The lungs of sensitized horses were exposed to aerosolized ovalbumin. Some horses (n = 4) were given ovalbumin in 1 lung only, whereas in others (n = 7), ovalbumin or vehicle were inoculated in the cranial, ventral, and caudal regions of the caudal lung lobe. Horses were exercised 5 hours after ovalbumin exposure. Immediately before exercise, endoscopy failed to reveal any abnormality. After exercise, endoscopic examination of horses subjected to unilateral ovalbumin exposure revealed extensive blood in airways leading to the exposed lung in all horses. Blood was not observed in the airways leading to the control lung. Mean (+/- SEM) minimum volume of the exposed and control lungs was 9.5 +/- 1.5 and 5.5 +/- 1.6 L, respectively; this difference was statistically significant (P < 0.05). Bronchoscopy of horses subjected to regional ovalbumin or vehicle exposure and exercise revealed a small amount of blood-tinged fluid in the bronchi serving the regions of the lung inoculated with ovalbumin. Minimum volumes of such regions were not significantly different from one another. However, their minimum volume was significantly (P < 0.05) larger than that of vehicle-inoculated regions. Gross and histologic examination confirmed inflammation and hemorrhage in the ovalbumin-exposed, but not the control lungs or lung regions. Thus, exercise can cause blood from an injured region of lung to appear in the larger airways. Regional differences in lung structure and function do not influence the appearance of blood in the airways.

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%.

Concentrations of serum and vitreous humor constituents at time of death, and concentrations of vitreous humor constituents at time of death and at 7 postmortem intervals were compared in 70 domestic, female New Zealand White rabbits (Oryctolagus cuniculus). Urea nitrogen concentration was significantly (P = 0.0094) different, but was linearly correlated in serum and vitreous humor at time of death and at the 4- and 8-hour postmortem intervals. Concentrations of gamma-glutamyltransferase were not significantly different in serum and vitreous humor at time of death, nor were concentrations significantly different in vitreous humor at time of death and at the 4-hour postmortem interval. The vitreous humor concentrations of glucose, triglycerides, sodium, potassium, cholesterol, total protein, albumin, lactate dehydrogenase, creatine kinase, aspartate transaminase, bilirubin, cortisol, and IgG were neither similar to nor predictive of serum constituents. Vitreous humor can be used as a source for estimates of serum urea nitrogen and gamma-glutamyltransferase up to 8 and 4 hours after death, respectively.

Disposition kinetics of indocyanine green (ICG) were used to evaluate hepatic function in healthy Beagles (group 1; n = 6) and Beagles with progressive hepatic disease induced by oral administration of dimethylnitrosamine, a hepatospecific toxin. Three classes of hepatic disease were defined by histologic features: mild (group 2; n = 5), moderate (group 3; n = 6), and severe (group 4; n = 5). Disposition of ICG was studied 3 weeks following the last dose of toxin. A rapid IV injection of 0.5 mg of ICG/kg was administered and serum samples were obtained at certain intervals during 60-minute periods. Serum ICG was analyzed by use of visible spectrophotometry. Disposition kinetics were determined from serum ICG concentrations vs 15- and 60-minute time curves and compared between one another and among groups. Data based on 60-minute time curves were not significantly different from those based on 15-minute curves. Area under the curve for ICG was greatest in group 3. Clearance of ICG was decreased and mean resident time was increased in groups 3 and 4, compared with those in groups 1 and 2. When disposition data (60 minutes) were normalized for differences in hepatic weight among dogs, group-3 mean resident time was significantly greater than that of group 4. This study supports the diagnostic benefits of using ICG disposition kinetics as a method of evaluating hepatic function in dogs with progressive liver disease.

The relationship between colloid osmotic pressure (COP) and protein concentration was investigated for purified proteins and plasma samples obtained from cattle, horses, dogs, and cats. At equivalent concentrations, bovine albumin exerted a cop that exceeded that of gamma-globulins by a mean factor of 4.4. Similar relationships between cop and protein were observed in the other species. Consequently, for a given total protein concentration, COP was dependent on the albumin/gamma-globulins ratio. A commonly used nomogram for estimating cop from protein concentration, the Landis-Pappenheimer equation, did not provide reliable results for plasma samples from these species.

Collection of exocrine pancreatic secretions from cattle by use of a single-unit cannula was performed. The major advantage of the cannula was simple technical management. A small pouch of the duodenum into which the major pancreatic duct drains was formed. Continuity of the duodenum was reestablished by end-to-end anastomosis. A side arm of the cannula was inserted into the pouch to collect exocrine secretions, and the main portion of the cannula was placed cranial to the anastomosis to return pancreatic secretions to the small intestine between collection periods. The accessory pancreatic duct was ligated in 2 of 4 cattle to evaluate possible secretory contribution from this source. All cattle remained healthy after cannulation, and cattle gained approximately 100 kg of body weight in the 5 months after surgery. The mean secretory rate for exocrine pancreatic secretion in cattle was 106 +/- 6.8 ml/h. There was no effect of feeding on the pattern of secretion nor were there significant differences between cattle. A fistula formed between the pouch and duodenum approximately 120 days after surgery in the first 2 cattle used. Development of fistulas was prevented for 300 days in subsequently prepared cattle by use of surgical mesh around the cannulas, leading to functional cannulation sites. Preparation of a duodenal pouch appeared useful for long-term studies of pancreatic exocrine secretion in cattle.

