The vasculature of 22 small colons from dead adult ponies was perfused with latex or barium sulphate solution. The vascular anatomy was studied by use of dissection and alkali digestion of the latex specimens and microangiography of the barium sulphate-perfused specimens. The small colon is supplied by the caudal mesentric artery. The left colic artery arises from the caudal mesenteric artery, which then becomes the cranial rectal artery. Branches from the left colic and cranial rectal arteries form anastomosing arcades that become narrower distally along the length of the small colon. From these arcades arise terminal arteries, which enter the small colon wall and give rise to a subserosal, an intermuscular, and a large submucosal plexus, with frequent anastomoses between them. The venous drainage closely parallels the arterial supply, except near to its origin from the portal vein, when the left colic vein and caudal mesentric vein are separate from the corresponding arteries.

The in vitro and in vivo binding of a monoclonal antibody (MAB) that recognizes a tumor-associated carbohydrate antigen was studied in dogs. Monoclonal antibody 155H.7 was raised in response to inoculation of mice with beta-galactose(1-3)betaN-acetylgalactosamine conjugated to human serum albumin. Avidin-biotin-complex immunohistochemical staining of cryostat sections of normal and neoplastic canine tissue specimens revealed heterogenous binding of MAB 155H.7 to the cells of many canine mammary and lung carcinomas and homogenous staining of many sarcomas, including osteogenic sarcoma. In addition, there was variable staining of a variety of normal tissues including some ductual epithelium, peripheral nerve fibers, and some endothelial cells and fibroblasts. Immunoscintigraphy with 131I-labeled MAB 155H.7 was used to study the in vitro distribution of the antibody. The 131I-labeled MAB 155.H.7 was administered to 1 clinically normal dog, 7 dogs with osteogenic sarcoma, 1 dog with undifferentiated sarcoma, and 2 dogs with mammary tumor. Scintigraphy revealed concentration of radioactivity in 8 of 10 tumor sites within 24 hours after MAB administration. The ratio of 131I in tumor sites to 131I in the surrounding normal tissues, compared with the similar ratio of 99mTc-labeled erythrocytes ranged from 1.1 to 4.3 in tumor vs normal tissue with a mean value of 2, confirming tumor localization of the radiolabeled MAB in excess of that associated with enhanced tumor vascularization.

Strain gauge rosettes were bonded to the dorsal, lateral, medial, and plantar aspects of the third metatarsal bone in the hind limbs of 6 ponies. The maximal compressive principal strain was approximately -600 X 10(-6) m/m, and exceeded the amplitudes of the tensile strains at all aspects of the bone. After transformation, the shear strain and the principal strains parallel and perpendicular to the bone were obtained. The first peak in the bending strain was higher in the dorsal and lateral aspects, and the second peak was higher in the medial and plantar aspects. Young modulus of elasticity was determined in a 4-point bending test at the dorsal and plantar sides; it averaged 19.5 GPa in tension and compression. Applying linear bending theory, the eccentricity of an axial force parallel or a bending force perpendicular to the bone were calculated. The position where the total force penetrated the tarsometatarsal joint surface was largely within the joint surface, indicating that the joint is merely loaded in (eccentric) compression.

