The bicipital tendons and bursae of 25 healthy adult Quarter Horses were ultrasonographically examined. Cross-sectional images of the right and left bicipital tendons were obtained from each horse, using a 7.5-MHz transducer held in the frontal plane at the point of the shoulder. The bicipital tendon at the point of the shoulder appeared as a bilobate structure overlying the echogenic surface of the humerus. Median distance from the skin surface to the cranial surface of the tendon on the medial sagittal plane of the tendon was 23 mm (range, 16.5 to 30 mm); median distance on the lateral sagittal plane was 14 mm (range, 8.5 to 19 mm). Median distance from the skin surface to the tendon on the midsagittal plane of the tendon was 17 mm (range, 10.5 to 22 mm). Median cranial-to-caudal widths of the lateral and medial lobes of the tendon at their greatest dimensions were 20.5 mm (range, 18 to 27.5 mm) and 16 mm (range, 13 to 20.5 mm), respectively. The median cranial-tocaudal width of the central (midsagittal) portion of the tendon was 10 mm (range, 7 to 13.5 mm). The bicipital bursa was less than or equal to 3 mm wide at all locations at which it was measured. Ultrasonographic imaging was easily performed and allowed evaluation of the bicipital tendon, bursa, and surface of the underlying humerus.

Selenium concentration was measured in paired maternal blood samples and fetal liver specimens collected at a San Joaquin County, Calif, slaughterhouse (beef = 19, dairy = 54) and from bovine aborted fetuses submitted to the California Veterinary Diagnostic Laboratory System (CVDLS; beef = 20, dairy = 20). Of the slaughterhouse samples and specimens, dairy maternal blood selenium concentration was significantly (P < 0.001) higher (mean +/- SD; 0.22 +/- 0.056 micrograms/ml) than that for beef breeds (0.137 +/- 0.082 micrograms/ml). The CVDLS mean maternal blood selenium concentration for the dairy-breed samples (0.192 +/- 0.028 micrograms/ml) was similar to that for the slaughterhouse dairy-breed samples, but was greater than that for the slaughterhouse beef-breed samples. Slaughterhouse mean fetal liver selenium content also was higher (P < 0.001) for the dairy breeds (0.777 +/- 0.408 micrograms/g), compared with the beef breeds (0.443 +/- 0.038 micrograms/g). Mean fetal liver selenium content for slaughterhouse specimens was higher (P < 0.002) than that for the CVDLS specimens (beef, 0.244 +/- 0.149 micrograms/g; dairy, 0.390 +/- 0.165 micrograms/g). At the CVDLS, dairy fetal liver content was greater (P < 0.001) than that for beef breeds. Mean ratio of fetal liver selenium content to maternal blood selenium concentration was 3.53 +/- 1.89 for dairy breeds at the slaughterhouse (liver-to-blood correlation [r] = 0.38), and was 2.11 +/- 1.00 for dairy breeds at the CVDLS (r = 0.31) and 3.43 +/- 1.50 for beef breeds (r = 0.58). Both slaughterhouse breed ratios were significantly (P < 0.002) greater than the CVDLS dairy-breed ratio. On the basis of these results, breed and source location should be taken into account when interpreting selenium values. Fetal liver selenium content should only be used as a screening test and combined with whole blood selenium concentration from clinically normal herdmates to evaluate herd selenium status.

An ELISA was developed to determine serum concentration of apolipoprotein B-100, a major triglyceride-binding protein in very low-density lipoproteins and a putative maker for hepatic lipidosis of dairy cows. Serum apolipoprotein B-100 was prepared electrophoretically, and antibodies to this protein were raised in rabbits. The antiserum prepared was further purified by affinity chromatography, using bovine serum albumin-Sepharose 4B, to remove antibodies to albumin. For the ELISA, addition of 2-mercaptoethanol to the coating buffer (50 mM sodium carbonate, pH 9.6) was required to evaluate apolipoprotein B-100 concentration in serum. The ELISA developed was sensitive (detection limit was 300 to 400 ng/ml of serum) and reliable (coefficients of variance were in the range of 3.3 to 7.6%). By use of the established ELISA, the serum apolipoprotein B-100 concentration was found to be significantly (P < 0.01) lower during the early lactating stage than during other stages of lactation. Reduced hepatic synthesis or secretion of apolipoprotein B-100 during the early lactating stage, together with the excess uptake by the liver of serum nonesterified fatty acids, is suggested to be relevant in the accelerated accumulation of triglycerides in the liver of dairy cows during the periparturient period.

