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Dabareiner, R. M., Sullins, K. E., & White, N. A. 2nd. (1993). Progression of femoropatellar osteochondrosis in nine young horses. Clinical, radiographic and arthroscopic findings. Vet Surg, 22(6), 515–523.
Abstract: The clinical and radiographic progression, and arthroscopic findings for nine young horses (< 1 year of age) with femoropatellar osteochondrosis (OCD) are presented. Horses had a 2 to 12 week history of bilateral (8 horses) or unilateral (1 horse) hindlimb lameness. The most consistent clinical signs included femoropatellar joint distention and bilateral hindlimb lameness. At the onset of clinical signs, radiographic lesions were not present (4 horses) or subtle (5 horses), but were easily identified on radiographs taken 4 to 24 weeks later. Arthroscopic surgery was delayed until radiographic changes became obvious. Surgical findings in 20 femoropatellar joints were most commonly osteochondral “flaps” located on the proximal lateral trochlear ridge of the femur and were larger than had been indicated by the radiographs. Eight horses were being used for their intended purpose, which was racing (3 horses were racing and 3 were in race training), dressage (1 horse) or pleasure riding (1 horse). One horse required a second surgery when similar lesions developed on the opposite stifle, and was euthanatized 2 months later because of persistent lameness. One clinical signs are observed, osteochondrosis lesions of the distal femur can progress in foals younger than 9 months of age and the full extent of the radiographic lesion may take several weeks to develop.
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Carroll, G. L., Matthews, N. S., Hartsfield, S. M., Slater, M. R., Champney, T. H., & Erickson, S. W. (1997). The effect of detomidine and its antagonism with tolazoline on stress-related hormones, metabolites, physiologic responses, and behavior in awake ponies. Vet Surg, 26(1), 69–77.
Abstract: Six ponies were used to investigate the effect of tolazoline antagonism of detomidine on physiological responses, behavior, epinephrine, norepinephrine, cortisol, glucose, and free fatty acids in awake ponies. Each pony had a catheter inserted into a jugular vein 1 hour before beginning the study. Awake ponies were administered detomidine (0.04 mg/kg intravenously [i.v.]) followed 20 minutes later by either tolazoline (4.0 mg/kg i.v.) or saline. Blood samples were drawn from the catheter 5 minutes before detomidine administration (baseline), 5 minutes after detomidine administration, 20 minutes before detomidine administration which was immediately before the administration of tolazoline or saline (time [T] = 0), and at 5, 30, and 60 minutes after injections of tolazoline or saline (T = 5, 30, and 60 minutes, respectively). Compared with heart rate at T = 0, tolazoline antagonism increased heart rate 45% at 5 minutes. There was no difference in heart rate between treatments at 30 minutes. Blood pressure remained stable after tolazoline, while it decreased over time after saline. Compared with concentrations at T = 0, tolazoline antagonism of detomidine in awake ponies resulted in a 55% increase in cortisol at 30 minutes and a 52% increase in glucose at 5 minutes. The change in free fatty acids was different for tolazoline and saline over time. Free fatty acids decreased after detomidine administration. Free fatty acids did not change after saline administration. After tolazoline administration, free fatty acids increased transiently. Tolazoline tended to decrease sedation and analgesia at 15 and 60 minutes postantagonism. Antagonism of detomidine-induced physiological and behavioral effects with tolazoline in awake ponies that were not experiencing pain appears to precipitate a stress response as measured by cortisol, glucose, and free fatty acids. If antagonism of an alpha-agonist is contemplated, the potential effect on hormones and metabolites should be considered.
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