A study was performed to determine the effect of proadifen hydrochloride on prostacyclin (prostaglandin I2 [PGI2]) and thromboxane A2 (TxA2) synthesis by equine peritoneal macrophages and the effect of proadifen on endotoxin-induced synthesis of PGI2 and TxA2 by equine macrophages. Peritoneal macrophages (2.5 X 10(6)/ml) were incubated for 6 hours in tissue culture media containing 1) nothing (nontreated control), 2) proadifen hydrochloride (20, 100, 250, and 500 micromol/L, 3) endotoxin (5 ng/ml), or 4) the calcium ionophore A23187 (0.95 micromol/L). In a second series of experiments, peritoneal macrophages were incubated with endotoxin (5 ng/ml) and proadifen (250 micromol/L), for 6 hours. Concentrations of 6-keto-prostaglandin F 1alpha (6-keto-PGF 1alpha) and thromboxane B2, the stable metabolites of PGI2 and TxA2, were determined in the incubation media by radioimmunoassay. Proadifen caused increased synthesis of PGI2 by equine macrophages, without affecting TxA2 production. The increased PGI2 production was similar to that induced by endotoxin and calcium ionophore; however, the latter 2 agents significantly stimulated TxA2 production as well (P less than 0.05). There were no significant differences among mean concentrations of 6-keto-PGF 1alpha in media from macrophages treated with 100, 250, or 500 micromol/L proadifen, but there was a significant curvilinear regression between their concentrations. The ratio of thromboxane B2 to 6-keto-PGF 1alpha was significantly lower than baseline in incubation media from macrophages exposed to proadifen, endotoxin, and calcium ionophore. Proadifen hydrochloride did not significantly change equine peritoneal macrophage production of PGI2 or TxA2 in response to endotoxin.

Cell proliferation kinetic values were established for the epidermis, hair follicle epithelium, and sebaceous glands of 8 Cocker Spaniels with primary idiopathic seborrhea. Values were established by intradermal pulse labeling injections of tritiated thymidine followed by cutaneous biopsy and autoradiography.The epidermal basal cell-labeling index was 4.96 +/- 0.97%, and the epidermal nucleated cell-labeling index was 3.33 +/- 0.71%. Calculated epidermal cell renewal time for the viable layers of the epidermis was 7.85 +/- 1.80 days. The hair follicle infundibulum basal cell-labeling index was 5.48 +/- 2.01%, and the sebaceous gland basal cell-labeling index was 5.94 +/- 4.15%. When compared with previously reported cell kinetic values for Cocker Spaniels and Beagles with healthy skin, these data indicate accelerated cellular proliferation in all 3 cutaneous structures in seborrheic Cocker Spaniels.

Efficacy of oral administration of 20 mg of triclaben-dazole/kg of body weight was evaluated against 12-week Fascioloides magna infections in 12 sheep, each inoculated orally with 250 viable metacercariae. From 6 sheep treated with triclabendazole, 1 immature F magna was recovered, whereas 116 F magna with a mean length of 19 +/- 6.5 mm were recovered from 6 untreated control sheep. Efficacy of triclabendazole was 99.14%. Signs of toxicosis or illness were not observed in the sheep.

A study was conducted to compare immunogenicity of a Brucella abortus lipopolysaccharide (LPS) and the duration of infection in 5 strains of mice. Mice of strains CBA/NJ, BALB/c, CD-1, C3H/HeN, and C3H/HeJ were allotted into 2 large groups (vaccinated with proteinase K-treated LPS or nonvaccinated) and 6 subgroups based on the intervals between challenge exposure to B abortus strain 2308 and the week the response data were obtained. Criteria used in comparing responses between the various strains of mice as well as betweeen vaccinated and nonvaccinated mice were splenomegaly, colony-forming units (CFU) from spleens, and antibody titers. Responses were evaluated at 1, 2, 3, 5, 8, and 12 weeks after challenge exposure. Results indicated that all strains of mice became infected and maintained infection throughout the 12-week period, the percentages of mice infected were significantly (P less than 0.05) less in vaccinated mice for the first 5 weeks after challenge exposure, and there were no direct correlations between increased immunoglobulins (IgM and IgG titers) and reduction in CFU. Vaccinated mice of strains BALB/c, CD-1, C3H/HeN, and C3H/HeJ had increased titers when challenge exposed and also had significantly (P less than 0.05) smaller spleens and lower CFU. Vaccinated CBA/NJ mice did not have marked antibody titers. The overall results indicated that vaccination with LPS offers some initial protection against B abortus strain 2308 infection, but this protection disappears gradually and in various degrees in the 5 strains of mice studied.

