In this study, we tested the hypothesis that erythrocyte deformability is decreased in the development of cardiac failure induced by NaCl toxicosis. Deformability of erythrocytes and routine hematologic and biochemical variables were measured in 6 of 50 chickens that were given 5 g of NaCl/L in their drinking water from day 7 to day 42, and were compared with values in 6 of 50 healthy chickens given free access to tap water. Deformability was assessed by passing a 10% suspension of erythrocytes through a polycarbonate membrane with 5 micromoles pores. Chickens were euthanatized and heart and body weights were determined. Treatment with NaCl induced right-sided cardiac failure up to day 28. The ratios of heart weight to body weight were greater, for right ventricle by 20 to 64% and for left ventricle by 15 to 27%, attributable to NaCl treatment. Deformability of erythrocytes of NaCl-treated chickens was markedly decreased, in association with increased erythrocyte size and plasma Na+ concentration. However, only part of the decreased deformability could be explained by swelling of erythrocytes. Decreased deformability could not be explained by increased cell viscosity because mean corpuscular hemoglobin concentration, the primary determinant of erythrocyte viscosity, was decreased. Because decreased deformability of erythrocytes has been demonstrated previously to be associated with increased vascular resistance, decreased deformability may have contributed to the development of right-sided cardiac failure in these chickens.

The temporal response of blood and serum proteins to chronic plasmapheresis was determined in 8 horses used in a commercial antibody enterprise. Plasmapheresis of between 4 and 11 L induced significant decreases in total protein, albumin, and IgG values. With the exception of a high hematocrit value for the first postplasmapheresis blood sample, there were no changes in erythrocyte or leukocyte measurements, and no changes in the proportions of serum protein in an electrophoretic profile. Regression equations generated for recovery of proteins after plasmapheresis indicated a return to preplasmapheresis values of total protein and albumin at approximately 1 month. Complications of repeated plasmapheresis were not detected when plasma extractions were done between 7 and 19 times at 30-day intervals.

Serum lipoprotein concentrations, routine serum biochemical values, and morphologic changes of the liver were evaluated in cats undergoing weight loss. Food was withheld from 6 obese and 6 control cats for 3 days (days 0 to 2), followed by feeding 50% of previous food intake for 26 days (days 3 to 28). Percutaneous liver biopsy specimens were obtained from all cats on days 0, 7, 14, and 28. Blood samples for serum biochemical analysis and lipoprotein profiles were obtained on days 0, 3, 7, 14, and 28. All cats lost weight throughout the study, and none developed signs of chemical illness, including those of idiopathic hepatic lipidosis syndrome. Serum total cholesterol concentrations decreased initially in all cats, but rapidly returned to normal after day 3 in obese cats, suggesting altered cholesterol metabolism during dietary restriction. Low-density lipoprotein concentrations decreased throughout the study in control cats, but were unchanged in obese cats. Examination of liver biopsy specimens from each cat revealed minimal lipid accumulation in all specimens, although some specimens contained hydropic degeneration.

A selected group of pharmaceutical compounds were evaluated for the ability to inhibit the biochemical activity of fibrinoligase (coagulation factor XIIIa) in pooled equine plasma. Criteria for the pharmaceuticals selected were based on the mechanism of the transglutamination biochemical reaction mediated by coagulation factor XIIa . These criteria were complemented by recognition of the molecular configuration and chemical composition of amino acid residue side chains involved in the process of covalent fibrin monomer polymerization (cross-linking, transglutamination) mediated by this enzyme. Each pharmaceutical was evaluated individually and in combination with other potential coagulation factor XIIIa inhibitors in an effort to detect additive and synergistic phenomenon. In this context, pharmaceuticals with a carbonylamide (eg, cefuroxime, Girard's reagent-P, prolinamide) were applied in concert with compounds with a terminal amine (eg, D-arginine, L-lysine) functional group. In concept, this method theoretically served to competitively simulate glutamine and lysine amino acid residues within strands of fibrin monomer substrate involved in phase I (carbonylamide) and phase II (terminal amine) of the transglutamination reaction (covalent fibrin monomer cross-linking). Halogen-dinitro and ethylene compounds were also evaluated because of their reported ability to inactivate enzyme systems dependent on an intact sulfhydryl group located at their biochemically active site (eg, cystine amino acid residue). This group of pharmaceutical compounds failed to inhibit the biochemical activity mediated by coagulation factor XIIIa in equine plasma.

