Eight ponies were allotted to 2 groups of 4. Group-1 ponies (1-4) were given 0.2 g of indole/kg of body weight orally and group-2 ponies (5 to 8) were given 0.1 g of indole/kg. Various physical, hematologic, and physiologic measurements were obtained after administration of indole. Intravascular hemolysis and hemoglobinuria were detected in both groups within 24 hours of dosing. Hemolysis was reflected by decreases in PCV, hemoglobin concentration, and RBC count, and an increase in indirect bilirubin. Erythrocyte fragility appeared to increase in both groups at 8 hours after dosing and peaked at 16 hours after dosing. At 72 hours after dosing, the RBC fragility value was less than predose measurements. Heinz body formation was noticed in group-2 ponies, but not in group 1. Plasma indole concentrations increased in both groups from the nondetectable predose concentrations. Group-1 values were 203% of group-2 values. In group 2, plasma indole was nondetectable by 12 hours, whereas low concentrations could still be measured in the group-1 ponies at 24 hours. Ponies in group 1 died or were euthanatized between 24 and 72 hours after dosing, whereas group-2 ponies were euthanatized between 48 and 120 hours. At necropsy, all body fat, mucous membranes, and elastic tissue were stained yellow. Hemoglobinuric nephrosis was the most prominent microscopic lesion. Results of this study indicated that indole, a metabolite of the amino acid tryptophan, causes acute intravascular hemolysis in ponies.

Acidemia stimulates renal ammonia production and excretion. This adaptive response allows increased H+ secretion and generation of new bicarbonate. To determine whether a relationship existed between urine ammonium (NH4+) concentration and excretion and urine anion gap (Na+ + K+ - Cl-), ammonium chloride (NH4Cl) was administered per OS for 5 days to induce systemic acidemia in 12 healthy Beagles. During NH4Cl administration, a strong, statistically significant (P < 0.0001) relationship was apparent between urine NH4+ concentration measured in millimoles per liter and urine anion gap. Regression equation: urine [NH4+] = 8.2 - 0.416 X urine anion gap; r = -0.897. A statistically significant (P = 0.0001) relationship existed between urine NH4+ excretion measured in millimoles per kilogram of body weight per day and urine anion gap. Regression equation: urine NH4+ excretion = 0.74 - 0.38 X urine anion gap; r = -0.768. As urine NH4+ concentration or excretion increased, urine anion gap became more negative. Before NH4Cl administration (no systemic acidemia), a weak, but statistically significant (P = 0.015) relationship was observed between urine NH4+ concentration and urine anion gap. Regression equation: urine [NH4+] = 65.2 - 0.141 X urine anion gap; r = -0.41. However, a relationship was not evident between urine NH4+ excretion and urine anion gap before NH4Cl administration. Hence, urine anion gap is a reliable index of urine NH4+ concentration and excretion only in dogs with metabolic acidosis. In human beings with distal renal tubular acidosis, NH4+ excretion is inappropriately low and results in a positive urine anion gap. Therefore, as a reliable index of NH4+ excretion, urine anion gap may represent an easy and rapid method to aid in the diagnosis of distal renal tubular acidosis in dogs.

Furazolidone cardiotoxicosis was induced in 2 groups (FZ and FZ-CR groups) of newly hatched male Pekin ducklings (100/group) by feeding a ration containing 650 mg of furazolidone/kg of feed (ppm) for 28 days. A third group (control ration, CR group; n = 100) was fed the same ration without furazolidone. On day 28, the control ration was initiated for the FZ-CR group initially given the furazolidone-containing ration, to allow recovery from the effects of the drug, whereas ducklings of the FZ group continued to consume the furazolidone-containing ration. Biweekly, beginning with week 4, ducklings were euthanatized to assess severity of gross lesions and to obtain sections of myocardium for histologic and ultrastructural examination. Clinical evidence (increased weight gain, increased feed consumption, decreased mortality, reduced prevalence of palpable ascites) of regression of cardiotoxicosis of ducklings of the FZ-CR group was nearly complete by day 56 (28 days after cessation of furazolidone intake). Likewise, regression of gross lesions, as measured by overall prevalence of gross lesions, left ventricular volume, and ascites prevalence and severity, were also essentially complete by day 56. Myofibrillar lysis was not seen in sections from the heart (examined ultrastructurally) obtained from ducklings of the CR group that were euthanatized on day 28, 56, or 98. Myofibrillar lysis was detected in all ducklings (4/4) fed furazolidone (FZ and FZ-CR groups) and euthanatized on day 28. Myofibrillar lysis was not seen in the heart of ducklings of the FZ-CR group that were euthanatized on day 56 or 98. Myofibrillar lysis was detected in the heart from all ducklings of the FZ group that were euthanatized on day 56. Leptomeres were observed in cardiac myocytes of ducklings that had been fed furazolidone, but not in those fed only the control ration. Our clinical, gross pathologic, and ultrastructural findings indicate that regression of the cardiac lesions of furazolidone toxicosis may be essentially complete by 28 days after cessation of furazolidone intake. Our ultrastructural findings indicate that furazolidone consumption may result in cardiac dilatation by altering myofibrillar/cytoskeletal attachments of myocytes.