The relationship of serum complement activity and bacteriostatic activity was investigated in male guinea pigs given aflatoxin and/or rubratoxin. In experiment 1, guinea pigs were given 0.6 mg of aflatoxin/kg of body weight, PO, once. In experiment 2, guinea pigs were given 0.02 mg of aflatoxin/kg, PO, and/or 8 mg of rubratoxin, PO, 11 times. Aflatoxin (0.02 mg/kg) had no effect given alone, but potentiated the effect of rubratoxin. In both experiments, changes in complement activity were accompanied by similar but not always significant (P less than 0.05) changes in bacteriostatic activity of serum. Guinea pigs given 0.06 mg of aflatoxin/kg had significant (P less than 0.05) changes in complement titers and in serum alkaline phosphatase, alanine aminotransferase, and aspartate aminotransferase activities. Guinea pigs given repeated oral doses of aflatoxin and/or rubratoxin had changes in complement titers, bacteriostasis, and alkaline phosphatase and aspartate aminotransferase activities, but not in alanine aminotransferase activities. Significant differences were detected only when average values for all guinea pigs given rubratoxin or rubratoxin with aflatoxin were compared with average values for guinea pigs not given rubratoxin.

Thirty-eight tracheobronchial aspirates (TBA) were collected from twenty 1 to 6-month-old foals, which were free of clinical signs of respiratory tract or other infectious disease. We collected TBA from 9 of the foals 3 times when they were approximately 8, 16, and 24 weeks old. Aspirates were examined cytologically after staining with modified Wright-Giemsa, Gram, toluidine blue, and prussian blue stains. Aerobic bacterial culturing was performed on all aspirates. Of the 20 initial TBA, 4 (20%) were normal cytologically on the basis of previously defined criteria for TBA from clinically normal horses, 6 (30%) had a high percentage of eosinophils (> 5%), 8 (40%) were classified as indicative of subacute inflammation, and 2 (10%) were classified as indicative of acute inflammation. Nine (45%) were positive for mast cells and none were positive for hemosiderin-laden macrophages (hemosiderophages). Of the 9 foals from which samples were collected at 16 and 24 weeks of age, results were similar, except for an increase in the number of TBA classified as indicative of chronic inflammation (33% and 22% respectively) and the number positive for hemosiderophages (33% and 88%, respectively). One TBA was considered nondiagnostic because of pharyngeal contamination. Culturing of 12 of the 37 aspirates (32%) yielded a potential microbial pathogen. Only 2 were positive cultures from the same foal. The following organisms were isolated: beta-hemolytic Streptococci spp (4), Actinobacillus/Pasteurella spp (4), Rhodococcus equi (2), unidentified nonenteric Gram-negative rod (1), and Escherichia coli (1). Thirty-four of the 37 aspirates (92%) yielded light growth of various organisms considered to be nonpathogenic and normal inhabitants of the upper respiratory tract. It was concluded that the presence of inflammatory cells, eosinophils, and mast cells in the tracheobronchial aspirates from clinically normal foals is a common finding. These cytologic findings were consistent in the samples collected from foals at 8, 16, and 24 weeks of age. It was also concluded that bacteria with recognized pathogenicity can be isolated from TBA from clinically normal foals and were most frequently isolated from 1- to 2-month-old foals or those with cytologic evidence of inflammation, even in the absence of clinical signs of respiratory tract disease.

Hemodynamic effects of spontaneous ventilation, intermittent positive-pressure ventilation (IPPV), and high-frequency oscillatory ventilation (HFOV) were compared in 6 dogs during halothane anesthesia. Anesthesia was induced with IV thiamylal Na and was maintained with halothane (end-tidal concentration, 1.09%). During placement of catheters, dogs breathed spontaneously through a conventional semiclosed anesthesia circuit. Data were collected, and dogs were mechanically ventilated, using IPPV or HFOV in random order. Ventilation was adjusted to maintain PaCO2 between 38 and 43 mm of Hg during IPPV and HFOV. Cardiac index, aortic blood pressure, and maximum rate of increase of left ventricular pressure were significantly (P less than 0.05) less during HFOV than during spontaneous ventilation, whereas right atrial and pulmonary artery pressure were significantly greater during HFOV than during spontaneous ventilation. During IPPV, only the maximum rate of increase of left ventricular pressure was significantly less than that during spontaneous ventilation.