A circular (5.5 mm diameter) full-thickness cartilage defect was created on the medial ridge of the talus in 12 skeletally mature dogs. In 6 dogs, the articular surface of the lesion was repaired, using an osteochondral graft obtained from the ipsilateral manus. The graft (digit I, first phalanx, distal articular surface and diaphysis) was contoured to obtain a press fit in the drilled talar recipient site. In 6 dogs, the lesion was not treated and healed by fibrous tissue replacement. Functional assessment (lameness, hock range of motion, joint stability, joint crepitus, and mid-femoral muscle circumference) was completed before surgery and at postoperative weeks 2 through 20. Radiographic assessment (periarticular soft tissue width, joint space width, osteophyte formation, and graft incorporation) was completed before surgery and at postoperative weeks 0, 6, 12, and 20. To facilitate histologic assessment, tissues were stained with toluidine blue and H&E. Histologic assessment of the articular surface on the surgically treated talus, ipsilateral tibia, and contralateral talus was completed, using a modification of the Mankin grading system. Subchondral bone was examined to assess graft viability and incorporation. Analysis of the ordinal data was completed, using a Mann-Whitney rank sum test. All dogs were fully weight bearing by postoperative week 7. Dogs without grafts had significantly (P = 0.036) better clinical function at postoperative week 6. Significant difference in functional assessment was not evident at postoperative week 20. Immediate postoperative radiographic assessment revealed significant (P = 0.005) difference between nongrafted and grafted groups. Significant difference was not observed at postoperative week 6, 12, or 20. All grafts appeared radiographically incorporated by postoperative week 12. All grafts restored joint surface congruity, whereas 3 of 6 nongrafted lesions had poor articular congruity. Of 6 grafts, 4 partially retained normal hyaline cartilage, resulting in significantly (P = 0.014) lower Mankin grades. Significant histologic differences between groups were not apparent when the apposing tibia and control talus were examined. Talar reconstruction by use of a phalangeal osteochondral graft is a viable surgical procedure. These data indicate that normal articular and subchondral architecture are more closely approximated by osteochondral reconstruction than by fibrous tissue repair.

We examined the efficacy of ivermectin in the control of ear mites (Psoroptes cuniculi) in rabbits. The study involved 40 female and 35 male rabbits that were known to be naturally infested with ear mites. After a period of acclimation to the animal care facilities, the rabbits were ranked on the visual appearance of any ear lesion and the number of mites on glycerin-dipped ear swabs. The rabbits were then randomly assigned to 1 of 4 treatment groups; vehicle only (group 1), 50 micrograms of ivermectin/kg of body weight (group 2), 100 micrograms of ivermectin/kg (group 3) and 200 micrograms of ivermectin/kg (group 4). The rabbits were treated by SC injections on day 0 and day 14 of the trial; thus, the total dose of ivermectin given to groups 1 through 4, was 0, 100, 200, or 400 micrograms/kg, respectively. The study ended 2 weeks after the last treatment. Ear lesions of the treated rabbits improved significantly (P < 0.001). By 28 days after the first treatment, the mean number of mites on the ear swabs (both ears) was 57.5 for untreated rabbits and 9.1, 0.5, and 2.5, respectively, for rabbits in groups 2, 3, and 4. The mean number of mites recovered from the ears of the untreated rabbits at necropsy was 24,297. For groups 2, 3, and 4, the mean number of mites recovered from the ears was 5,352, 96, and 96, respectively. The efficacy of treatment with a total dose of 100 micrograms/kg was 77.96%, with 200 micrograms/kg was 99.61%, and for 400 micrograms/kg was 99.61%.

