Thirty-two bovine field isolates of bluetongue virus (BTV), 6 field isolates of epizootic hemorrhagic disease virus (EHDV) from deer, 4 BTV prototype serotypes (10, 11, 13, and 17), and 2 EHDV prototype serotypes (1 and 2) were coelectrophoresed, using polyacrylamide gels. Field isolates were obtained from various regions of the United States. Analysis of polyacrylamide gels and scattered plots generated for comparison of migration patterns for different isolates within each serotype of BTV revealed wide variation among the individual segments. The BTV serotypes 10 and 11 had more variation, compared with BTV serotypes 13 and 17, especially for migration of genome segment 5. A definitive correlation was not seen between the double-stranded RNA migration profiles on polyacrylamide gel electrophoresis, geographic origin, herd of origin, or year of collection. One BTV field isolate contained more than 1 electropherotype, with 2 bands at the segment-7 position, and it was further characterized as BTV serotype 11. Segments 2 and 5 of EHDV isolates were more variable in their migration than were the other gene segments. Generally, migration profiles for EHDV double-stranded RNA were more variable, compared with those of BTV isolates. Although a correlation was found between migration profiles and serotype of 2 isolates of EHDV, a study of additional EHDV isolates is required before the diversity of electrophoretic patterns of EHDV can be determined.

Liquid mercury strain gauges were implanted in the forelimb proximal sesamoidean ligaments (PSL) of 8 adult horses. The gauges measured PSL strain while horses were standing with or without external support. In 6 of the horses, the gauges also measured PSL strain in horses at a walk, with or without external support. Gauges were enclosed within sliding polypropylene tubes to prevent nonaxial deformation. Each gauge was placed in 1 arm of a low-resistance half-bridge circuit. To provide temperature compensation, a dummy gauge was placed in the adjacent arm of the bridge circuit and was implanted next to the active gauge in the surrounding fascial tissue. External support included fiberglass cast support (CAST), dorsal fetlock splint support (DFS), support wraps of 3 bandage materials (SW1, SW2, and SW3), and support wrap with caudal splint (SW4). The cast was applied, with the fetlock and foot in weightbearing position, from the proximal portion of the metacarpus distal to and including the foot. The DFS was applied by placing the cranial half of the fiberglass cast on the dorsal aspect of the instrumented limb. The SW1, SW2, and SW3 were applied in a figure-8 pattern around the fetlock, using 50% of the linear stretch capacity of the bandage material, with the horse standing squarely on all 4 limbs. The SW4 was applied identically to the other support wraps, with the exception of addition of a flexible caudal splint incorporated in the support wrap. Mean maximal strain while standing without external support for 8 horses was 6.0% (range, 3.8 to 7.5%). Mean maximal strain at a walk without external support for 6 horses was 5.9% (range, 4.1 to 8.2%). Only cast and DFS significantly reduced mean maximal strain while standing. Cast support reduced mean maximal strain while standing to a mean +/- SEM 1.4 +/- 0.2%, 77% reduction in total strain (P < 0.0001). Use of DFS reduced mean maximal strain while standing to a mean 4.2 +/- 0.3%, 30% reduction in total strain (P < 0.0001). The SW1, SW2, and SW3 did not significantly reduce mean maximal strain while standing (power > 0.8, delta = 20%). Conclusions cannot be made for reduction of mean maximal strain while standing with SW4 (power < 0.8, delta = 20%) because of low sample size. Only CAST and DFS significantly reduced mean maximal strain while walking. Cast support reduced mean maximal strain while walking to a mean 2.0 +/- 0.3%, 67% reduction in total strain (P < 0.0001). The DFS reduced mean maximal strain while walking to a mean 4.4 +/- 0.4%, 25% reduction in total strain (P < 0.008). The SW1, SW2, and SW3 did not significantly reduce mean maximal strain while walking (power > 0.8, delta = 20%). Conclusions cannot be made for reduction of mean maximal strain while walking with SW4 (power < 0.8, delta = 20%) because of low sample size.

Albendazole (10 mg(kg of body weight) was administered as a drench suspension or as a feed additive to 24 cattle with naturally acquired infections of Fasciola hepatica and Fascioloides magna. Cattle were euthanatized 16 to 30 days after treatment, and the number of viable flukes was counted. Viable F hepatica and F magna were decreased by 91.4% and 70.6% for drench administration and by 82.9% and 71.9% for the feed additive treatment, respectively. There was no significant difference between the efficacy of the 2 formulations in decreasing viable fluke numbers, compared with untreated controls.

