Brain capillary function was assessed in 4- to 6-week-old calves given lead acetate (15 mg/kg of body weight) orally for 7 to 8 days. Neurologic signs of lead poisoning included CNS depression, blindness, and hyperesthesia. Brain capillaries were isolated from cerebral cortex of control and lead-treated calves and evaluated for metabolic indicators, ion transport, and prolyl hydroxylase activity. In lead-treated calves, the rate of glucose metabolism was less than half that in controls. Ion efflux of 45Ca or 36Cl from endothelial cell suspensions was not affected by lead treatment. Prolyl hydroxylase activity in endothelium and proline-to-hydroxyproline ratio in endothelial basement membranes were similar in control and lead-poisoned calves. Results indicate that lead may inhibit energy metabolism, but not ion transport or collagen biosynthesis in brain capillaries of calves and, compared with suckling rats, damage to the blood-brain barrier is less important. In calves, neuronal tissue may be the primary target for the CNS effects of lead.

A murine IgM monoclonal antibody causing bacterial agglutination was used in an immunoaffinity procedure to purify a serotype 1-specific polysaccharide epitope from Pasteurella haemolytica. The P haemolytica serotype 1-specific antibody was precipitated from peritoneal ascitic fluid, dialyzed, and covalently attached to cyanogen bromide-activated Sepharose 4B beads. Retention of purified antibody activity and coupling efficiency were > 99% when evaluated by ELISA, agglutination testing, and protein determination. Potassium thiocyanate was selected as an eluant on the basis of reversible dissociation of bacterial agglutination and was titrated for the lowest effective concentration. Immunobead activity was observed microscopically by immobilization of encapsulated P haemolytica serotype 1 and its reversible dissociation after elution with 0.4M potassium thiocyanate. Specificity of immobilization was visualized, using P haemolytica serotypes 2 and 5, which were not bound, and by blocking serotype-1 binding with homologous capsular material. Saline-extractable capsular material from P haemolytica serotype 1 was used as an antigen source. After elution of the serotype 1-specific polysaccharide epitope, the product was dialyzed and analyzed, using chemical and immunologic methods. The immunoaffinity product contained no detectable protein and greater than half the original hexosamine content. Using defined monoclonal antibodies in ELISA, titration of the original capsular material and the immunoaffinity product revealed specific retention of lipopolysaccharide, a 10- to 30-kd polysaccharide antigen common to all P haemolytica and P multocida serotypes, and serotype 1-specific capsular polysaccharide, indicating possible epitope sharing among polysaccharide antigens of P haemolytica serotype 1.

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.

Pharmacokinetics and recovery characteristics of propofol in Greyhounds and mixed-breed dogs were compared. In all dogs, disposition of propofol was adequately described by a 2-compartment open model, with a rapid distribution phase followed by a slower elimination phase. When findings in Greyhounds were compared with those in mixed-breed dogs, significant differences were observed in mean concentrations of propofol in blood, recovery characteristics, and estimates for apparent volume of distribution, volume of distribution at steady state, and total body clearance. In addition, Greyhounds recovered from anesthesia at higher concentrations of propofol than did mixed-breed dogs. A secondary peak in blood propofol concentration was observed in 8 of 10 Greyhounds and in 5 of 8 mixed-breed dogs. This peak corresponded to the time of return of the righting reflex.

Twelve resected canine gallbladders (in vitro) and the gallbladder in each of 14 dogs (in vivo) were ultrasonographically examined. Gallbladder volume was calculated from ultrasonographically measured geometric dimensions, using 4 volumetric model formulas: cone, ellipse, biplanar ellipse, and prolate ellipse. Calculated volume was compared with true gallbladder volume, as measured by water displacement. AU examined models for calculation of gallbladder volume were closely associated with true gallbladder volume (P < 0.005), and all models provided accurate predictions of true gallbladder volume (r2 > 0.80). Calculated volumes can be corrected mathematically by use of the regression coefficient and constant for each model. Body weight was not significantly associated with gallbladder volume in any of the models considered. Use of ultrasonography to accurately measure gallbladder volume could be combined with synthetic cholecystokinin-stimulated gallbladder emptying to provide information about biliary function and patency in icteric animals. Such information could aid the clinical decision between surgical or medical treatment. Correction of calculated volumes would not be necessary in association with induced emptying studies, because volume change is more important than absolute volume.

