Traumatic tarsal luxation repaired without internal fixation in three horses and three ponies.

Three horses and three ponies were treated for traumatic luxation of the proximal intertarsal or tarsometatarsal joint. In each case, there were fractures of one or more tarsal bones. Three of the animals had disruption of one of the collateral ligaments. Five animals were treated by closed reduction and external coaptation. One pony was treated by open curettage, a cancellous bone graft, and cast immobilization. No internal fixation was used in any of these animals. From this series of cases, it would appear that closed reduction and external coaption alone is adequate treatment for most cases of tarsal luxation.

Noniatrogenic rectal tears in three horses.

Rectal tears were detected in three horses treated for colic. Based on historical, clinical, and postmortem findings, the tears could not be attributed to the attending veterinarian and were therefore not iatrogenic (physician induced). One tear was attributable to an infarction that presumably resulted from thromboembolism; 1 tear occurred without any evidence of external cause and resulted in such severe peritonitis that the cause and resulted in such severe peritonitis that the cause could not be determined, and 1 tear occurred during rectal palpation by the owner, before he called the veterinarian. Postmortem examination of the last horse revealed lesions suggestive of thromboembolism. It was concluded that thromboembolism may have caused or predisposed to two of the rectal tears and could not be ruled out in the third.

Effect of exercise, phenylbutazone, and furosemide on the plasma renin activity and angiotensin I in horses.

Circulating concentrations of angiotensin I and plasma renin activity (PRA) were determined in 45 Thoroughbreds before prerace medication (at rest), 1 to 1 1/2 hours before racing but after prerace medication (prerace), within 15 minutes after racing (immediately postrace), and between 1 to 2 hours after racing. Angiotensin I was measured by radioimmunoassay, and PRA was determined by the rate of generation of angiotensin I in plasma incubated at 37 C. Irrespective of prerace medication, there was a marked increase in angiotensin I (0.478 +/- 0.034 to 0.848 +/- 0.051 ng/ml) and PRA (0.191 +/- 0.018 to 0.522 +/- 0.061 ng/hour/ml) from the at-rest samples to the immediate-postrace samples, with the exception of anhidrotic horses in which increases in angiotensin I (0.7131 +/- 0.0794 to 0.8081 +/- 0.0608 ng/ml) and PRA (0.1635 +/- 0.0379 to 0.2176 +/- 0.0437 ng/hour/ml) were not as marked as they were in other horses. Administration of 1 mg of furosemide/kg 2 hours before racing caused an increase in PRA from 0.2438 +/- 0.0324 to 0.3706 +/- 0.1110 ng/hour/ml, whereas horses under the influence of 4 mg of phenylbutazone/kg had a decrease in PRA from 0.2090 +/- 0.0440 to 0.0669 +/- 0.0206 ng/hour/ml. Marked increases in angiotensin I and in PRA did not occur when horses were administered furosemide and phenylbutazone as prerace medication.