On the basis of results in dogs, conditioning exercise may increase sensitivity to nondepolarizing muscle relaxants. Five Thoroughbreds were exercised/conditioned 3 times weekly on a treadmill for 8 months. Increasing maximal rate of O2 consumption verified that the horses were responding to exercise conditioning. Six nonexercised Thoroughbreds served as the control group. Studies were done with horses under general anesthesia by use of halothane during partial paralysis by a brief constant-rate infusion with the muscle relaxant, metocurine iodide. Quantification of degree of paralysis of the hoof twitch (eg, digital extensor) occurred with simultaneous quantification of blood values of metocurine. Pharmacokinetic and pharmacodynamic analyses of the data were done by a nonlinear regression program, using the Hill equation. There were no differences in findings between exercised and nonexercised horses. The mean blood concentration for the 50% paralyzing dose of metocurine was 0.44 +/- 0.11 (SD) micrograms/ml in exercised horses, and 0.58 +/- 0.22 micrograms/ml in nonexercised horses. Despite evidence for a response to conditioning, a significant change in the sensitivity of the neuromuscular junction to metocurine was not found.

Twelve Beagles were inoculated with concanavalin A, and after a mean ninefold increase in antibody titer, 1 mg of concanavalin A was infused into each renal artery of each dog to induce in situ immune complex glomerulonephritis. Starting 4 weeks after renal arterial infusion, 6 dogs were treated orally 3 times daily with 30 mg of 3-methyl-2 (3 pyridyl)-1-indoleoctanoic acid (CGS 12970)/kg of body weight, a thromboxane synthetase inhibitor, and 6 dogs (control group) received a gelatin capsule 3 times daily. Endogenous creatinine clearance and 24-hour urinary excretion of protein and thromboxane B2 were determined for each dog prior to renal arterial infusion, at the initiation of treatment and at 2, 4, 6, and 8 weeks after initiation of treatment. In addition, methyoxy-(3)H inulin clearance was determined at initiation of treatment and 4 and 8 weeks later. Renal specimens were examined histologically at the initiation of treatment and 4 and 8 weeks later. Glomerular mononuclear profiles/micrometers(3) were determined from at least 10 equatorially sectioned glomeruli from each dog. Paired t tests were used to compare mean values at the various time points to the respective mean baseline value and 2-sample t tests were used to evaluate differences between treatment groups. At the start of treatment (4 weeks after renal arterial infusion of concanavalin A), histologic evaluation of renal specimens revealed glomerular epithelial crescent formation, mononuclear cell proliferation, and infiltration of neutrophils. Mononuclear cell profiles and urinary excretion of protein and thromboxane B2 were significantly increased, but endogenous creatinine clearance values were unchanged. Treatment with CGS 12970 did not affect endogenous creatinine clearance, methyoxy-(3)H inulin clearance, or glomeruli, however, CGS 12970 treatment significantly decreased urinary excretion of protein and thromboxane B2 when compared with values in the control group. These findings suggested that thromboxane has a role in the pathogenesis of established glomerulonephritis and that thromboxane synthetase inhibition treatment may be beneficial in dogs with established glomerulonephritis.

Several pharmaceutical compounds were evaluated for their ability to selectively inhibit activated coagulation factor-XIII-like enzyme activity (eg, XIIIa) in pooled equine plasma. Presence of coagulation factor-XIIIa -like enzyme activity in plasma was established by assay procedures involving incorporation of the fluorescent amine compound, monodansylcadaverine, into purified casein, which served as a protein substrate. Pharmaceuticals inhibitory to coagulation factor-XIIIa -like enzyme activity were recognized by plasma gel formation of high spectrophotometric transmittance (transparency), solubility of transparent fibrin gels in concentrated urea solution, in conjunction with simultaneous depletion of native fibrinogen fractions, and production of fibrin monomer. Compounds acting primarily as anticoagulants were recognized by lack of plasma gel formation, but retaining high spectrophotometric transmittance and no detectable depletion of native fibrinogen fractions. Compounds failing to inhibit either thrombin-mediated fibrinogen-fibrin transformation (ie, coagulation) or coagulation factor-XIIIa -like enzyme activity were recognized by opaque plasma gels caused by fibrin polymerization, low spectrophotometric transmittance values, and coinciding with depletion of native fibrinogen fractions. Pharmaceuticals capable of exerting selective inhibition of coagulation factor-XIIIa -like enzyme activity were further classified as competitive inhibitors of phase 1 (carbamide) or phase 2 (terminal amine) of the transglutamination process.

