Cortical bone screws were implanted into the proximal portion of the right and left radius and ulna of 6 newborn Quarter Horse foals as radiographic markers for measurement of growth. Distance between markers on a lateral radiographic view was measured. Radiographs were taken at 2-week intervals until the horses were 8 weeks old, at 4-week intervals until they were 48 weeks old, and at 12-week intervals until they were 72 weeks old. The proximal radius and ulna grew at similar rates during the 72-week period of evaluation, and growth continued throughout 72 weeks. The proximal radius grew 3.5 cm, and the ulna grew 3.4 cm. Although the rates of growth were similar, growth from the ulnar physis contributed only to the length of the olecranon; growth was not transmitted to the ulnar diaphysis distal to the cubital joint. The proximal radius slid distally in relation to the ulna as growth occurred at the proximal radial physis. These findings suggest that transfixing the ulna to the radius while growth is occurring at the proximal radial physis impedes the natural shifting process, and subluxation of the elbow can result. Severity of subluxation would be inversely related to the age of the horse at the time of transfixation.

Plasma luteinizing hormone and progesterone concentrations, time to onset of estrus, and pregnancy rates were determined in nonlactating anestrous does given 1 of 4 treatments: subcutaneous ear implants containing 3 mg of norgestomet for 9 days (NOR; n = 6); subcutaneous administration, using osmotic minipumps, of 250 ng of gonadotropin-releasing hormone (GnRH)/h for 48 hours (GnRH; n = 6); 3 mg of NOR for 9 days, followed immediately by 250 ng of GnRH/h for 48 hours (NOR + GnRH; n = 6); or no treatment (control; n = 6). During the 72-hour period after removal of NOR or insertion of GnRH pumps, 6 of 6, 0 of 6, 6 of 6, and 3 of 6 does were observed in estrus at a mean (+/- SE) of 49 (+/- 3.0), 0(+/- 0), 32 (+/- 2.0), and 35 (+/- 13.8) hours in groups NOR, GnRH, NOR + GnRH, and control, respectively. Time from end of treatment to peak concentrations of luteinizing hormone were 56 +/-4.0, 28 +/- 4.7, 34 +/- 4.3, and 41 +/- 9.7 hours (mean +/- SE) for NOR, GnRH, Nor +/- GnRH, and control, respectively. Peak concentrations of luteinizing hormone were significantly greater and occurred significantly later in does given NOR. Progesterone concentrations in does that became pregnant increased to concentrations greater than or equal to 1.0 ng/ml 3 to 5 days after breeding and remained high. Functional corpora lutea (CL) was found in 6 does that did not become pregnant, 1 CL was associated with pseudopregnancy and 1 CL was associated with ovulation prior to placement of the GnRH pumps. Functional CL failed to form in 10 of the 12 does in groups GnRH and control. Does had either continual low concentrations of progesterone (3 does) or short-term increases in concentrations of progesterone (7 does). Conception rates for does in groups NOR, GnRH, NOR + GnRH, and control were 83%, 0%, 50% and 0%, respectively. Four does given GnRH and 3 control does were observed in estrus and were bred during the subsequent 2-week period. All of these does, except 1 control became pregnant subsequent to these breedings. The treatments NOR and NOR + GnRH were effective in inducing a synchronized estrus in dairy goats. However, the use of bucks to detect estrus may have introduced the buck effect and enhanced the performance of NOR alone, which has not been this effective in other studies with small ruminants.

A study was conducted to determine whether dietary supplements with alpha-linolenic acid altered the ability of equine peritoneal macrophages to produce tumor necrosis factor (TNF) in response to endotoxin. Peritoneal macrophages were harvested from 6 healthy adult horses before and after the horses were fed a nutritionally balanced ration that contained 8% linseed oil as a source of alpha-linolenic acid. The macrophages were cultured in media containing no additives (control), endotoxin (0.5 to 50 ng/ml), or the calcium ionophore, A23187. Macrophage supernatants were collected after 6 and 24 hours' incubation and stored at -70 C. Tumor necrosis factor activity was estimated by a modified in vitro cytotoxicity bioassay, using the murine fibrosarcoma cell line, WEHI 164 clone 13. The TNF activity after 6 and 24 hours' incubation was greater in culture media of macrophages exposed to endotoxin than in media from control macrophages. For macrophages cultured in media that contained endotoxin, neither the concentration of endotoxin nor incubation time had any effect on TNF activity. Endotoxin-induced macrophage production of TNF, as determined by measurement of TNF activity, was significantly less after horses were fed the alpha-linolenic acid-rich ration for 8 weeks.