Fourteen adult beavers (Castor canadensis) weighing 16.5 +/- 4.14 kg (mean +/- SD) were anesthetized for surgical implantation of radio telemetry devices. Beavers were anesthetized with diazepam (0.1 mg/kg) and ketamine (25 mg/kg) administered IM, which provided smooth anesthetic induction and facilitated tracheal intubation. Anesthesia was maintained with halothane in oxygen via a semiclosed circle anesthetic circuit. Values for heart rate, respiratory rate, esophageal temperature, direct arterial blood pressure, end-tidal halothane concentration, and end-tidal CO2 tension were recorded every 15 minutes during the surgical procedure. Arterial blood samples were collected every 30 minutes to determine pH, PaO2, and PaCO2. Values for plasma bicarbonate, total CO2, and base excess were calculated. Ventilation was spontaneous in 7 beavers and controlled to maintain normocapnia (PaCO2 approx 40 mm of Hg) in 7 others. Vaporizer settings were adjusted to maintain a light surgical plane of anesthesia. Throughout the surgical procedure, all beavers had mean arterial pressure < 60 mm of Hg and esophageal temperature < 35 C. Mean values for arterial pH, end-tidal CO2, PaO2, and PaCO2 were significantly (P < 0.05) different in spontaneously ventilating beavers, compared with those in which ventilation was controlled. Respiratory acidosis during halothane anesthesia was observed in spontaneously ventilating beavers, but not in beavers maintained with controlled ventilation. All beavers recovered unremarkably from anesthesia.

Bovine whey samples were evaluated by use of lymphocyte-transformation tests to determine their effect on lymphocyte blastogenesis. Whey samples from mammary glands with clinical mastitis strongly inhibited DNA synthesis and blastogenesis in lymphocytes stimulated with mitogens or dividing because of bovine leukemia virus infection. Whey samples from apparently healthy glands either did not inhibit lymphocyte DNA synthesis or inhibited it to a lesser degree than did whey from mastitic glands. Degree of inhibition was dose-dependent. The molecules causing inhibition were noncytotoxic and underwent minimal binding to the lymphocytes. Inhibitory molecules were susceptible to various proteolytic and glycolytic enzymes, indicating a glycoprotein-like structure. Whey inhibited incorporation of thymidine if it was in the cell cultures during the early stages of stimulation. Incubation of lymphocytes in whey that inhibited thymidine incorporation did not affect DNA synthesis in subsequent culturing of the same cells without whey. Degree of inhibition was affected by the method of whey preparation.

The effects of a potent new histamine-2 (H2) receptor antagonist, BMY-25368, were studied on gastric acid secretion in 5 foals from which food was withheld. Doses of 0.02, 0.11, 0.22, and 1.10 mg/kg of body weight were administered IM in a randomly assigned treatment sequence. Following BMY-25368 administration, hydrogen ion concentration was decreased and mean pH was higher than baseline values in a dose-response pattern. At the 0.22 and 1.10 mg/kg doses, the high pH was sustained for > 4 hours. The BMY-25368 thus may be useful for treating gastric ulcer disease in horses.

