Toxoplasma gondii-specific IgA, IgM, and IgG were measured by ELISA in the serum and aqueous humor of 29 client-owned cats with indigenous aviates and 7 specific-pathogen-free cats tested sequentially for 20 weeks after inoculation with T. gondii. Local antibody production in aqueous humor was estimated by multiplying the aqueous humor-to-serum T gondii-specific antibody ratio by the serum-to-aqueous humor total IgG (C value) or IgG (C value) ratio. Evidence for local production of antibody in aqueous humor was defined as C value greater than 8 or CTC value greater than 1. Toxoplasma gondii-specific IgM CTC values, IgG CTC values, or IgA CTC values greater than 1 were detected in the aqueous humor of 18 of 29 (62.1%) client-owned cats with endogenous uveitis; 2 cats had IgA CTC values greater than 1 without detectable IgM or IgG in aqueous humor. Toxoplasma gondii-specific IgM was not detected in the aqueous humor of experimentally inoculated cats before or after inoculation. Immunoglobulin G C values greater than 8 were detected in all 7 experimentally inoculated cats and ranged from 10.4 to 145.5. Immunoglobulin G C values greater than 8 were first detected 4 to 8 weeks after T gondii inoculation and were undetectable by week 16 after inoculation. Immunoglobulin A C values greater than 8 were detected in 4 of 7 cats and ranged from 12.7 to 264.3. Immunoglobulin A C values greater than 8 were first detected 4 to 8 weeks after inoculation, and were detected in 2 cats during week 20 after inoculation. It was concluded that some cats infected with T gondii develop detectable concentrations of T gondii-specific IgA in aqueous humor.

Arterial blood samples were obtained at rest, just before, and 5 minutes after a 704-m race, to quantify changes in hematologic variables, plasma electrolyte and protein concentrations, osmolality, and acid/base variables. Changes in plasma volume were estimated from the change in plasma protein concentration. Immediately prior to the race, plasma volume decreased by 10% from rest and total circulating RBC volume increased by 60%, attributable to increased RBC number rather than size. Increases in blood volume (VB) by 24% and PCV by 29% also were detected before the race. Five minutes after the race, plasma volume was 21% below the resting value and total circulating RBC volume had increased 73% above the resting value, resulting in a 40% increase in PCV. Contraction of the spleen appeared responsible for increased PCV and VB before the race and maintenance of VB after the race. Plasma chloride concentration was the same before and after the race; the chloride content of the plasma decreased by the same fraction (22%) as did the plasma volume, indicating Cl- loss from the plasma. Plasma Na+ content decreased by a smaller fraction (13%), causing Na+ concentration to increase from 151 mEq/L at rest to 167 mEq/L after the race. Assuming that Na+ concentration was the same throughout the extracellular fluid, H20 likely moved into the intracellular compartment. As a consequence of these changes, the inorganic strong ion difference in plasma increased by about 16 mEq/L, tending to minimize the acid/base disturbance induced by the 33 mEq/L increase in lactate concentration. Results indicated that the physiologic changes taking effect during strenuous sprint exercise in Greyhounds enhance blood volume and aid in acid/base homeostasis, both of which are adaptive for this type of exercise.

Ocular biometry, using A-scan ultrasonography and ultrasonographic pachymetry, was performed in 52 Samoyeds, 2 months to 13 years old, without intraocular or systemic diseases. Furthermore, the relative depth of the opening of the ciliary cleft was estimated from goniophotographs. The values were analyzed, and statistical models of changes in ocular distances with increasing age were identified. It was found that the changes in corneal thickness, axial anterior chamber depth, lens thickness, relative lens position, length of the vitreous body, and axial length could best be described by 1 of the 2 nonlinear models (...). The course began with a period of rapid increase, after which the ocular distance either increased at a progressively slower rate toward infinity (corneal and lens thickness) or to a finite limit (relative lens position and axial length), or ceased to grow and finally started to decrease toward minus infinity (axial anterior chamber depth and length of the vitreous body). However, suitable model for determining relative depth of the opening of the ciliary cleft could not be established. Results indicated that age-related changes, mainly in lens thickness, cause a shallow anterior chamber, and it was suggested that this may be of importance for development of a relative pupillary block and, thus, primary angle-closure glaucoma, at least in preconditioned eyes of Samoyeds.

