Limb symmetry was evaluated by measuring ground reaction forces in 2 groups of normal-gaited dogs at a trot. Data were collected from 2 groups of 21 dogs trotted at dog/handler velocities of 1.25 to 1.55 m/s and 1.85 to 2.05 m/s, respectively. Of these dogs, 9 participated in both groups to allow comparison of data at both velocities. Additionally, 16 of the dogs in group 1 were measured in 2 directions of movement to determine whether directional dependence was present. Collected data were then applied to 3 described symmetry indices. Each index was easy to calculate, but all had limitations. A major limitation was variation in magnitude of ground reaction forces measured between the different axes and the effect of this variation on precision of the derived indices. Vertical ground forces provided the most consistent symmetry indices, in part because of their large magnitude. The indices indicated that no dog had perfect right-to-left symmetry during a trotting gait. Statistical differences were not found in any of the measurements of directional dependence. Likewise, comparing symmetry data in dogs trotted at both velocities indicated no significant differences in any axis. However, further analysis of the data revealed the actual amount that a variance attributable to right-left limb variation was negligible. Most of the variance was attributable to trial variation. Thus, the aforementioned indices, which use nonconsecutive footfall methods to evaluate limb symmetry, actually measure principally trial variation and not limb-to-limb variation.

Concentration of dexamethasone was determined in plasma or serum samples from dogs after IV administration of a low dose (0.01 mg/kg of body weight) or high dose (0.1 mg/kg) of dexamethasone. On the basis of history, clinical signs of disease, and degree of cortisol suppression in response to dexamethasone, dogs were assigned to these groups: healthy dogs, dogs with nonadrenal illness, and dogs with hyperadrenocorticism. Four hours after administration of the low dose of dexamethasone, concentration of the steroid was reduced (P < 0.05) in dogs with hyperadrenocorticism, compared with healthy dogs, but not compared with values from dogs with nonadrenal illness. By 8 hours after dexamethasone administration, values were similar across groups. Dexamethasone concentration 4 and 8 hours after high-dose administration was similar between healthy dogs and dogs with hyperadrenocorticism. Concentration of dexamethasone 4 and 8 hours after its administration overlapped after the 2 doses. For example, in 11 of 66 dogs from all groups, concentration measured 4 hours after the low dose was greater than the minimal concentration determined in the 18 dogs given the high dose. These data indicate that dexamethasone metabolism may be altered in dogs with hyperadrenocorticism, and that individuals may have appreciable variability in dexamethasone clearance. Such variability provides a possible explanation for false-positive and false-negative results associated with dexamethasone suppression testing in dogs.

Twelve healthy dogs were used to determine the cardiorespiratory effects of IV administered ketamine (10 mg/kg of body weight) and midazolam (0.5 mg/ kg). Half the dogs received a ketamine-midazolam combination (K-M) as a bolus over 30 seconds and the other half received the K-M as an infusion over 15 minutes. Induction of anesthesia by use of K-M was good in all dogs. Ketamine-midazolam combination as a bolus or infusion induced minimal cardiorespiratory effects, except for significant (p < 0.05) increases in mean heart rate and rate-pressure product. The increase in heart rate was greater in dogs of the infusion group. Mild and transient respiratory depression was observed in dogs of both groups immediately after administration of K-M, but was greater in dogs of the bolus group than in dogs of the infusion group. Duration of action of K-M for chemical restraint was short. Salivation and defecation were observed in a few dogs. Extreme muscular tone developed in 1 dog after K-M bolus administration.

Changes in platelet indices (platelet count and platelet size) and PCV associated with thyroid disease were studied in 7 dogs with hypothyroidism and 21 cats with hyperthyroidism that were admitted to the veterinary teaching hospital. Compared with control (euthyroid) dogs, dogs with hypothyroidism had higher platelet count (P = 0.003), smaller platelet size (P = 0.01), and lower PCV (P = 0.02). Comparison of the group of hyperthyroid cats with a group of similarly aged, clinically normal cats with normal thyroxine values indicated that the group of hyperthyroid cats had significantly (P = 0.03) higher mean platelet size than did control cats, but differences were not found in mean platelet count or PCV. Results of this investigation indicate that the changes in platelet size reported in human beings with thyroid endocrinopathies also are found in animals so-affected. Although the pathogenesis of platelet abnormalities in animals with thyroid derangement is unclear and likely is multifactorial, the observed relation between platelet and erythrocyte production in this group of dogs is consistent with reports of an inverse relation between thrombocytopoiesis and erythropoiesis in iatrogenically hyperthyroid mice and in mice exposed to hypoxia.