Twelve calves (mean weight, 175.5 kg) were used to confirm efficacy of ivermectin delivered from a prototype sustained-release bolus against naturally acquired gastrointestinal nematodes including early fourth-stage (inhibited) larvae of Ostertagia ostertagi. The calves were allocated by restricted randomization on weight to 1 of 2 groups: controls, to which a placebo bolus was given orally, and treated calves, to which a sustained-release bolus designed to deliver 8 mg of ivermectin/day at a steady rate was given orally. After treatment, the 2 groups were housed in separate pens with concrete flooring. Twenty-eight days after treatment, all calves were euthanatized and necropsied. The ivermectin-treated calves had no larval or adult Ostertagia spp and significantly (P < 0.01) fewer adult Trichostrongylus axei and adult Cooperia (C oncophora, C punctata and C surnabada) than control calves. Efficacy of ivermectin was > 99% for Cooperia spp, and 100% for other parasites. Drug-related adverse reactions were not observed.

Tear samples were collected from 1 eye of each of 40 cows, 27 sheep, 5 goats, and 5 human beings. Additionally, 10 bovine tear samples were pooled and concentrated. Spectrophotometric assays, using Micrococcus lysodeikticus, were performed on each sample to detect lysozyme activity expressed in hen egg lysozyme (HEL) equivalents. Lysozyme activity was not detected in tears of cows, but 158.8 +/- 159.3 mg of HEL/ml was detected in tears of sheep, 220.7 +/- 37.5 mg of HEL/ml in tears of goats, and 216.3 +/- 86.2 mg of HEL/ml in tears of human beings. In pooled bovine tear samples, lysozyme activity was not detected on plate assay and lysozyme protein was not detected on polyacrylamide gel electrophoresis, column chromatography, or immunoelectrophoresis with rabbit anti-bovine tear antibodies. On the basis of these observations, we concluded that the basic ocular protective mechanism in bovine tears is not lysozyme. Other antibacterial proteins such as lactoferrin, transferrin, complement, or beta-lysin may, therefore, be of primary importance in protecting the bovine eye.

The effect of flunixin meglumine on renal function was studied in 6 healthy horses by use of nonimaging nuclear medicine techniques. Effective renal plasma flow (ERPF) and effective renal blood flow (ERBF) were determined by plasma clearance of 131I-orthoiodohippuric acid before and after administration of flunixin meglumine. Mean ERPF and ERBF was 6.03 ml/min/kg and 10.7 ml/min/kg, respectively, before treatment and was 5.7 ml/min/kg and 9.7 ml/min/kg, respectively, after treatment. Although ERPF and ERBF decreased after flunixin meglumine administration, the difference was not statistically significant.

Ten colostrum-deprived calves were assigned to 1 of 2 treatment groups (5 calves/group), and fed colostrum that had either low (naturally infected cows) or high (immunized cows) antibody titers to bovine coronavirus (BCV). All calves were inoculated orally and intranasally with virulent BCV when they were 24 to 48 hours old and challenge exposed 21 days later. Blood, feces, nasal secretions, tears, saliva, and bronchoalveolar lavage (BAL) fluids were collected weekly from each calf for 5 weeks after inoculation. The titers to whole BCV or the relative amounts of isotype-specific antibodies to BCV structural proteins were evaluated in these samples by ELISA or immunoblotting, respectively. Both pools of colostrum contained primarily IgG1, IgG2, and IgA antibodies to the E2 and E3 BCV proteins. Calves fed the high-titer colostrum had correspondingly higher amounts of passive IgG1 and IgA antibodies to whole BCV and to the E2 and E3 BCV proteins in serum, feces, and BAL fluid at postinoculation week 1 than those calves fed low-titer colostrum. Active IgG1, IgA and IgM antibody responses in serum and active IgA and IgM antibody responses in most mucosal secretions to whole BCV and to the E2 and E3 proteins were lower or delayed in calves fed high-titer colostrum, compared with responses in calves fed low-titer colostrum. In contrast, increased responses to the BCV N protein were observed in all samples (except in serum and BAL fluid) in the calves fed high-titer colostrum, compared with calves fed low-titer colostrum. Upon challenge exposure, responses to E2 and E3 BCV proteins in serum and BAL fluid were lower in the group fed high-titer colostrum, compared with those in the group fed low-titer colostrum. Our findings indicate that the level of passive immunity in calves at the time of BCV inoculation can influence the development of active antibody responses in serum, feces, and mucosal secretions to whole BCV and to some BCV proteins individually.