Exertion has an effect on plasma, serum, and/or urine prostanoid concentrations in many species. We investigated the effect of exercise intensity on plasma prostaglandin concentrations during and after exercise in horses. Six Thoroughbreds completed 4 trials: 3 exercise trials (low-, medium-, and high-speed) and 1 nonexercise (control) trial on a high-speed treadmill. Blood samples were collected from a jugular catheter before, during and after exercise. The PCV and blood lactate, plasma protein, plasma prostacyclin (6-keto-PGF1 alpha), thromboxane B2 (TXB2), and prostaglandin E2 (PGE2) concentrations were measured before, during, and after exercise. Exercise significantly (P = 0.001) increased plasma TXB2 concentration during and after exercise in the low-, medium-, and high-speed trials, although effect of exercise intensity was not detected. Exercise was associated with an increase in PCV and blood lactate and plasma protein concentrations. There was no effect of exercise on plasma 6-keto-PGF1 alpha concentrations; PGE2 was not detected in plasma from any horse in any trial.

The effect of oxytetracycline (OTC) on bovine blood mononuclear cells and neutrophil functions was examined in vitro. Neutrophil functions tested include respiratory burst, peroxidase, and antibacterial activities. Neutrophils were treated with OTC (10 to 1,500 > microgram/ml) before exposure to either opsonized zymosan or bacteria. A dose-response inhibition of antibacterial activity to high concentrations of OTC (500 to 1,000 microgram/ml) was observed. Beginning at a concentration of 15 microgram/ml, OTC treatment of neutrophil Iysates resulted in decreased peroxidase activity. A dose response was not observed. In contrast, respiratory burst, measured by nitroblue tetrazolium dye reduction, increased after OTC exposure, but only at high concentrations (500 and 1,000 microgram/ml) of OTC. Mitogen-induced proliferation of blood mononuclear cells cocultured with OTC and concanavalin A, phytohemagglutinin-P, or pokeweed mitogen was inhibited at an OTC concentration of 100 microgram/ml at 48 and 72 hours of culture. These results indicate that blood mononuclear cells are more sensitive to the inhibitory effects of OTC than are neutrophils. Furthermore, the OTC-mediated inhibition of neutrophil antimicrobial activity is inversely related to the increase in nitroblue tetrazolium reduction. This suggests that OTC is uncoupling the hexose monophosphate shunt from production of secreted oxygen radicals. These results also suggest that the peroxidase enzyme system has a large biological reserve capacity.

Six horses, highly trained for dressage competition, were used to study the stride kinematics of the walk, and to compare the kinematics of the collected, medium, and extended walks. Horses were filmed in a sagittal plane at a rate of 150 frames/s; temporal, linear, and angular data were extracted from the films. Results of ANOVA and Duncan's multiple range test indicated that the speed of the collected walk (1.37 m/s) was significantly (P < 0.01) slower than that of the medium (1.73 m/s) and extended (1.82 m/s) walks, values for which were not significantly different from each other. The increase in speed was associated with a significant increase in stride length, from 157 cm in the collected walk to 193 am in the extended walk. This was a result of an increase in the over-tracking distance, whereas there was no significant difference in the distance between lateral placements of the limbs. Stride duration decreased (P < 0.01) from the collected walk (1,159 ms) to the extended walk (1,064 ms). Angles of the metacarpal and metatarsal segments, measured on the palmar/plantar aspect, were higher at impact and lower at lift off in the collected than in the extended walk (P < 0.01). This indicated greater range of angular motion of this segment during the stance phase in the extended walk. Only 1 of the 6 horses had a regular 4-beat rhythm of the footfalls, with equal time elapsing between the lateral and diagonal footfalls.