Sixty-three drugs, belonging to 10 chemical classes, were tested in vitro to determine effects on phagocytosis of 32P-labeled Staphylococcus aureus by neutrophils isolated from milk. Within each class, the number of antibiotics tested were: nonsteroidal anti-inflammatory drugs (NSAID; 8), peptolids (2), aminoglycosides (8), tetracyclines and fusidic acid (4), beta-lactam antibiotics (25), secretolytic agents (2), macrolides (5), polypeptides (2), and antibacterial quinolones (8). Percentage of phagocytosis was determined after incubating (2 hours at 37 C) 12.5 X 10(6) viable neutrophils, 200 X 10(6) 32P-labeled S aureus with antibiotics and 5% skimmed milk. Concentrations of antibiotics tested were 1,000, 500, and 10 microgram/ml of incubation media. When compared with nonantibiotic controls at the highest drug concentration, the NSAID acetylsalicylic acid and centrophenoxine increased phagocytosis 23.2 and 8.8%, respectively, and benzydamine, indomethacin, phenylbutazone, ibuprofen, and acetominophen decreased phagocytosis 22.8, 14.2, 9.8, 27.0, and 18.2%, respectively. The peptolids novobiocin and pristinamycin decreased phagocytosis 24.5 and 22.0%, respectively. The aminoglycosides tobramycin, amikacin, and gentamicin decreased phagocytosis 21.1, 15.4, and 19.2%, respectively. For the tetracyclines and fusidic acid, minocycline and doxycycline decreased phagocytosis 39.8 and 54.2%, respectively. The beta-lactam antibiotics carfecillin, cephapirin sodium, and cephacetrile sodium decreased phagocytosis 11.2, 12.8, and 23.8%, respectively. The secretolytic agent, bromhexin, increased phagocytosis 10.8%. These data indicate that the potential for enhanced phagocytosis exists through use of some NSAID, and for depressed phagocytosis through use of aminoglycosides, peptolids, tetracyclines, and beta-lactams, as well as certain other NSAID.

The vaccine efficacy of a genetically engineered deletion mutant strain of pseudorabies virus, strain 783, was compared with that of the conventionally attenuated Bartha strain. Strain 783 has deletions in the genes coding for glycoprotein I and thymidine kinase. In experiment 1, which had a 3-month interval between vaccination and challenge exposure, strain 783 protected pigs significantly (P < 0.05) better against virulent virus challenge exposure than did the Bartha strain. The growth of pigs vaccinated with strain 783 was not arrested, whereas that of pigs vaccinated with the Bartha strain was arrested for 7 days. Of 8 pigs given strain 783, 4 were fully protected against challenge exposure; none of the pigs given strain Bartha was fully protected. In experiment 2, which had a 3-week interval between vaccination and challenge exposure, the growth of pigs vaccinated with strain 783 was arrested for 3.5 days, whereas that of pigs vaccinated with the Bartha strain was arrested for 6 days. In experiment 3, pigs with moderate titer of maternal antibodies were vaccinated twice IM or once intranasally with either strain 783 or Bartha and were challenge-exposed 3 months after vaccination. Pigs given strain 783 twice IM were significantly (P < 0.05) better protected than were the other pigs. They had growth arrest of only 6 days, compared with 9 days for pigs of other groups, and shed less virus after challenge exposure. Results of this study indicate that the vaccine based on the deletion mutant strain 783 is more efficacious than is the Bartha strain of pseudorabies virus.