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.

Hyperxanthinuria and xanthine uroliths have been recognized with increased frequency in dogs with ammonium urate uroliths that had been given allopurinol. We hypothesized that dietary modification might reduce the magnitude of uric acid and xanthine excretion in urine of dogs given allopurinol. To test this hypothesis, excretion of metabolites, volume, and pH were determined in 24-hour urine samples produced by 6 healthy Beagles during periods of allopurinol administration (15 mg/kg of body weight, PO, q 12 h) and consumption of 2 special purpose diets: a 10.4% protein (dry matter), casein-based diet and a 31.4% protein (dry matter), meat-based diet. Significantly lower values of uric acid (P = 0.004), xanthine (P = 0.003), ammonia (P = 0.0002), net acid (P = 0.0001), titratable acid (P = 0.0002), and creatinine (P = 0.01) excreted during a 24-hour period were detected when dogs consumed the casein-based diet and were given allopurinol, compared with the 24-hour period when the same dogs consumed the meat-based diet and were given allopurinol. For the same 24-hour period, urine pH values, urine volumes, and urine bicarbonate values were significantly (P = 0.0004, P = 0.04, and P = 0.002, respectively) higher during the period when the dogs were fed the casein-based diet and given allopurinol than when they were fed the meat-based diet and given allopurinol. Endogenous creatinine clearance was significantly (P = 0.006) lower when dogs were fed the casein-based diet and given allopurinol than when they were fed the meat-based diet and given allopurinol. Significantly lower concentrations of plasma uric acid (P = 0.0001), plasma xanthine (P = 0.01), and serum urea nitrogen (P = 0.0001) were detected when dogs consumed the casen-based diet and were given allopurinol than when they consumed the meat-based diet and were given allopurinol. On the basis of these results, use of the casein-based diet and allopurinol in protocols designed for dissolution of urate uroliths may be beneficial in preventing hyperxanthinuria and xanthine urolith formation.

The partitioning of total pulmonary resistance (RL) into upper airway resistance and lower airway resistance (Rl) was studied in 8 Thoroughbred geldings. In addition, the phase shift and amplitude distortion of 3 catheters used for pressure measurements in this study were evaluated under static and dynamic conditions. Flow rate was obtained from a heated pneumotachograph attached to a tight-fitting mask placed over the nose. Electronic integration of the flow signal gave tidal volume. Transpulmonary pressure (PL) was obtained from calculation of the difference between the esophageal balloon catheter pressure and mask pressure. Lateral tracheal pressure was measured from a polyethylene catheter placed percutaneously in the middle portion of the trachea. Lower airway pressure (Pl) was calculated as the difference between esophageal pressure and lateral tracheal pressure. Similarly, upper airway pressure was defined as the difference between lateral tracheal pressure and mask pressure. Pressures are reported as the difference between the maximal and the minimal pressures recorded during a respiratory cycle. Airway resistance was calculated, using the isovolume method, at 50% of tidal volume. There were individual and group variations in Pl and Pl/PL, although P1 accounted for more than 60% of PL in all horses. In 6 horses, Rl was more than 50% of RL whereas in 2 horses, Rl was only 30 and 34% of RL. Amplitude distortion was minimal for the 3 catheters under static conditions in the in vitro study. Under dynamic conditions, amplitude distortion varied according to the catheter studied, the frequency, and the resistance of the system. There were no phase differences under static conditions at low frequency. However, phase discrepancy, which was variable through the cycle, was observed for some catheters at high frequency under static and dynamic conditions. It was concluded that, until measuring techniques are standardized in horses, variations in the partitioning of RL are likely to be obtained between studies and between animals within studies. However, phase discrepancy, which was variable through the cycle, was observed for some catheters at high frequency under static and dynamic conditions. It was concluded that, until measuring techniques are standardized in horses, variations in the partitioning of RL are likely to be obtained between studies and between animals within studies.