When Salmonella typhimurium and Clostridium perfringens were tested in conventional chickens, larger numbers of S typhimurium and C perfringens adhered to Eimeria tenella-infected ceca than to uninfected ceca. In germ-free chickens, S typhimurium and C perfringens adhered to the E tenella-infected cecal mucosa more than to the uninfected cecal mucosa, but fewer Bacteroides vulgatus and Bifidobacterium thermophilum adhered to the E tenella-infected ceca than to the uninfected ceca. Many bacteria adhered to the lesions caused by E tenella as observed by scanning electron microscopy. On the basis of our findings, we suggest that infection with E tenella upsets the balance of competitive adherence of bacteria, allowing more colonization of S typhimurium and C perfringens.

The nature of Mycoplasma arthritidis antigens responsible for eliciting protective immunity in rats was studied by inoculation of rats with mycoplasmal components that had been subjected to a variety of physical and chemical treatments. All inocula tested induced good protection against development of clinical illness, as assessed by changes in body weight and appearance of joint swelling and/or temporary hind limb paralysis. Although all preparations stimulated development in inoculated rats of high titer of antimycoplasmal antibodies measured by ELISA, the complement-fixation antibody response was poor and, in some cases, lacking altogether. This indicated that completion-fixation antibodies may not be involved in protecting rats against M arthritidis-induced illness. Protective antigens were stable to heat (100 C for 10 minutes), formalin, and denaturation by sodium dodecyl sulfate (SDS). Inoculation with membrane and soluble cytoplasmic fractions was protective, as was inoculation with 5 M arthritidis fractions separated according to molecular weight by SDS-polyacrylamide gel electrophoresis (SDS-PAGE). For this latter experiment, rat antisera obtained after vaccination, but prior to challenge exposure, were tested by immunoblot analysis against electrophoretically separated M arthritidis membrane proteins. Interestingly, all antisera from these rats recognized antigens migrating far outside the molecular weight range of the cell fractions with which rats were inoculated. This indicated either that the protective antigens may be composed of numerous antigenically related subunits that separated by SDS-PAGE into a variety of molecular weight ranges or that a few major antigens may exist in several forms or phases within a given population of M arthritidis.

Atracurium besylate, a nondepolarizing neuromuscular blocking agent, was administered to 24 isoflurane-anesthetized domestic chickens. Birds were randomly assigned to 4 groups, and atracurium was administered at dosage of 0.15, 0.25, 0.35 or 0.45 mg/kg of body weight. The time of onset of twitch depression, the amount of maximal twitch depression, and the duration of muscular relaxation were recorded. After return to control twitch height, atracurium was further administered to achieve > 75% twitch depression. When twitch depression reached 75% during noninduced recovery, 0.5 mg of edrophonium/kg was administered to reverse the muscle relaxation. Throughout the experimental period, cardiovascular, arterial blood gas, and acid-base variables were monitored. The effective dosage of atracurium to result in 95% twitch depression in 50% of birds, (ED95/9595) was calculated, using probit analysis, to be 0.25 mg/kg, whereas the ED95/95 the dosage of atracurium to result in 95% twitch depression in 95% of birds, was calculated by probit analysis to be 0.46 mg/kg. The total duration of action at dosage of 0.25 mg/kg was 34.5 +/- 5.8 minutes; at the highest dosage (0.45 mg/kg), total duration increased to 47.8 +/- 10.3 minutes. The return to control twitch height was greatly hastened by administration of edrophonium. Small, but statistically significant changes in heart rate and systolic blood pressure, were associated with administration of atracurium and edrophonium. These changes would not be clinically relevant. In this study, atracurium was found to be safe and reliable for induction of muscle relaxation in isoflurane anesthetized chickens.

Clindamycin phosphate was administered to dogs at dosage of 11 mg/kg of body weight via IV and IM routes. The disposition curve for IV administration was best represented as a 2-compartment open model. Mean elimination half life was 194.6 +/- 24.5 minutes for IV administration and 234.8 +/- 27.3 minutes for IM administration. Bioavailability after IM administration was 87%. Dosage of 11 mg/kg, IV, given every 8 hours, provided serum concentration of clindamycin that exceeded the minimal inhibitory concentration for all Staphylococcus spp, as well as most pathogenic anaerobes, throughout the dosing interval. Intramuscular administration induced signs of pain and cannot be recommended.