Right atrial (RA), right ventricular (RV), pulmonary artery (PA), and pulmonary artery wedge (Paw) pressures were examined, using catheter-mounted micromanometers, in 8 healthy horses at rest and during galloping on a treadmill at belt speeds of 8, 10, and 13 m/s. The in vivo signals from the micromanometers were matched with those from conventional fluid-filled catheter transducers leveled at the scapulohumeral joint. Thirty minutes after completing control exercise measurements, furosemide was administered IV at a dosage of 1 mg/kg of body weight, and resting, as well as exercise, measurements were repeated 4 hours later. Studies also were performed on a separate day, when only postfurosemide resting and exercise data were collected. Prefurosemide and postfurosemide heart rate values for rest (37 +/- 2 beats/min, mean +/- SEM), as well as for exercise (213 +/- 5 beats/min at 13 m/s), were similar. Prefurosemide mean RA, PA, and PAW pressures were increased significantly (P < 0.05) from resting values of 8 +/-2, 31 +/- 2, and 18 +/- 2 mm of Hg, respectively, to 44 +/- 4, 89 +/- 5, and 56 +/- 4 mm of Hg with exercise at 13 m/s. Furosemide administration resulted in marked diuresis, and resting mean RA, PA, and PAW pressures decreased significantly (P < 0.05) to 1 +/-1, 27 +/- 2, and 11 +/- 2 mm of Hg, respectively, 4 hours after furosemide administration. Although pressures increased markedly with exercise (corresponding values being 31 +/- 5, 79 +/- 6, and 44 +/- 4 mm of Hg), these 4-hour postfurosemide exercise values were significantly (P < 0.05) less than those recorded with prefurosemide exertion. Intravascular pulmonary capillary pressure, calculated as the average of mean PA and PAW pressures, during prefurosemide exercise (73 +/- 5 mm of Hg) significantly (P < 0.05) exceeded that during exercise performed 4 hours after furosemide administration (61 +/- 5 mm of Hg). Attenuation by furosemide of the exercise-induced increase in pulmonary capillary pressure may have a role in limiting or reducing the extent of exercise-induced pulmonary hemorrhage in horses.

Six calves with areas of pulmonary consolidation attributable to bronchopneumonia, and 6 calves with no areas of consolidation were given IV injections of danofloxacin. This injection was followed approximately 55 minutes later by injection of 15-micrometer radio-labeled microspheres to measure regional pulmonary blood flow. Calves were euthanatized exactly 1 hour after the danofloxacin injection. Six samples for determination of danofloxacin concentration, each surrounded by 4 samples for determination of gamma emission counts, were taken from each lung, Additional samples focusing on the line of demarcation between consolidated and nonconsolidated tissue were taken from calves with pulmonary consolidation. Data from calves with no areas of pulmonary consolidation indicated that blood flow was significantly reduced in the caudodorsal position of the left lung and the caudodorsal and cranioventral positions of the right lung, compared with that in other positions within the lungs. Danofloxacin concentrations in the cranioventral positions of the right and left lungs were significantly lower than those in the middle-dorsal positions. Differences in danofloxacin concentrations and blood flow were analyzed in consolidated and nonconsolidated cranioventral and middle-ventral positions of the lungs from calves with pulmonary consolidation. Decreases in blood flow in consolidated lung tissue ranged from 83.3 to 91.7%. Danofloxacin concentrations in consolidated lung tissue were significantly reduced by 41% in the middleventral position of the left lung. The line of demarcation step study revealed a significant reduction of blood flow at 2 and 4 cm into consolidated lung tissue, with reductions of 84 and 88%, respectively. Danofloxacin concentration did not significantly decrease in consolidated tissue.

