Prednisone was given orally to 12 dogs daily for 35 days at an anti-inflammatory dosage (1.1 mg/kg of body weight in divided dose, q 12 h) to study its effect on thyroxine (T4) and triiodothyronine (T3) metabolism. Six of these dogs were surgically thyroidectomized (THX-Pred) and maintained in euthyroid status by daily SC injections of T4 to study peripheral metabolism while receiving prednisone; 6 dogs with intact thyroid gland (Pred) were given prednisone; and 6 additional dogs were given gelatin capsule vehicle as a control group (Ctrl). Baseline T4 concentration after 4 weeks of treatment was not significantly different in dogs of the THX-Pred or Pred group (mean +/- SEM, 2.58 +/- 0.28 or 3.38 +/- 0.58 microgram/dl, respectively) vs dogs of the Ctrl group (2.12 +/- 0.30 microgram/dl). A supranormal response of T4 to thyrotropin was observed in dogs of the Pred group, but the T4 response to thyrotropin-releasing hormone was normal. Baseline T3 concentration in dogs of both steroid-treated groups was significantly (P < 0.05) lower after 2 and 4 weeks of prednisone administration vs pretreatment values, but normalized 2 weeks after prednisone was stopped. Free T3 (FT3) and T4 (FT4) fractions and absolute FT3 and FT, concentrations were not altered by prednisone administration. Reverse T3 (rT3) concentration in vehicle-treated Ctrl dogs (26.6 +/- 3.5 ng/dl) was not different from rT3 concentration in dogs of the THX-Pred (25.7 +/- 4.3 ng/dl) and Pred (28.9 +/- 3.8 ng/dl) groups after 4 weeks of medication. These data indicate that daily oral administration of such anti-inflammatory dose of prednisone for 1 month reduces baseline serum T3 concentration, does not alter serum T4 concentration, and enhances thyroidal sensitivity to thyrotropin.

Paired CSF and serum samples were obtained from 109 rhesus macaques aged 1 to 18 years. The CSF and serum IgG and albumin concentrations were determined, using radial immunodiffusion; CSF total protein and glucose were determined, using colorimetric methods; and Na, K, and Cl concentrations were determined, using ion-specific electrodes. The CSF protein values were lower than those reported for nonhuman primates, and this finding was confirmed by results of agar gel electrophoresis. Animal age and sex had no significant effects on CSF composition, but serum IgG concentration increased with age. Concentrations of total protein, albumin, and IgG were greater, and concentrations of glucose and potassium were lower in CSF obtained from the lumbar rather than the cisternal site. Composition of CSF was not significantly altered by contamination with blood at values up to 10,000 RBC/microliter. The CSF albumin quotient, IgG quotient, and IgG index were determined and differed markedly from values reported for human beings, indicating that the properties and specificity of the blood-brain barrier may be species-specific.

The mechanism of estrogen-induced myelotoxicosis is unknown, although evidence indicates that estrogen does not directly damage the bone marrow granulocyte-macrophage progenitor cells and that the thymus is a probable mediator of the bone marrow suppression. Estrogen-induced production of a myelopoiesis-inhibitory factor by canine thymic stromal cells in vitro has been observed. Then, presence of a myelopoiesis-inhibitory factor in canine serum was investigated immediately after estrogen administration in vivo. Maximal reduction in colony-forming units-granulocyte/macrophage growth by sera from individual dogs varied. Individual dog sensitivity to estrogen-induced myelotoxicosis is seen clinically, and the cause is unknown. This serum factor could have a role in the eventual bone marrow hypoplasia seen in estrogen-treated dogs and is possibly the same factor produced by cultured thymic stromal cells exposed to estrogen.

