin sensitivity was maintained during deconditioning.

Summary Pericarditis and pericardial effusion are considered to occur rarely in the horse. The clinical and laboratory features of idiopathic pericarditis with effusion diagnosed in 10 horses over a seven‐year period were reviewed. Consistent physical findings included tachycardia, ventral oedema, jugular venous distention and diminished heart sounds. Electrocardiographic features included diminished voltages and electrical alternans, and the effusion was identified by echocardiography in the six horses in which it was performed. Pericardiocentesis relieved clinical signs in nine horses. Laboratory anaylsis of pericardial fluid samples classified six cases as aseptic serofibrinous, three cases as eosinophilic, and one case as histiocytic. One horse died and three were destroyed. The remaining six horses recovered following pericardiocentesis (performed once or twice) with or without corticosteroid treatment, and were alive one month to seven years after diagnosis.

Summary Case records of horses with muscle disorders presenting to the Veterinary Medical Teaching Hospital of the University of California, Davis, over a nine year period were evaluated. The objectives of the review were to identify the common myogenic muscle problems and their clinical features. Muscle disease of idiopathic aetiology following exercise was by far the most common condition noted. Other causes of myogenic muscle disorders included congenital, infectious, immune‐mediated and nutritional factors.

Five thoroughbred foals (4 fillies and 1 colt), all in good to excellent body condition, ranging in age from 4 days to 5 weeks at the time of onset of signs, were presented to 2 Kentucky equine hospitals from 1992 through 1996. All 5 foals presented with tachycardia, hyperhidrosis, diarrhea or a recent history of diarrhea, and muscle rigidity or stiff gait. Four of the 5 foals presented for recumbency, seizure-like activity with opisthotonos, or pronounced extensor muscle ive cases of idiopathic hypocalcemia in foals resembled F several hypocalcemic syndromes noted in human neonates. These cases appear to be representative of distinct and as yet undescribed syndromes of idiopathic hypocalcemia in young foals. The etiopathogenesis of the syndromes remains unknown.Neonatal hypocalcemic syndromes are not recognized commonly in veterinary medicine, but there are 2 chromosomal abnormalities and 3 neonatal syndromes associated with hypocalcemia in human beings. A chromosomal point deletion in human beings (DiGeorge syndrome) can manifest itself as cardiac anomalies, cleft palate, facial dysmorphism, and hypocalcemia owing to aplasia of the parathyroid gland.' There are varying degrees of expression of these phenotypic manifestations.' Investigators have reported a second, unrelated mutation in the calcium receptor gene in human kindreds, which results in a gain of function of the protein receptor and subsequent hypocalcemia.' There are at least 3 additional syndromes of neonatal hypocalcemia in human beings not associated with a chromosomal abnormality described as ( 1) early neonatal hypocalcemia, (2) hypocalcemia of infants of diabetic mothers, and (3) late neonatal hypocal~e m i a .~ Early hypocalcemia of neonates is characterized by transient, often subclinical, hypocalcemia within the first 72 hours of life accompanied by an appropriate increase in parathyroid hormone (PTH) concentration.' Late neonatal hypocalcemia is characterized by clinical manifestations of hypocalcemia ranging from tremor to convulsions occurring from the third day to the end of the first month of life with inappropriate PTH response.' In contrast to the DiGeorge syndrome, late neonatal hypocalcemia is not due to an absence of the parathyroid glands.' Materials and Methods Selection of PatientsPatients were selected based on the presence of hypocalcemia, clinical signs, and response to IV calcium therapy. Idiopathic hypoFrom Hagyard-David..ton-McGee Associates, P.S. C.

Ponies were evaluated for their response to feed withholding and exogenous administration of corticosteroids (dexamethasone 0.04 mg/kg intramuscular [IMJ) in an attempt to reproduce the hyperlipemia syndrome. Because insulin resistance has been associated with hyperlipemia, all ponies were initially evaluated for insulin response to an oral glucose load and normal dexamethasone suppression of serum cortisol. Four ponies were identified as hyperinsulinemic reflecting insulin resistance. All ponies had suppressed cortisol concentrations following dexamethasone administration. Feed withdrawal resulted in hypertriglyceridemia by 48 hours in all ponies. Very low density lipoprotein-triglyceride (VLDL) fraction was primarily elevated. The administration of dexamethasone failed to increase the degree of triglyceridemia. Although insulin resistance has been proposed as the likely cause of the hypertriglyceridemia in ponies, in this study four of eight ponies were considered to have normal insulin responses and yet still developed hypertriglyceridemia. (Journal of Veterinary Internal Medicine 1991; 5~15-22)

Summary Twenty‐three well‐conditioned ponies were evaluated for insulin and glucose response following oral glucose administration (1 g/kg bodyweight [bwt] as a 20 per cent solution). Ponies were defined as normal if total insulin secretion (TIS) was less than 149 μiu/ml h and the glucose concentration was below 11.1 ± 0.11 mmol/litre (200 ± 2 mg/dl) at all times following oral glucose administration. When glucose concentrations were maintained below 11.1 ± 0.11 mmol/litre, the area under the glucose curve (TG) was less than 17.4 mmol/litre/h (314 mg/dl/h). The ponies were assigned to four groups based on insulin and glucose response: Group 1 (n=7), normal; Group 2 (n=5), high insulin, normal glucose; Group 3 (n=8), high insulin, high glucose and Group 4 (n=3), high glucose, normal insulin. This classification is an initial attempt to define normal insulin and glucose response in ponies. Additional data need to be accumulated to define further insulin resistance and diabetes in ponies.