Epidermal growth factor was injected intracamerally into the anterior chamber of the right eye of 9 cats. The central portion of the cornea in 8 of the 9 cats that had been cryoinjured. Effect of epidermal growth factor on the repair of endothelial cells in cats was evaluated by endothelial specular microscopy. Endothelial cell density and corneal thickness were studied quantitatively, as a measure of endothelial cell function. The repair process also was evaluated qualitatively by studying morphologic changes, developing as a result of reendothelialization and return to normal function. Seemingly, differences between rate of healing of cryoinjured eyes injected with epidermal growth factor and that in nontreated eyes were not significant (P = 0.86). The endothelial repair process was characterized by enlargement and migration of adjacent noninjured cells.

Renal ultrasonographic changes were evaluated in 5 dogs administered 10 ml of commercial antifreeze (95% ethylene glycol)/kg of body weight, PO, and in 2 dogs given placebos. Studies were made prior to and after ingestion on an hourly basis over a period of 8 to 10 hours. All dogs were anesthetized immediately after toxin or placebo ingestion for the duration of the study. Renal cortical echogenicity was evaluated in comparison with that of the adjacent liver and spleen. Echogenicity of the renal medulla and definition of the corticomedullary juction were assessed. Within 4 hours after ethylene glycol administration, renal cortical echogenicity of all intoxicated dogs increased from normal to surpass that of the liver and approach or equal that of the spleen. Medullary echogenicity in all intoxicated dogs progressively increased over the course of the study, with changes recognized within 5 hours after ethylene glycol administration. An ultrasonographic pattern consisting of nearly equal, marked increase in cortical and medullary echogenicity and relatively hypoechoic corticomedullary junction and central medullary regions was recognized concurrent with the development of anuria in 3 of the 5 intoxicated dogs. Mild, transient increases in cortical and medullary echogenicity were observed in anesthetized control dogs. However, no statistical difference (P less than 0.05) was detected between baseline, peak, and terminal echogenicity values in these dogs. Blood and urine samples were collected hourly from intoxicated dogs to coincide with ultrasonographic studies. Most clinicopathologic values derived from these samples were not statistically different (P less than 0.05) from those reported in a study that used a similar intoxication protocol in nonanesthetized dogs.

Ontogeny of the third component of complement (C3) was monitored in 10 neonatal swine, using a radial immunodiffusion technique. Significant differences in mean serum C3 concentrations, expressed as percentage of C3 concentration in a pooled standard drawn from 15 adult swine, were not observed between serum samples collected before pigs suckled and at 2 days of age (P = 0.2583). Serum C3 concentrations increased significantly between 2 and 7 days of age (P less than 0.0001) and 7 and 14 days of age (P less than 0.0001). Concentrations comparable with those in adults were not observed at 14 days of age and significant changes were not observed thereafter. Acquisition of adult concentrations of C3 appeared to be a function of endogenous production by the neonate, rather than by passive colostral transfer.

The effect of aspirin on bovine platelet function and thromboxane A2 (TXA2) production in stimulated platelets was evaluated. A single dose of aspirin (100 mg/kg of body weight) was administered orally to Holstein cows, and blood samples were obtained before and at regular intervals for 7 days after treatment. The production of TXA2 was assessed by measuring the stable metabolite thromboxane B2, using a specific radioimmunoassay. Within 4 hours of aspirin administration, the production of TXA2 was significantly (P less than 0.05) decreased, irrespective of whether collagen, adenosine diphosphate, or platelet activating factor was used to initiate platelet aggregation. Despite the inhibition of TXA2 release from the stimulated platelets, platelet function, assessed by initial rate of aggregate formation and extent of aggregation, was unaffected by aspirin administration. The extent of aggregate formation in response to collagen, adenosine diphosphate, or platelet activating factor was independent of the amount of TXA2 released from platelets before and after aspirin treatment. The results suggested that TXA2 formation is not the primary biochemical pathway involved in the aggregation of stimulated bovine platelets.