To determine the role of thromboxane A2 in the pathogenesis of experimentally induced immune complex glomerulonephritis, 12 concanavalin A-immunized Beagles were infused with 1 mg of concanavalin A via each renal artery and treated twice daily for 8 days with either 30 mg of CGS 12970/kg, PO, a specific thromboxane synthetase inhibitor, or placebo. The effect of treatment was assessed by measuring endogenous creatinine clearance and urine protein and eicosanoid excretion, and by evaluating changes in glomerular morphometric characteristics. On postinfusion day 8, urine protein, thromboxane B2, and 11-dehydro-thromboxane B2 excretion, glomerular epithelial crescent formation, and glomerular cell proliferation in the CGS 12970-treated dogs were significantly decreased when compared with values in the placebo-treated group. Differences were not observed in endogenous creatinine clearance, urine prostaglandin E2 and 6-keto-prostaglandin F1 alpha excretion, or glomerular polymorphonuclear leukocyte infiltration between groups in this study. These findings suggest thromboxane A2 has a role in the development of immune complex glomerulonephritis and that thromboxane synthetase inhibition may be beneficial in attenuating some of the functional and histologic changes associated with immune complex glomerulonephritis.

In mammalian species studied previously, pepsinogen consisted of biochemically different groups of isozymogens. By use of gel filtration chromatography and electrophoresis, we isolated a predominant pepsinogen from the gastric mucosa of a horse. Peptide mapping with V8 protease revealed differences with its porcine homologue. However, porcine and equine pepsinogens, when activated to pepsin, had a similar pattern of activity when hemoglobin was used as substrate. Those results suggest that differences must exist in the primary structure of the pepsinogens of the 2 species.

The thiamylal sparing effect of midazolam was studied in 30 healthy Beagle and mixed-breed dogs. Using a replicated Latin square design, all dogs were given placebo (saline solution) and 0.025, 0.05, 0.1, and 0.2 mg of midazolam/kg of body weight prior to IV administration of thiamylal sodium. The 0.1 and 0.2 mg/kg dosages significantly decreased the amount of thiamylal required to obtund swallowing reflex and easily achieve endotracheal intubation. Midazolam at 0.1 and 0.2 mg/kg reduced thiamylal requirement by 16.4% and 18.9%, respectively, whereas the 0.05 mg/kg dosage decreased thiamylal requirement by only 6.8%. The 0.2 mg/kg dosage did not further decrease thiamylal requirement beyond that achieved with the 0.1 mg/kg dosage of midazolam. This study demonstrates that the preanesthetic IV administration of midazolam reduces the thiamylal dose necessary to accomplish intubation. The optimal preanesthetic dosage (lowest dosage with significant effect) was 0.1 mg/kg.

Bone marrow fibroblast colony-forming units (CFU-F) were evaluated in cats experimentally infected with different isolates of FeLV. Cats infected with the Kawakami-Theilen isolate of FeLV (FeLV-KT) had progressive decrease in the number of CFU-F at 2, 4, and 6 weeks after infection. The number of CFU-F in FeLV-KT-infected cats ranged from 38 to 70% of the preinoculation CFU-F value. Of 3 cats with FeLV-KT-induced suppression of CFU-F, 2 developed fatal nonregenerative anemia. Cats infected with the Rickard isolate of FeLV (FeLV-R) had more moderate decrease in the number of CFU-F at 2, 4, and 6 weeks after infection. The number of CFU-F in FeLV-R-infected cats ranged from 62 to 82% of the preinoculation CFU-F value. The FeLV-R-infected cats did not become anemic.

Five adult 40- to 50-kg female sheep were surgically fitted with a reentrant cannulae placed in the proximal part of the duodenum just distal to the pylorus. By diversion of abomasal outflow, this model has been shown to produce hypochloremic metabolic alkalosis accompanied by dehydration, hypokalemia, and hyponatremia. Each sheep was subjected to 3 separate, 12-hour IV treatment trials, in each case preceded by a control period of 48 hours, and a diversion period of 36 to 96 hours, during which a hypochloremic (Cl- less than or equal to 60 +/- 2 mEq/L) metabolic alkalosis with hypokalemia and hyponatremia was produced. Treatment 1, consisting of 6 L of isotonic Na gluconate, was designed to replace volume without replenishing the Cl- deficit. Although hydration improved, plasma Cl- decreased further, and the sheep became increasingly weak and depressed. Treatment 2, consisting of 2 L of 1.8% NaCl, was designed to replace the Cl- deficit without replacing total volume. Plasma Na+ and Cl- concentrations returned to normal during the 12 hours of treatment; acid-base balance and plasma K+ concentrations returned to normal within 36 hours of treatment. During treatment 3 (control, no treatment), measured metabolic values changed minimally. We concluded that the IV replacement of Cl- without K+ is effective in the correction of experimentally induced hypochloremic metabolic alkalosis in sheep.