We examined the electromyographic activity of the costal portion of the diaphragm and the transverse abdominal and external oblique muscles in 6 chronically instrumented awake adult horses during eupneic breathing during 2 levels of hypercapnia (fractional concentration of inspired CO2; FICO2 = 0.4 and 0.6), and during 2 levels of hypocapnic hypoxia (FIO2 = 0.15 and 0.12). Using the inert gas technique, we also measured the end-expiratory lung volumes of the 6 horses during eupnea, 6% CO2 challenge, and 12% O2 breathing. During eupneic breathing, phasic electrical activity of these 3 muscles was always present and was preceded by the onset of mechanical flow. At progressive levels of hypercapnia, the magnitude of inspiratory and expiratory electrical activity increased, and for the expiratory muscles, this recruitment coincided with significant (P < 0.05) increases in peak expiratory gastric pressure. However, during hypocapnic hypoxia, differential recruitment patterns of the respiratory muscles were found. The electrical activity of the diaphragm increased in magnitude and occurred sooner relative to the onset of mechanical flow. The magnitude and onset of abdominal expiratory activity failed to increase significantly during these episodes of hyperpnea and this pattern of activity coincided with decrements in peak expiratory gastric pressure. Despite alterations in muscle recruitment patterns during these hyperpneic episodes, end-expiratory lung volume remained unchanged. Thus, we conclude that adult horses respond similarly to awake dogs during peripheral and central chemoreceptor stimulation.

Six healthy, adult horses, with normal (mean +/- SEM) baseline serum concentrations of total triiodothyronine (T3, 1.02 +/- 0.16 nmol/L), free T3 (FT3, 2.05 +/- 0.33 pmol/L), total thyroxine (T4, 19.87 +/- 1.74 nmol/L), free T4 (FT4, 11.55 +/- 0.70 pmol/L), total reverse T3 (rT3, 0.68 +/- 0.06 nmol/L), and cortisol (152.75 +/- 17.50 nmol/L), were judged to be euthyroid on the basis of response to a standardized thyroid-stimulating hormone response test. Serum concentrations of T3, FT3, T4, FT4, rT3, and cortisol were determined immediately before and every 24 hours during a 4-day period of food deprivation, when water was available ad libitum. Similar variables were measured 72 hours after refeeding. Decreases (to percentage of baseline, prefood deprivation value) in circulating T3 (42%), T4 (38%), FT3 (30%), and FT4 (24%) concentrations were maximal after 2, 4, 2, and 4 days of food deprivation, respectively (P < 0.05). Increases (compared with baseline, prefood deprivation value) in rT3 (31%) and cortisol (41%) concentrations were maximal after 1 and 2 days of food deprivation, respectively (P < 0.05). Refeeding resulted in increase in serum T4 and FT4, and decrease in rT3 and cortisol concentrations toward baseline values, after 72 hours (P < 0.05). Refeeding did not effect a return of T3 or FT3 concentration to baseline values after 72 hours (P < 0.05). Food deprivation appears to cause changes in serum concentrations of T3, FT3, T4, FT4, rT3, and cortisol in horses that are similar to those in human beings. This effect of food deprivation should be considered when results of serum thyroid hormone and cortisol assays are interpreted in the face of clinical disease. These results further emphasize the invalidity of making a clinical diagnosis of hypothyroidism on the basis of baseline, serum thyroid hormone concentrations in horses, especially if the horses have been anorectic or inappetent.