Somatosensory evoked potentials (SEP) were recorded at the scalp and at various levels along the lumbar and caudal thoracic parts of the spine in response to tibial nerve stimulations. The SEP were observed in 24 diseased dogs, 2 with a vertebral fracture, 1 with a spinal cord tumor, 1 with a vertebral tumor, and 20 with disk herniation. Cord compression location was confirmed by myelography, laminectomy, or both. The clinical state had significant (P < 0.0001) influence on SEP characteristics. The scalp-recorded SEP latency changed only in association with the most severe lesions; spine-recorded SEP conduction velocity was lower in association with mild lesions; scalp-recorded SEP amplitude changed with lesions of intermediary severity. Because these 3 electrophysiologic variables were influenced differently by cord damage, it was possible to discriminate the various clinical grades by use of these techniques. However, dogs with signs of pain only could not be differentiated from clinically normal dogs. The evoked injury potential was observed in all but 4 diseased dogs, and its maximal amplitude corresponded, in all cases, with cord damage location. Increased duration (P < 0.05) of the spine-recorded SEP was associated with longstanding problems, but not necessarily with clinically detectable malfunction. Use of SEP and evoked injury potential for identifying lateralized cord damage may be of value.

Twelve mature (5 sexually intact males, 4 castrated males, and 3 females) mixed-breed dogs were surgically thyroidectomized and used in a Latin-square design pharmacokinetic study of orally administered L-thyroxine. The dogs were treated with 44, 22, and 11 Kg of L-thyroxine/kg as a single morning dose or in divided doses, morning and evening. Serum concentration of thyroxine (T4) was evaluated to determine a number of pharmacokinetic variables for comparison. Mean steady-state concentrations (C(SS)) were determined from the area under the curve. Variables were analyzed for comparisons between dosages by use of ANOVA. Concentration at steady state was highest for dogs of the 44-micrograms/kg of body weight once-daily group and was lowest for dogs of the group given 11 micrograms/kg in 2 daily doses. Single daily administration resulted in higher C(SS), except at the 22-micrograms/kg/d dosage. Clearance was faster for the 22- and 44-micrograms/kg/d dosages than for the 11-micrograms/kg/d dosage. The half-life (t(1/2)) and mean residence time (MRT) also were shorter for the 44-micrograms/kg/d dosage, possibly indicating more rapid elimination of the drug at higher doses and dose-dependent kinetics. Perhaps, as the dogs' metabolism increased with higher iodothyronine concentrations, hormone degradation was accelerated. Interval (divided vs single dose) caused some expected changes: maximal concentration was higher and minimal concentration was lower when single administration was used. These undulations resulted in iodothyronine concentrations above the physiologic range for a number of hours, whereas concentration closer to physiologic ranges was achieved by use of divided doses. Delayed absorption (lag time) was seen in 37 of the 72 data sets, but was generally short, about 0.25 hour. Mean time to maximal concentration was 3 to 4 hours. At the higher dosages, serum total T4 concentration was high normal or above normal during most of the time after L-thyroxine administration, but serum concentration of total 3,5,3'-triiodothyronine did not remain within the normal range until the 44-micrograms/kg/d dosage was used. The customary dosage of 22 micrograms/kg/d (0.1 mg/10 lb/d) may not be adequate for most dogs. Pharmacokinetic variables appear to be highly dependent on the individual dog. Those with rapid absorption and higher concentration tended to have these characteristics at each dosage in this study. The pharmacokinetic variables, therefore, appear to be highly individualized, and dosages recommended for treatment of hypothyroidism should be considered to be only a starting point for the average dog. To avoid underdosing or overdosing, monitoring of treatment to adjust dose for individual dog kinetic variables seems to be imperative.

Eight dogs were determined to be orthopedically normal on the basis of prelavage physical examination, stifle radiography, synovial fluid analysis, and force plate analysis (peak vertical force normalized for body weight, and time on the force plate). Each dog had 1 stifle randomly assigned to be lavaged with 100 ml of a commercially available 0.05% (w/v) chlorhexidine diacetate solution, and the contralateral stifle was lavaged with lactated Ringer's solution. Difference was not detected between the chlorhexidine diacetate and lactated Ringer's solution-treated joints, with regard to results of synovial fluid analysis and clinical lameness evaluations on days 4 and 8 after lavage. Chlorhexidine diacetate caused a more intense synovitis than did lactated Ringer's solution, as determined by histologic evaluation of synovial membrane specimens after necropsy on day 8; however, a difference in the intensity of toluidine blue staining of articular cartilage was not found between treatments. Chlorhexidine diacetate, as a 0.05% (w/v) solution, cannot be recommended as a joint lavage fluid until the duration of inflammatory changes in the synovial membrane are determined or until the chemical constituents of chlorhexidine diacetate causing the synovitis can be identified and removed.