The uptake of colostral IgG and IgM, their serum half-lives, and the rates of endogenous synthesis of IgG and IgM were evaluated in 6 newborn foals fed bovine colostrum (principals) and 6 foals allowed to suckle their dams (controls). The principal foals were fed 400 ml of bovine colostrum (IgG, 10,000 mg/dl and IgM, 200 mg/dl) at 2-hour intervals, from 2 to 20 hours after foaling (total dose, 4 L). Serum IgG and IgM concentrations were determined by single radial immunodiffusion from birth to 98 days of age. At foaling, principal foals had no detectable serum equine IgG, but 1 control foal had serum equine IgG of 185 mg/dl. AFter ingestion of colostrum, there was no significant difference in the maximal serum bovine IgG concentration (range, 1,350 to 3,300 mg/dl) in the principal foals, and maximal serum equine IgG concentration (range, 500 to 6,000 mg/dl). The calculated biological bovine and equine IgG half-life in the principal and control groups was 9.4 and 26 days, respectively. Endogenous IgG synthesis was first detected in 1 principal foal at 3 days of age, but was detected first between 28 and 42 days in the other principal foals. Starting on day 56 there was no significant difference in serum equine IgG concentration between groups. At foaling, foals in both groups had low equine IgM concentrations. In the control foals, there was marked individual variation in the increases in equine IgM concentration (range, 5 to 73 mg/dl) after ingestion of colostrum. With the exception of day 49 after foaling, there was no statistical difference between groups for serum IgM concentration after day 3, and both groups had parallel rates of IgM synthesis. Bovine IgM was undetectable at foaling and maximal serum concentration ranged from 200 to 350 mg/dl following ingestion of colostrum. The calculated bovine and equine IgM half-lives were 8 and 5 days, respectively. The coefficients of absorption of bovine IgG and IgM were 30.9 and 84, respectively, in the principal foals. In the control foals, the coefficient of absorption of equine IgG and IgM was 35 and 30, respectively. One principal foal was excluded from the study because it died of aspiration pneumonia at 2 days of age.

Tissue specimens from muscle, liver, kidney, and injection sites were collected, and serum was obtained from 3 calves euthanatized on each of posttreatment days 5 and 22. Calves were treated with 6.7, 13.4, or 20 mg of oxytetracycline (OTC)/kg of body weight, IM, once daily for 3 days; these dosages are 1, 2, and 3 times the label dose, respectively. One control calf was euthanatized on each of posttreatment days 5 and 22. In treated male calves killed 2 days after the last injection, OTC residues were detected in all tissues and serum, using high-performance liquid chromatography. Tissues from all injection sites also were considered positive for antimicrobial residues, using swab test on premises (STOP), microbial inhibition test (MIT), and thin-layer chromatography-biautography (TLCB) test. Kidney tissues from a calf given 13.4 mg of OTC/kg and kidney and liver tissues from a calf given 20 mg of OTC/kg also were considered positive, using the MIT and TLCB. Results of the STOP only were considered positive for the liver and kidney of a calf given 20 mg of OTC/kg, but substitution of Saskatoon antibiotic medium-3 for the original medium (antibiotic medium-5) allowed the STOP to detect residues in these tissues from all treated calves. In female calves killed 19 days after the last injection, the STOP, MIT, and TLCB procedures revealed positive results for tissues from some injection sites, but revealed negative results for other tissues. High-performance liquid chromatographic analyses detected OTC in tissues from injection sites from all treated calves, in muscle and liver from a calf given 20 mg of OTC/kg, and in kidneys from calves given 13.4 or 20 mg of OTC/kg. The STOP, MIT, and TLCB procedures lacked the sensitivity of high-performance liquid chromatography for detection of OTC residues. However, the STOP procedure with Saskatoon antibiotic medium-3 did perform appropriately in that it failed to detect label doses in tissues from injection sites, but did detect 2 and 3 times extralabel doses after the recommended withdrawal time, and results were considered positive for all tissues after 2 days of withdrawal. A significant (P less than 0.05) loss of OTC was not observed after samples were stored at -20 C for 80 days. The highest concentration of OTC residues persisted in kidneys and tissues from injection sites.