Pepsinogen and protein concentrations were determined in blood samples, collected from the left gastroepiploic artery and vein, and in abomasal lymph from 15 steers naturally infected with Ostertagia ostertagi and 4 uninfected steers. In steers with type-1 ostertagiosis, the concentration gradient between the mucosal interstitium and the blood alone could account for higher than normal serum pepsinogen concentrations. High interstitial pepsinogen concentrations may have resulted from increased epithelial permeability or increased pepsinogen production and secretion. However, in steers with type-2 ostertagiosis, the concentration gradient could not entirely account for the high serum pepsinogen concentrations, suggesting that capillary permeability or surface area may have been altered. Lymphatic uptake contributed pepsinogen to the blood in all infected steers.

The severity of pulmonary thromboembolism and pulmonary hypertension induced by heartworms dying after administration of 2 adulticides was evaluated. Because melarsomine dihydrochloride (RM340) has been shown to be more effective in killing Dirofilaria immitis (heartworms) than the traditional approved adulticide, thiacetarsamide, an attempt was made to determine whether this new adulticide induced more severe lung disease. Before adulticide treatment, 32 dogs with naturally acquired heartworm infections received physical examinations, semiquantitative antigen concentration tests, CBC, platelet counts, serum biochemistry analyses, arterial blood gas determinations, thoracic radiography, pulmonary arteriography, and pulmonary hemodynamic tests. Eight dogs with a low burden and 9 dogs with a high burden of heartworms were treated with thiacetarsamide, and 7 dogs with a low burden and 8 dogs with a high burden were treated with RM340. Except for the heartworm-burden test, tests were repeated at regular intervals during the first 7 weeks after treatment. None of the dogs coughed or had dyspnea after treatment. Six of 9 dogs with high worm burdens and 4 of 8 dogs with low worm burdens had surviving heartworms after thiacetarsamide treatment, in contrast to only 3 of 15 RM340-treated dogs. Differences between the 2 adulticide treatments were minimal as determined by thoracic radiography, pulmonary hemodynamic tests, clinical laboratory analyses, pulmonary arteriography, or necropsy. The RM340 treatment was a more effective adulticide, but it did not increase the severity of hypertension and thromboembolism.

Fifteen 2-week-old kittens were randomly assigned to 1 of 3 milk treatment groups as the sole source of nutrition for 4 weeks: queen's milk, commercially available kitten milk replacer (CMR), and an experimental milk replacer (EXP). Kittens fed queen's milk suckled ad libitum, whereas CMR- and EXP-fed kittens were tube-fed every 6 hours. Kittens were weaned at 6 weeks of age and were fed a feline growth diet ad libitum for an additional 4 weeks. Kittens were examined at 2, 4, 6, 8 and 10 weeks of age; the procedure included an ophthalmic examination and blood sample collection for CBC and serum biochemical and amino acid analyses. Kittens fed CMR and EXP diets had weight gain greater than that for queen's milk-fed kittens. The kittens fed CMR, however, had diarrhea throughout most of the milk-feeding trial and developed diffuse anterior and posterior lens opacification and vacuolation at the posterior Y-sutures. The lens opacities noticed in the kittens during the milk treatments resolved to a residual perinuclear halo, and a few incipient cortical opacities were observed by the end of the growth diet-feeding period. Serum arginine concentration was significantly (P < 0.05) lower in the CMR-fed kittens, but was not different during the growth diet-feeding period. We concluded that the EXP diet supported normal growth in 2- to 6-week-old kittens; CMR supported normal kitten growth rate, but resulted in diarrhea and cataract formation; and serum amino acid data indicated that low arginine concentration may have been related to the CMR-induced cataract formation.

Saline (0.9% NaCl) solution or 1 of 3 nonsteroidal anti-inflammatory drugs (NSAID) was administered IV to 5 neonatal calves 15 minutes after the start of a 3-hour IV infusion of Escherichia coli lipopolysaccharide (LPS; 2 micrograms/kg/h). Four additional calves were given a 3-hour IV infusion of saline solution alone. Clinical attitude, mean arterial blood pressure, PCV, WBC, and plasma lactate, glucose, and eicosanoid concentrations (thromboxane B2, 6-keto-PGF(1 alpha)) were monitored for 12 hours. Flunixin meglumine (1.1 mg/kg of body weight, IV), ketoprofen (2.2 mg/kg, IV), and ketorolac tromethamine (1.1 mg/kg, IV) each ameliorated the clinical signs of endotoxemia and LPS-induced lacticemia, but failed to significantly alter the degree of leukopenia or hypoglycemia associated with infusion of LPS. Although the 3 NSAID prevented eicosanoid production, they provided only partial protection against LPS-induced hypotension. Each NSAID modified the response to LPS, but none was clearly superior to the others in modulating the clinical signs or physiologic alterations induced by infusion of LPS in neonatal calves.