In each of 5 groups of dogs, 0.05 ml of 1 of the following solutions was injected into the anterior chamber of both eyes: phosphate-buffered saline solution, 0.001 microg of prostaglandin F2 alpha (PGF2 alpha), 0.01 microg of PGF2 alpha, 0.1 microg of leukotriene D4 (LTD4), and 1 microg of LTD4. A 10% solution of sodium fluorescein was injected IV (14 mg/kg of body weight) at the same time, and pupil size, intraocular pressure, and anterior chamber fluorescence were measured for 1 hour after injections. In a dose-dependent manner, Pgf2 alpha was a potent miotic. A significant effect on intraocular pressure was not detected when the groups given PGF2 alpha were compared with the control group. When compared with LTD4, PGF2 alpha Significantly (P < 0.05) increased the breakdown of the blood-aqueous barrier, as evidenced by increased fluorescein leakage into the anterior chamber. Leukotriene D4 caused a decrease in pupil size only at 5 minutes, compared with that of the control group. Intraocular pressure was greater (but not significantly) in the group given 1 microg of LTD4.

Monensin is an ionophoretic antibiotic, which selectively transports alkali metal cations across biological membranes. In growing swine, monensin toxicosis causes acute, degenerative cardiac and skeletal myopathy resembling vitamin E-selenium deficiency. Selenium is an essential trace element incorporated in glutathione peroxidase (GSH-Px), an antioxidant enzyme system that protects subcellular membranes. In our study, we examined the effects of monensin on body weight, Se balance, antioxidant status, and serum concentrations of selected minerals in growing pigs that were genetically hypo- or hyperselenemic (hypo-Se and hyper-Se, respectively). Three groups of eight 8-week-old pigs, each comprised of 4 hypo-Se and 4 hyper-Se pigs (76.4 +/- 3.0 and 106.3 +/- 10.3 ng of Se/ml of serum, respectively), were fed standard diets containing 0.1 mg of supplemental Se/kg of body weight, and either 0, 200, or 400 mg of monensin/kg for a 77-day period, followed by a 28-day monensin withdrawal period. On days 0, 7, 28, 56, 70, and 98, all pigs were weighed and blood was collected for determination of serum GSH-Px, creatine phosphokinase, and aspartate transaminase values, as well as serum concentrations of vitamin E, Se, Ca, Cu, Fe, K, Mg, Na, P, and Zn. Significance of main effects of monensin treatment, genetic Se status, and their interactions was tested by Fisher's variance ratio test, followed by conditional comparison of treatment means with a Bonferroni test. Signs of monensin toxicosis were not observed and monensin consumption had no effect on body weight, or serum creatine phosphokinase, aspartate transaminase, or Se values. However, pigs consuming monensin had consistently higher serum GSH-Px activities, possibly because of increased synthesis of this adaptive antioxidant enzyme. Interactions were not found between monensin and genetic Se status. Hyperselenemic pigs were heavier and had higher serum Se and GSH-Px values than hypo-Se pigs. Furthermore, hypo-Se and hyper-Se pigs were hypo- and hypercupremic, respectively, suggesting genetic regulation of copper status. It is likely that pigs with inadequate antioxidant status (hyposelenemia, hypocupremia) are more susceptible to diseases associated with cellular membrane damage, such as vitamin E-Se deficiency disease and monensin toxicosis.

Superficial digital flexor tendinitis was induced in each forelimb of 8 horses by injecting 4,000 U of collagenase into the midmetacarpal region of the tendon. In each horse, each tendon was treated 24 and 96 hours after the collagenase injection with sc injections of sodium hyaluronate (treated limbs) or an equal volume of 0.9% NaCl solution (control limbs). Exercise was restricted for the first 3 weeks of the study, and a controlled exercise program was instituted for the remainder of the study. Horses were evaluated clinically for lameness, tendon swelling, and midmetacarpal limb circumference. Ultrasonographic examinations were performed regularly (11 examinations/horse) throughout the study, and all horses were euthanatized 12 weeks after collagenase injections. Tendons from 4 horses were harvested for biomechanical testing, and samples were obtained from tendons from the remaining 4 horses for biochemical analysis of collagen. Samples were obtained from all tendons for microscopic evaluation. Significant differences between treated and control tendons were not noticed in any of the variables examined in live horses, although trends toward less lameness in treated limbs and toward better healing on ultrasonographic examination in control limbs were recorded. Significant differences were not noticed in biomechanical or biochemical evaluations, and the only significant (P < 0.05) microscopic finding was more severe inflammation in tendons from treated limbs. This study did not reveal significant benefits of treatment with sodium hyaluronate outside a synovial sheath on tendon repair in collagenase-induced tendinitis.

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.