To investigate the effect of chloramphenicol, a cytochrome P-450 inhibitor, on the pharmacokinetics of propofol, either chloramphenicol (50 mg/kg of body weight, IV) or saline solution was administered IV to 5 Greyhounds in randomized manner, with at least 2 weeks between trials. Thirty minutes after either chloramphenicol or saline treatment, a bolus dose of propofol (10 mg/kg IV) was administered, followed by a 2-hour infusion of propofol (0.4 mg/kg/min, IV). Samples for determination of blood propofol concentration were collected sequentially over a 6-hour period during each trial. After termination of propofol infusion, the time to spontaneous head lift, extubation, sternal recumbency, and standing was recorded. Blood propofol concentration was determined by use of high-performance liquid chromatography. Concentration-time data were fitted to a two-compartment open pharmacokinetic model and pharmacokinetic variables were determined, using a microcomputer program for modeling and simulation of concentration-time data. The effect of chloramphenicol on the pharmacokinetics of propofol and recovery time were evaluated, using paired t-tests and Wilcoxon's test for parameters that are not normally distributed (t1/2(beta), Vd(ss), Cl(B)). Significant (P < 0.05) effects of chloramphenicol pretreatment included increased t1/2(5) (by 209%), and decreased Cl(B) (by 45%), and prolonged recovery indices (by 768 to 946%). These results indicate that cytochrome P-450 metabolic pathways have an important role in propofol clearance and propofol anesthetic recovery in Greyhounds.

Intraocular production of Toxoplasma gondii-specific antibody in cats has been estimated by comparing the ratio of T gondii-specific antibody in aqueous humor and serum with the ratio of total immunoglobulins in serum and aqueous humor (Goldmann-Witmer coefficient; aqueous antibody coefficient; C value). It has been proposed that in human beings, comparison of the ratio of T gondii-specific antibody in aqueous humor and serum with the ratio of antibodies against a nonocular pathogen in serum and aqueous humor is more accurate than methods using total immunoglobulin quantification. We developed an ELISA for detection of calicivirus-specific antibodies in the serum and aqueous humor of cats. By evaluating calicivirus-specific antibody concentrations in the aqueous humor of healthy and diseased cats, calicivirus was assessed as a nonintraocular pathogen. The ratio of T gondii-specific antibodies in the aqueous humor and serum and the ratio of calicivirus-specific antibodies in serum and aqueous humor were evaluated as a means of estimating intraocular T gondii-specific antibody production. A field strain of feline calicivirus was isolated, cultured, and purified. A calicivirus-specific IgG ELISA was developed for detection of feline calicivirus-specific IgG in serum and aqueous humor. Calicivirus-specific IgG was measured in the serum and aqueous humor from 3 groups of control cats. Results suggested that calicivirus is a nonintraocular pathogen in cats and that calicivirus IgG detected in aqueous humor is attributable to leakage across a damaged blood-ocular barrier. Intraocular production of T gondii-specific antibodies was estimated, using 2 formulas. The C value was calculated by multiplying the ratio of T gondii-specific IgM or IgG in aqueous humor and serum by the ratio of total immunoglobulins (using the corresponding IgM or IgG class) in serum and aqueous humor. The Ctc value (Toxoplasma-calicivirus Goldmann-Witmer coefficient) was calculated by multiplying the ratio of T gondii-specific IgM or IgG in aqueous humor and serum by the ratio of calicivirus-specific IgG in serum and aqueous humor. Serum and aqueous humor samples were obtained from 41 client-owned cats with uveitis, and T gondii-specific C values and Ctc values were calculated. Toxoplasma gondii-specific IgM or IgG C values of 10 or greater or T gondii-specific IgM or IgG Ctc values of 1 or greater were considered to be suggestive of intraocular T gondii-specific antibody production. Of the 41 cats, 20 (48.7%) had evidence of intraocular production of T gondii-specific antibody on the basis of either an IgM or IgG C value of 10 or greater. A Ctc value could not be calculated in 3 cats because calicivirus-specific IgG was not present in aqueous humor. Of the 38 cats for which Ctc values could be calculated, 25 (65.8%) had evidence of intraocular production of T gondii-specific antibody on the basis of either an IgM or IgG Ctc value of 1 or greater. The C values and Ctc values were in agreement for 75.9% of IgM containing samples and 75% of IgG containing samples. Sensitivity, specificity, predictive value of a positive test result, and predictive value of a negative test result for an IgM or IgG C value, when compared with the corresponding IgM or IgG Ctc value were determined. The results indicate that use of the C value for estimation of intraocular T gondii-specific antibody production will result in 28.6 (IgM) to 50% IgG) false-negative results and 12.5% (IgM and IgG) false-positive results, when compared with the Ctc value.