Intranasal (IN) and intratracheal (IT) oxygen administration techniques were compared by measuring inspired oxygen concentrations (FI(O2)) and partial pressures of arterial oxygen (Pa(O2)) in 5 healthy dogs at various IN (50, 100, 150, and 200 ml/kg of body weight/min) and IT (10, 25, 50, 100, 150, 200, and 250 ml/kg/min) oxygen flow rates. Intratracheal administration of oxygen permitted lower oxygen flow rates than IN administration. Each IT oxygen flow rate produced significantly higher FI(O2) and Pa(O2), than the corresponding IN flow rate. An IT oxygen flow-rate of 25 ml/kg/min produced FI(O2) and Pa(O2) Values equivalent to those produced by an IN oxygen flow rate of 50 ml/kg/min. An IT oxygen flow rate of 50 ml/kg/min produced FI(O2) and Pa(O2) values equivalent to those produced by IN oxygen flow rates of 100 and 150 ml/kg/min. All IT oxygen flow rates greater than or equal to 100 ml/kg/min produced FI(O2) and Pa(O2) values that were greater than FI(O2) and Pa(O2) values produced by IN oxygen flow rates of 200 ml/kg/min. The lowest flow rates studied (50 ml/kg/min, IN, and 10 ml/kg/min, IT) produced Pa(O2), capable of maintaining 97% hemoglobin saturation, which should be adequate for most clinical situations. Arterial blood gas analysis and FI(O2) measurements are necessary to accurately guide oxygen flow adjustments to achieve the desired Pa(O2) and to prevent oxygen toxicity produced by excessive FI(O2).

Sixty-eight cattle under general anesthesia were splenectomized. The transthoracic approach was used to provide better access to the spleen and to facilitate ligature of the major splenic vessels. The procedure was easier and less time-consuming, compared with other surgical approaches, and is considered to be less stressful to the animals. Postoperative recovery was complete in 67 of 68 cattle. After surgery, 1 animal developed respiratory tract disease that was thought to have been unrelated to the surgery.

A murine hybridoma monoclonal antibody (MAB), IBF9, was generated by fusing myeloma cells (P3X63Ag8.653) with spleen cells from a BALB/c mouse immunized with the canine melanoma cell line CML-10c7. Initial screening of hybridoma antibodies was performed by use of an indirect immunoperomidase assay on formalin-fixed CML-10c7 cells. The isotype of MAB IBF9 was IgG1 as determined by radial gel immunodiffusion. The antibody was tested for reactivity against a panel of formalin-fixed, paraffin-embedded normal and neoplastic canine tissues, using immunoperoxidase staining. Immunostaining was observed in melanomas (24 of 38), a few carcinomas, basal cell tumors, and cutaneous lymphosarcomas. Immunostaining was not observed in fibrosarcomas, hemangiosarcomas, hemangiopericytomas, or histiocytomas. Staining of normal adult canine tissues was limited to a few epithehal tissues and a small percentage of lymphocytes. Fetal tissues were not reactive with MAB IBF9. There were statistically significant differences in frequency of reactivity among melanomas with regard to oral vs non-oral, malignant vs benign, and mitotic indices greater than or equal to 1 vs mitotic indices < 1. Differences were not significant when tumors were compared for degree of pigmentation or histologic type. On the basis of these findings, we suggest that MAB IBF9 may be of assistance in diagnosis of nonpigmented melanomas and in assessing the malignant potential of melanomas.

Because hepatocyte-stimulating factor/interleukin 6 (IL-6) the principal inducer of acute-phase protein synthesis in the liver, quantification of its activity in blood provides an early and sensitive assessment of the acute-phase response. Circulating IL-6 activity was monitored in 4 adult horses for 72 hours after IV administration of endotoxin. In 4 experiments performed at weekly intervals and in randomized order, each horse was given endotoxin-1,000, 30, 1, and 0 ng/kg of body weight. Plasma IL-6 activity was quantified as the ability to promote growth of the IL-6-dependent B-cell hybridoma, B13.29 clone B9. Interleukin-6 activity (171 +/- 10.2 U/ml) was found in all pretreatment plasma samples and was significantly (P < 0.05) increased above baseline from 2 to 12 hours after 1,000 ng of endotoxin/kg was given and at 3 hours after 30 ng of endotoxin/kg was given. After 1,000- or 30-ng/kg dosage of endotoxin, peak plasma IL-6 activity (10,128 +/- 4,096 and 1,555 +/- 1,326 U/ml, respectively) was observed for 3 hours. The IL-6 response of endotoxin-treated horses began about 1 hour after tumor necrosis factor appeared in the circulation, and its course closely approximated the endotoxin-induced febrile reaction. Significant increase in plasma IL-6 activity was not detected in horses given 1 ng of endotoxin/kg or control buffer.