Eight Holstein cows, 4 inoculated intracisternally in 1 quarter of the mammary gland with Escherichia coli and 4 noninfected controls, were administered ceftiofur sodium (3 mg/kg of body weight, IV, q 12 hours) for 24 hours, beginning at 14 hours after inoculation of infected cows. All challenge-exposed cows became infected, with mean +/- SEM peak log10 bacterial concentration in milk of 5.03 +/- 0.69 colony-forming units/ml. The infection resulted in systemic signs (mean peak rectal temperature, 41.5 +/- 0.3 C; anorexia; signs of depression) and local inflammation (mean peak albumin concentration in milk, 7.89 +/- 1.71 mg/ml). Ceftiofur was detectable in milk from all challenge-exposed cows, compared with only 1 of 4 noninfected cows, and the mean period after inoculation that ceftiofur was detectable in milk was longer (P < 0.05) in infected (147.7 +/- 27.5 hours) than noninfected cows (1.3 +/- 1.3 hours). However, maximal ceftiofur concentration attained in milk for all cows was 0.28 micrograms/ml, and was 0.20 micrograms/ml or less for all but 2 milk samples collected for 10 days after challenge exposure. Mean serum concentration of ceftiofur peaked at 1.0 +/- 0.3 micrograms/ml and 0.7 +/- 0.1 micrograms/ml for infected and noninfected COWS, respectively. After each ceftiofur dose, mean peak and trough concentrations of ceftiofur in serum did not differ between groups; however, concentration of ceftiofur in serum was higher at 7 hours after each dose in noninfected cows, suggesting more rapid clearance of the drug in infected cows. Ceftiofur was not detected in serum (< 0.05 micrograms/ml) of any cow at or after 120 hours following inoculation of infected cows. Storage of serum samples at -20 C for 3 weeks resulted in a 98.8% decrease in ceftiofur activity, compared with that in fresh serum samples. Eighty-seven percent of this loss occurred 30 minutes after mixing serum and ceftiofur; thus, about 13% of the original activity was lost in storage. Storage of milk samples under similar conditions did not result in loss of ceftiofur activity. Despite acute inflammation, the dosage of ceftiofur used in this trial would not result in drug concentrations in milk above FDA safe concentrations, or above the reported minimum inhibitory concentration for coliform bacteria.

Sixteen German Shepherd Dogs from 4 litters were IgA-deficient on the basis of at least 1 of 2 serum IgA determinations, and all had small intestinal bacterial overgrowth, as documented by quantitated small intestinal bacterial culture in another study. These dogs were fed 2 diets that differed principally in their protein source (chicken vs beef, milk, and wheat). All dogs were fed each diet for 2 weeks before the study began. Next, all dogs were fed the chicken-based diet for 2 months. Then, half the dogs (group 1) were randomly assigned to continue eating the chicken-based diet, while the other half (group 2) ate a diet containing beef, milk, and wheat proteins. The small intestine was biopsied at the beginning of the study and after dogs had eaten the assigned diet for 2 and 4 months. At 2 months, group-2 dogs had more colonic mucosal mast cells, but this difference did not persist at 4 months. At the end of the study (ie, 4 months), although all dogs were clinically normal, group-2 dogs had significantly (P = 0.010) decreased numbers of jejunal villus plasma cells. However, these histologic changes were not considered clinically important. There were no significant differences in blood eosinophil counts, serum trypsin-like immunoreactivity, or cobalamin, folate, or IgA concentration. Clinical differences were not detected between the 2 groups, before or after the study. Changes were seen in serum IgM and IgG concentrations. Although results of this study suggest that dietary protein may influence intestinal mucosal cell populations, there was no evidence that the protein sources in these 2 diets caused intestinal disease in these dogs under the conditions of this study.

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.

Porcine fetuses were exposed in utero to porcine reproductive and respiratory syndrome virus (PRRSV) at stages of gestation ranging from 34 to 85 days and examined 17 to 31 days later to determine the effect of gestational age on fetal susceptibility. For each of the 8 litters tested during the study, all of the fetuses of 1 horn of the uterus were exposed to virus by intraamniotic injection; those of the other horn were exposed similarly to a sham inoculum that consisted of sterile cell culture medium. Viral infectivity titers associated with fetal tissues collected at necropsy indicated that, regardless of gestational age, the virus had replicated in fetuses exposed intraamniotically. In addition, virus had also spread and replicated in sham-inoculated littermates in 3 litters. On the basis of these findings it appears that there may be little or no temporal difference in fetal susceptibility to infection with PRRSV. If so, the lack of early fetal death as a commonly recognized feature of naturally occurring cases of PRRS may be due to a greater resistance of early gestational fetuses to the lethal effects of PRRSV, as suggested by this study, and/or a greater likelihood of transplacental infection during late gestation.