Four healthy cats were given clindamycin orally in daily doses of 25 or 50 mg/kg of body weight for 6 weeks. Significant change in Factor-VII activity was not found, compared with pretreatment values. In 2 cats tested, toxin produced by Clostridium difficile was not detected in fecal samples obtained before treatment and at 6 weeks after treatment, suggesting that intestinal overgrowth by C difficile did not develop. Results of the study seemed to indicate that orally administered clindamycin does not measurably reduce synthesis of vitamin K-dependent clotting factors in healthy cats.

Serologic recognition of common lipopolysaccharide core antigens has been related to enhanced resistance to gram-negative bacterial disease in several species. Class-specific titers (IgG, IgM) were determined by direct ELISA, using intact Escherichia coli (J5) as a plate antigen. Serum samples were obtained from 224 neonatal swine between the ages of 36 and 60 hours. The mean (+/- SEM) log(10) IgG titer against gram-negative core antigens was 1:1,713 +/- 0.4718 and the mean log(10) IgM titer was 1:202 +/- 0.5644. The IgG titer was directly related with litter size, birth weight, and serum total IgG concentration; IgM titer was directly related with dam parity and serum total IgG concentration.

Antiparasitic efficacy of ivermectin against migrating Gasterophilus intestinalis was evaluated in 36 treated and 24 nontreated (n = 12) or vehicle-treated (n = 12) ponies experimentally and naturally infected with G intestinalis and naturally infected with G nasalis. Each pony was experimentally infected with 500 G intestinalis lst instars in 2 divided doses on days -14 and -7 before treatment. On day 0, ivermectin was administered at the rate of 200 microgram/kg of body weight by IV (n = 12) or IM injection (n = 12) or given as an oral paste (n = 12). Ponies were euthanatized and necropsied 21 days after treatment. In each nontreated or vehicle-treated pony, late lst-, lst- to 2nd-instar molt, and early 2nd-instars of G intestinalis were found in the mouth, and 2nd- and 3rd instars of G intestinalis and 3rd instars of G nasalis were found in the stomach. Bots were not found in any ivermectin-treated pony and, thus, ivermectin was 100% effective against oral and gastric stages. Adverse reactions were not observed in ponies given ivermectin by IM injection or orally, but 1 pony given the vehicle IV and 1 pony given ivermectin (in the vehicle) IV had an anaphylactic reaction, resulting in death of the ivermectin-treated pony. It was speculated that the adverse reaction was caused by histamines released in response to vehicle components given by IV injection.

The effects of pneumonia on the pharmacokinetics of erythromycin administered IM and the tissue concentration changes with time were evaluated in 2-month-old calves. Pneumonia was induced by injection of Pasteurella haemolytica cultures through the thoracic wall into each lung. Six days prior to induction of pneumonia, erythromycin (15 mg/kg) was administered in a single IM dose. Erythromycin was administered again 48, 72, and 96 hours after injection of P haemolytica. On the third day of erythromycin administration (96 hours), the calves were serially euthanatized in groups of 4 calves each at 2, 5, 8, 12, 18, and 24 hours after the final dose was given. Tissue concentrations of erythromycin in kidney, liver, lung, muscle, CSF, and serum were determined. Neither the serum concentrations nor the overall pharmacokinetic values were significantly (P less than or equal to 0.05) changed by pneumonia. The concentrations of erythromycin were maximal at 5 hours for liver, muscle, and serum and at 8 hours for CSF, kidney, and lung. Serum and muscle concentrations were similar, whereas concentrations in CSF were lower than in serum and higher in kidney, liver, and lung. The lung/serum ratios were approximately 2.5 to 3 at 8 through 24 hours after IM administration. The peak concentration in lung was approximately 6 microgram/per gram at 8 hours.