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.

Pharmacologic effects of alpha-methylfentanyl and 3-methylfentanyl, analogs of fentanyl, were investigated in mares. The ability of an 125I-labeled fentanyl radioimmunoassay (125I-RIA) to detect these methylated fentanyl analogs in individual and pooled urine samples from horses was evaluated. Also, the ability of 7 fentanyl antibodies to react with fentanyl and fentanyl derivatives (sufentanil, alfentanil, and carfentanil) was investigated. Mares were studied in a locomotor test to determine the amount of stimulation methylated fentanyl analogs might induce. Two mares each were given alpha-methylfentanyl at 1, 2, 4, 8, or 13 microgram/kg of body weight, IV, or 3-methylfentanyl at 0.4, 0.7, or 1 microgram/kg IV. The cross-reactivity of sufentanil, alfentanil, carfentanil, alpha-methylfentanyl, and 3-methylfentanyl with 7 fentanyl antibodies was studied, using the 125I-RIA. All fentanyl analogs, with the exception of alfentanil, cross-reacted well with a C1 antibody raised to fentanyl. Less satisfactory cross-reactivity was determined with 6 other antibodies raised to fentanyl derivatives. When the C1 antibody was combined with an iodinated analog to fentanyl, good detectability of alpha-methylfentanyl and 3-methylfentanyl, in terms of fentanyl equivalents, was obtained from urine samples of dosed mares. The ability of the 125I-RIA to detect methylated fentanyl analogs in forensic urine samples pooled in groups of up to 20 samples was evaluated. When these methylated analogs were administered to mares in doses that induced measurable locomotor stimulation, the analog's presence was readily detected in individual or pooled samples.

Lumbar and thoracic vertebrae of the extinct horse, Equus occidentalis, were examined for gross and radiographic evidence of overriding spinous processes. Of 2,661 vertebrae examined, 580 had intact spinous processes. Thirty-six intact spinous processes, which appeared grossly similar to overriding spinous processes in the modern domestic horse, E caballus caballus, were radiographed. Of these 36 vertebrae, 2 had radiographic signs compatible with a radiographic diagnosis of overriding spinous processes, ie, radiographically observed lysis and/or sclerosis. Seemingly, weight bearing or other stresses imposed by human beings may not have induced the signs of overriding spinous processes.

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.

Resistance of gram-negative bacteria to gentamicin has become an increasingly common problem among clinical isolates from human beings. Susceptibility of isolates from horses to gentamicin and amikacin was evaluated for the period from July, 1983 to June, 1985. All isolates of Escherichia coli, and species of Enterobacter, Klebsiella, Proteus, and Pseudomonas examined were susceptible to amikacin, except 2 of the 46 Pseudomonas isolates. In contrast, 13 to 50% of isolates were resistant to gentamicin. Escherichia coli, and Klebsiella, Proteus, and Enterobacter species isolates were highly significantly more susceptible to amikacin (P less than 0.01) than to gentamicin. Pseudomonas spp (P = 0.13) were not significantly different in susceptibility to the 2 drugs. There was significant variation among genera in their susceptibility to gentamicin (P = 0.002), primarily because of the frequency of resistance in isolates of Klebsiella spp and Proteus spp, compared with the other 3 organisms (E coli, Enterobacter spp, and Pseudomonas spp). There was no significant difference of susceptibility to amikacin among the genera studied (P = 0.06).

Arthrotomies of middle carpal joints were done on 13 horses, and a 1-cm partial thickness, round defect was made on the radial facet of both third carpal bones. In one joint, 1-mm diameter 1-cm deep holes were drilled within the defect, and one joint was used as a control. Horses were assigned to 2 groups--group 1 (n = 6 horses), 5 drill holes; group 2 (n = 7 horses), 11 drill holes. At 1 and 3 weeks after surgery, differences between joints in synovial fluid total protein values, WBC counts, or results of mucin precipitate tests were not significant (P = 0.005). Physically and radiographically, horses were the same during the 12 initial weeks they were housed in stalls and the 9 weeks they were kept in paddocks. Twenty-one weeks after surgery, horses were euthanatized. Joints with drill holes had a significantly greater area (P less than 0.05) of healthy fibrocartilage new tissue: group 1--33 to 68% new tissue, compared with 0 to 23% new tissue in controls; and group 2--22 to 64% new tissue, compared with 0 to 37% new tissue in controls. Differences between healing of defects with drill holes in groups 1 and 2 were not significant. Thickness of new tissue over drill holes was 33 to 61% of thickness of cartilage adjacent to the defect, and thickness of tissue between drill holes was 11 to 43% (group 1) and 8 to 79% (group 2) of the thickness of cartilage adjacent to the defect. In all defects with drill holes, new tissue in the form of fibrocartilage was detected deep in drill holes, whereas fibrous tissue was observed superficially and adjacent to drill holes.

Eight adult cats were inoculated IV (n = 6) or SC (n = 2) with Ehrlichia risticii-infected P388Dl (continuous murine macrophage) cells or with E risticii released from P388D1 cells. Three additional cats were inoculated with organism-free P388D1 cultured monocytes, and 1 cat, which served as a medium control, was inoculated with balanced salt solution. Clinical signs of illness were observed in the IV inoculated cats from which E risticii was isolated. One cat developed intermittent diarrhea between postinoculation days (PID) 8 and 18, and the other cat developed lymphadenopathy, acute depression, and anorexia between PID 20 and 24. Ehrlichia risticii was isolated in cultures from 2 of 6 IV inoculated cats on PID 6, 10, and 17. Both cats were inoculated with E risticii released from the P388D1 cells. Ehrlichia risticii was not isolated from SC inoculated cats or from control cats. All 8 cats inoculated with E risticii seroconverted between PID 10 and 23. A pony inoculated with E risticii isolated from 1 of the inoculated cats developed clinical signs of equine monocytic ehrlichiosis including fever, anorexia, depression, and mild colic. Ehrlichia risticii was isolated from the blood of this pony on PID 7, 9, 11, and 16.