Relationships between electrocardiographic findings, racing performance and training in Standardbred horses

SUMMARY The presence of abnormal T waves in three or more electrocardiographic leads has been used to diagnose the cause of poor race performance in horses. This study investigated the relationship between previous racing performance in Standardbred horses and T waves, and the effect of training on the T wave. Thirty-two horses were electrocardiographed in two Sydney racing stables. Sixteen horses (50%) had ECGs with three or more leads with abnormal T waves, and these horses had won more races, had a greater ratio of wins per start and a greater number of dollars earned per start than horses with less than three abnormal T waves (P < 0.05). Horses with abnormal T waves also had significantly faster racing times (P < 0.01). There were significant (P < 0.01) correlations between the number of abnormal T waves and both number of wins (R = 0.47) and dollars earned per start (R = 0.45). Fastest winning mile rate was also negatively correlated with number of leads with abnormal T waves (R =?0.52, P < 0.01). Twenty two horses were also electrocardiographed within seven days of good racing performance. The mean number of abnormal T waves was 2.7 ± 0.41, and the mean T wave amplitude in the four chest leads (CV, CR, CL, CF) was 0.9 ± 0.15 mV. Thirteen horses (59%) had abnormal T waves in three or more leads. The effect of training on the T wave was also investigated in nine previously untrained and unraced Standardbred racehorses. There were significant effects of training (P < 0.01) on the number of abnormal T waves and mean chest lead T wave amplitude. These increases occurred in the second phase of training during which faster exercise, race trials and racing were conducted. We concluded that abnormal T waves are a common finding in the race-fit Standardbred horse, and can be found in more than 50% of horses currently performing well in races. In addition, chest lead T waves become more positive after training.     

Xenobiotic metabolism in suspensions and primary cultures of isolated hepatocytes prepared from the caudate process of bovine liver

Isolated hepatocytes were prepared from 100- to 125-kg Holstein male calves (n = 10) by perfusion of the caudate process of the caudate lobe of the liver. The 11th or 12th rib on the right side was resected to provide exposure of the caudate process. Complete postsurgical recovery of the donor from partial lobectomy was confirmed by growth data and serum chemical and hematologic criteria. Hepatocytes were isolated under aseptic conditions, using a 2-step collagenase vascular perfusion procedure. Hepatocyte preparations averaged 85% viability, and the yield averaged 1.2 X 10(7) viable hepatocytes/g of (wet weight) liver. Morphologic characteristics of hepatocytes examined under light and scanning electron microscopy were considered normal, except for occasional surface blebs. Freshly isolated hepatocytes in suspension rapidly decreased in viability and xenobiotic metabolizing capacity (aldrin epoxidation and ethoxycoumarin 0-deethylation and 7-hydroxycoumarin glucuronidation and sulfation), and hepatocytes surviving the initial 2 to 3 hours appeared to undergo repair. As an alternative, primary monolayer cultures on collagen-coated plates were evaluated. Hepatocytes attached to the collagen surface within 4 hours and appeared flattened by 12 hours. Although metabolic activity decreased about 30% over 8 hours in culture, the pattern of ethoxycoumarin metabolites was relatively constant. It was not determined to what extent the apparent loss of metabolic capacity was caused by hepatocyte detachment from the collagen surface. Although complicated by the requirement for asepsis, primary cultures were superior to suspensions for xenobiotic metabolism studies in cattle.     

Clinical features and treatment of renal tubular acidosis in two horses

Two horses were admitted separately for evaluation and treatment of profound hyperchloremic metabolic acidosis without azotemia. One, an 11-year-old Quarter Horse mare, had been depressed and ataxic for 2 days. The other, a 2-year-old Quarter Horse colt, had a 6-week history of depression, anorexia, and weight loss. Both horses responded to fluid and electrolyte therapy, but required daily oral administration of sodium bicarbonate for maintenance. In each case, the diagnosis was renal tubular acidosis.     

Effect of source of calcium and phosphate,autoclaving, vitamin D3 level and strain of turkey poults on the rachitogenic activity of isolated soybean protein 1

This study was conducted to ascertain the effect of autoclaving, source of calcium and phosphate, vitamin D₃ level and strain of turkey poults on the rachitogenic activity of isolated soybean protein (C‐1 protein‐Skidmore). One‐day‐old poults were fed purified diets of the glucose—C‐1 protein type. The diets contained calcium, phosphorus and vitamin D₃ at levels equal to or greater than the National Research Council's (1960) recommendations. The findings demonstrate that USP hydrated dicalcium phosphate was more effective than food‐grade dicalcium phosphate in overcoming the rachitogenic activity of the C‐1 protein. Autoclaving the C‐1 protein for 80 min destroyed its rachitogenic activity: Vitamin D₃ was also effective in reducing the rachitogenic effect of C‐1 protein. The Broad Breasted White strain proved to be more susceptible to the rachitogenic property of C‐1 protein than the Wrolstad Small White strain. Substituting USP hydrated dicalcium phosphate for food‐grade dicalcium phosphate, autoclaving the C‐1 protein or increasing the vitamin D₃ level increased body weight gains and tibia ash values. The interactions which were shown to exist between source of calcium and phosphate × autoclaving, strain × autoclaving, and vitamin D₃ level × strain demonstrate an interrelationship between these factors.     

Bacterial diskospondylitis associated with posterior paresis/paralysis in North American farmed mink (Mustela vison)

Posterior paresis/paralysis in farmed mink is responsible for significant morbidity and mortality, with individual farms reporting the loss of as many as 700 animals each year. Although this disease has been recognized by North American mink farmers for approximately 40 years, there are few published reports focusing on this entity. The objective of this study was to investigate the etiology and pathogenesis of the disease. Complete necropsy examinations were done on 40 clinically affected mink, ranging from 7 to 10 weeks of age, and on three normal animals in the same age range from two mink farms. Thirty-two of the 40 clinically affected animals had an isolated vertebral lesion characterized by bone lysis and proliferation that usually was centered on an intervertebral disk space in the midthoracic area. An inflammatory reaction, composed primarily of neutrophils, was present within the vertebral sections in 25 of the 40 affected animals (62.5%), and the presence of gram-positive cocci was confirmed in 8 of 10 animals (80%) in which bacterial organisms were observed histologically. Bacterial cultures from 15 affected animals yielded Streptococcus sp. from the intervertebral disk space in 13 of 15 (86.7%) animals and from heart blood in 6 of 8 (75%). A farm visit revealed no history or evidence of traumatic wounds as a source of infection in these animals, and the diet appeared to be adequate for skeletal development. We conclude that posterior paresis/paralysis in farmed mink is associated with bacterial diskospondylitis, likely occurring secondary to bacteremia/septicemia.