Efficacy of albendazole for treating giardiasis in dogs was assessed in 3 experiments. In experiment 1, Giardia cysts were cleared from feces of 5 of 7 dogs (as determined by the zinc-sulfate concentration technique) after the dogs received a single dose of albendazole (25 mg/kg of body weight, PO), whereas feces of 3 of 7 dogs became clear of cysts without treatment. In experiment 2, feces of 5 of 5 dogs became clear of cysts after albendazole treatment (25 mg/kg, PO, q 12 h for 4 doses); feces of 1 of 5 untreated control dogs became clear. In experiment 3, feces of 18 of 20 dogs became clear of cysts after albendazole 25 mg/kg, PO, q 12 h for 4 doses) was given; none of the 20 control dogs had feces clear of cysts. Signs of toxicosis were not observed in any dog. These results indicate that a single dose of albendazole (25 mg/kg, PO) is not effective for treating giardiasis in dogs. However, 4 doses of albendazole (25 mg/kg, PO, q 12 h) are highly effective and nontoxic for treatment of giardiasis in dogs.

The disposition of clorazepate, a benzodiazepine anticonvulsant, was determined in dogs after administration of a single oral dose of clorazepate (2 mg/kg of body weight) and after oral administration of clorazepate (2 mg/kg, q 12 h) concurrently with phenobarbital (5 mg/kg, q 12 h) for 44 consecutive days. Serum concentrations of nordiazepam, the active metabolite of clorazepate, were measured. After a single oral dose of clorazepate, maximal nordiazepam concentrations ranged from 569.6 to 1,387.9 ng/ml mean, 880.2 248.9 ng/ml) and were detected 16.8 to 131.4 minutes (mean, 85.2 36 minutes) after dosing. After administration of phenobarbital for 44 consecutive days, maximal nordiazepam concentrations were significantly (P < 0.01) lower, ranging from 209.6 to 698.5 ng/ml (mean, 399.3 +/- 155.6 ng/ml) at 68.4 to 145.8 minutes (mean, 93 +/- 25.8 minutes) after dosing. Mean area under the curve (AUC) on day 1 (mean, 3.37 +/- 0.598 ng-min/ml) was significantly (P < 0.001) greater than AUC on day 44 (1.66 +/- 0.308 ng-min/ml). Oral clearance was significantly (P < 0.01) greater on day 44 (12.44 +/- 2.55 ml/min/kg), compared with that on day 1 6.16 +/- 1.35 ml/min/kg). Values for area under the first moment curve, oral volume of distribution, mean residence time, and elimination half-life were not significantly altered by concurrent administration of phenobarbital. Administration of phenobarbital altered the disposition of clorazepate such that the amount of nordiazepam in circulation during each dose interval was significantly reduced. Adequate control of seizures in epileptic dogs, therefore, may require higher dosages of clorazepate when it is coadministered with phenobarbital.

Estradiol was administered to 3 steers (0.12 mg/kg of body weight/d for 14 consecutive days), followed by 2 days of nonfeeding (starvation). During estradiol administration, liver nuclear estrogen receptor and serum apolipoprotein B-100 (apoB-100), as well as serum triglycerides concentrations were increased, compared with values before administration. Starvation, together with interruption of estradiol administration, resulted in rapid decreases of the receptor, serum apoB-100, and serum triglycerides concentrations, and increase of nonesterified fatty acids concentration. Of the 3 steers, 2 had higher liver triglyceride content, compared with values before treatment. In the control group (3 steers that received vehicle alone, then starved similarly), these concentrations, except for serum nonesterified fatty acids and triglycerides concentrations after starvation, were not changed. In another experiment, serum apoB-100 concentration in dairy cows was significantly (P < 0.05) lower at parturition than values before and after parturition. These results indicate that estradiol may be involved in development of fatty liver in cattle.