A study was performed to determine whether experimentally induced bovine leukemia virus (BLV) infection in cattle could be detected earlier by use of polymerase chain reaction (PCR) amplification of genomic DNA extracted from leukocytes than by use of conventional agar-gel immunodiffusion (AGID). The PCR primers were designed to amplify a 375-basepair region of the proviral gag gene. Five cows were identified that were BLV-negative on the basis of AGID and PCR results. At day 0, these cows were inoculated IM with blood pooled from 3 naturally infected cows. Blood samples were taken on days 0, 1, and 7, and every 2 weeks thereafter until 3 months after inoculation. Three of the cows were BLV-positive by AGID test results 3 weeks after inoculation, and the remaining 2 seroconverted at 5 weeks. In contrast, all 5 cows were BLV-positive by PCR results 7 days after inoculation and remained positive for the duration of the study. Five cows that were BLV-positive by AGID test and PCR results on day 0 and from which samples were obtained at the same times as those from the other 5 cows, remained BLV-positive by results of both tests during the course of the study. Results indicate that under experimental conditions, BLV infection in cattle can be detected as much as 2 to 4 weeks earlier by use of PCR than by use of the AGID test.

Using catheter mounted microtip manometers, right atrial, pulmonary artery, and pulmonary artery wedge pressures were studied in 8 horses while they were standing quietly (rest), and during galloping at treadmill speeds of 8, 10, and 13 m/s. At rest, mean (+/- SEM) heart rate, mean right atrial pressure, mean pulmonary artery pressure, and mean pulmonary artery wedge pressure were 37 (+/- 2) beats/min, 8 (+/- 2) mm of Hg, 31 (+/- 2) mm of Hg, and 18 (+/- 2) mm of Hg, respectively. Exercise at treadmill belt speed of 8 m/s resulted in significant (P < 0.05) increments in heart rate, right atrial pressure, pulmonary artery systolic, mean, diastolic and pulse pressures, and pulmonary artery wedge pressure. All these variables registered further significant (P < 0.05) increments as work intensity increased to 10 m/s, and then to 13 m/s. Pulmonary artery diastolic pressure was, however, not different among the 3 work intensities. During exercise at belt speed of 13 m/s, heart rate, mean right atrial pressure, mean pulmonary artery pressure, pulmonary artery pulse pressure, and mean pulmonary artery wedge pressure were 213 (+/- 5) beats/min, 44 (+/- 4) mm of Hg, 89 (+/- 5) mm of Hg, 69 (+/- 4) mm of Hg, and 56 (+/- 4) mm of Hg, respectively. Assuming mean intravascular pulmonary capillary pressure to be halfway between the mean pulmonary arterial and venous pressures, its value during exercise at 13 m/s may have approached 72.5 mm of Hg. Transmural pressure (intravascular minus alveolar pressure) across pulmonary capillaries may be even higher because of the large negative pleural pressure swings in galloping horses. High transmural pressures may cause stress failure of pulmonary capillaries, resulting in exercise-induced pulmonary hemorrhage.

Prednisone was administered orally for 4 weeks at a dosage of 1.1 mg/kg of body weight/d, in divided dose every 12 hours, to a group of healthy adult dogs (n = 12). Intravenous glucose tolerance testing was performed before and after the 28-day regimen in each dog, as well as in dogs of a control group (n = 6). Glucose metabolism was evaluated by measurement of preprandial plasma insulin and glucose concentrations, total insulin secretion, and fractional clearance of glucose. Mean preprandial plasma insulin and glucose concentrations were not increased after the 4-week regimen of prednisone. Total insulin secretion in response to an IV administered glucose load was not increased in treated dogs, compared with pretreatment values or with values for control dogs. The fractional clearance of glucose was also not altered in dogs given prednisone. Results indicate that anti-inflammatory doses of prednisone, given orally for 4 weeks, probably do not alter insulin sensitivity or glucose tolerance in clinically normal dogs.