The effects of preanesthetic medication on ease of duodenal endoscopic intubation in dogs was evaluated. One of 12 combinations of preanesthetic medications (using atropine, glycopyrrolate, morphine, meperidine, acepromazine, and 0.9% NaCl solution) was administered IM to each of 12 dogs in a trial. Twelve endoscopic trials were performed so that each dog received each treatment combination once. Anesthesia was induced with thiamylal administered IV and maintained with halothane vaporized in oxygen. Electrocardiographic recordings, indirect blood pressure measurements, end-tidal carbon dioxide partial pressures, and halothane concentrations were monitored during the anesthetic period. The ease with which the fiberoptic endoscope was passed into the proximal portion of the duodenum was qualitatively scored on the basis of time and maneuvering effort. None of the preanesthetic combinations made intubation of the duodenum significantly easier than that with 0.9% Nacl solution (control). Only the combination of morphine and atropine induced gastropyloric conditions that resulted in significantly higher (more difficult) endoscopic scores than those after preanesthetic medication with 0.9% NaCl solution.

Rectal swab specimens were collected from 362 apparently healthy dogs of different origin, age, breed, and sex. Specimens were obtained in summer, autumn, and winter. Ninety-five thermophilic Campylobacter spp were isolated: C jejuni biotype I, n = 57, C jejuni biotype II, n = 1, C coli, n = 36, and C laridis, n = 1. Biotypes of C jejuni recovered were the same as those associated with Campylobacter-induced enteritis in human beings. Prevalence of C jejuni was significantly (P < 0.05) greater: in dogs < 6 months old than in adult dogs; in dogs living under high density and cohabitation housing conditions for long periods; and in autumn.

In 6 anesthetized ponies, 3 segments of jejunum and 3 segments of small colon were isolated from the peritoneal cavity in plastic bags filled with Hanks' balanced salt solution. One jejunal and 1 small colon segment were subjected to venous strangulation obstruction for 3 hours (VSO-3), venous strangulation obstruction for 6 hours (VSO-6), or a 6-hour sham procedure to control for changes induced by isolation in a plastic bag. Additional segments of jejunum and colon that were not placed in bags served as controls for histologic examination and collagenase measurements. Samples of fluid surrounding the intestine were obtained for chemical analyses, nucleated cell count, aerobic and anaerobic bacteriologic culture, and measurement of collagenase activity. Full-thickness tissue samples were obtained for histologic examination and measurement of collagenase content. Bacteria did not cross the intestinal wall after 3 and 6 hours of VSO, despite severe mucosal lesions in these segments. At 6 hours, P(O2) was significantly less and P(CO2) was significantly (P < 0.05) greater in the fluid surrounding the VSO-6 jejunal segments, compared with the sham jejunal segments. The pH was significantly (P < 0.05) less in fluid surrounding VSO-6 small colon segments, compared with the sham colon segments at 6 hours. For jejunum and small colon, phosphate and lactate concentrations were significantly (P < 0.05) greater in VSO-6 fluid than in the corresponding sham fluids at 6 hours. Fibrin formed around all VSO segments, although fibrinogen was not detected in the surrounding fluid, indicating possible rapid conversion of fibrinogen to fibrin. Fluid collagenase activity increased significantly (P < 0.05) in all segments over 6 hours. The preparation used in this study was successful in measuring local changes on the serosal surface of intestine subjected to VSO and in isolating segments under study in a sterile environment.