Eight dogs were determined to be orthopedically normal on the basis of prelavage physical examination, stifle radiography, synovial fluid analysis, and force plate analysis (peak vertical force normalized for body weight, and time on the force plate). Each dog had 1 stifle randomly assigned to be lavaged with 100 ml of a commercially available 0.05% (w/v) chlorhexidine diacetate solution, and the contralateral stifle was lavaged with lactated Ringer's solution. Difference was not detected between the chlorhexidine diacetate and lactated Ringer's solution-treated joints, with regard to results of synovial fluid analysis and clinical lameness evaluations on days 4 and 8 after lavage. Chlorhexidine diacetate caused a more intense synovitis than did lactated Ringer's solution, as determined by histologic evaluation of synovial membrane specimens after necropsy on day 8; however, a difference in the intensity of toluidine blue staining of articular cartilage was not found between treatments. Chlorhexidine diacetate, as a 0.05% (w/v) solution, cannot be recommended as a joint lavage fluid until the duration of inflammatory changes in the synovial membrane are determined or until the chemical constituents of chlorhexidine diacetate causing the synovitis can be identified and removed.

A rebreathing method for measurement of pulmonary diffusing capacity for carbon monoxide (DL(CO)) and functional residual capacity (FRC) was evaluated in conscious horses. Horses were manually ventilated through an endotracheal tube, using a custom-made syringe filled with a gas mixture containing 18-carbon monoxide (18CO) and helium (He). The 18CO and He concentrations were continuously monitored by use of a mass spectrometer connected to the rebreathing circuit. Values for DL(CO), and FRC were calculated from changes in the concentration of these 2 gases. In 11 Thoroughbreds, mean (+/- SD) DL(CO) was 330.3 +/- 56.9 ml.min-1.mm of Hg-1, and FRC was 20.21 +/- 3.35 L. Body weight normalization yielded mean (+/- SD) values of 0.652 +/- 0.114 ml.min-1.mm of Hg-1.kg-1 for DL(CO), and 39.9 +/- 6.4 ml.kg-1 for FRC.

The hemodynamic effects of 2 dosages of ephedrine were studied in 6 dogs anesthetized with isoflurane only (end-tidal concentration equivalent to 1.5 times minimum alveolar concentration). Following instrumentation, baseline (time 0) measurements included heart rate (HR), respiratory rate, mean arterial blood pressure (MAP), cardiac output, and blood gas tensions. Cardiac index (CI), stroke volume (SV), systemic vascular resistance (SVR), arterial oxygen content (CaO2), and oxygen delivery and consumption (DO2 and VO2, respectively) were calculated. Three dogs were given ephedrine IV at a dosage of 0.1 mg/ kg of body weight, and 3 dogs were given ephedrine IV at a dosage of 0.25 mg/kg. Measurements were recorded at 5, 10, 15, 30, and 60 minutes. Each dog then received the alternate dosage of ephedrine, and measurements were again recorded at the same intervals. Effects of ephedrine varied with dosage. Neither dosage was associated with significant changes in pH, PaO2, PaCO2, VO2, or respiratory rate. Ephedrine at a dosage of 0.1 mg/kg caused transient significant increases in MAP, CI, SV, CaO2, and DO2, significant decreases in HR and SVR, and a late, slight decrease in CaO2. Ephedrine at a dosage of 0.25 mg/kg caused a greater and more prolonged increase in MAP, as well as increases in CI, SV, and SVR, and a decrease in HR. The higher dosage of ephedrine also caused a pronounced increase in hemoglobin concentration and CaO2, resulting in a 20 to 35% increase in DO2 throughout the 60-minute experiment.

Cytologic and bacteriologic responses, and changes in cytokine activity were evaluated in secretions of Staphylococcus aureus-infected mammary glands after treatment of heifers with recombinant bovine interferon gamma (rbIFN gamma) or interleukin 2 (rbIL-2). Two groups of 4 heifers each, experimentally infected with 10(7) colony-forming units (CFU) of S aureus, were injected in 2 quarters via the teat canal, with 10(5) U of rbIFN gamma (trial 1) or 7.5 X 10(5) U of rbIL-2 (trial 2) 2 weeks after experimentally induced infection; control quarters received phosphate-buffered saline solution. Mammary secretion samples were taken on days 0, 1, 2, 3, 4, 7, and 14 after cytokine infusion. Secretions were diluted 1:10 and used to perform somatic cell counts (SCC), differential cell counts, and CFU enumerations, and to determine the number of leukocytes expressing major histocompatibility complex class-II (MHC II) antigens. In addition, mammary secretion samples taken on days 0, 1, and 2 were processed to obtain skimmed milk for evaluation of rbIFN gamma- and rbIL-2-like activities. Treatment with rbIFN gamma did not influence SCC, or differential or bacteria counts, or the number of leukocytes expressing MHC II antigens. However, rbIL-2 stimulated leukocytosis, which may have reduced bacteria counts early in the trial; treatment with this cytokine also increased the neutrophil, macrophage, lymphocyte, and eosinophil counts in secretions. Similarly, numbers of MHC II-positive leukocytes were greater in rbIL-2-treated quarters vs controls. Compared with day 0, IFN gamma-like activity was increased on only day 1 in both trials. Interleukin-2-like activity was not influenced in the rbIFN gamma trial, but was increased on days 1 and 2 in the rbIL-2 trials. Results indicated that neither cytokine may have had a major influence on the course of established S aureus infections. However, the increased SCC in rbIL-2-treated quarters may have accounted for the reduction in CFU throughout the trial after treatment with this cytokine. Greatest cytokine-like activity was observed on day 1; however, the consequences of cytokine activity, such as the sustained eosinophilia after rbIL-2 treatment, were detected over the 14-day trial period, indicating possible prolonged action.

One hundred two dogs without known gastric lesions were evaluated to establish a reference range of gastric rugal fold thickness (millimeters). Mucosal folds were measureable for 63 examinations, and the length of the second lumbar vertebra was measured for 61 of the 63 (centimeters). Body weight was available in the case records of 29 dogs. Measurements of the mucosal folds were related to body weight (n = 29) and length of the second lumbar vertebra (n = 61) by use of linear regression analysis. Reference range of normal gastric mucosal fold thickness, 1 to 8 mm, was defined by this study for dogs of any breed weighing between 2 and 50 kg.

Cardiopulmonary and behavioral responses to detomidine, a potent alpha 2-adrenergic agonist, were determined at 4 plasma concentrations in standing horses. After instrumentation and baseline measurements in 7 horses (mean +/- SD for age and body weight, 6 +/- 2 years, and 531 +/- 48.5 kg, respectively), detomidine was infused to maintain 4 plasma concentrations: 2.1 +/- 0.5 (infusion 1), 7.2 +/- 3.5 (infusion 2), 19.1 +/- 5.1 (infusion 3), and 42.9 +/- 10 (infusion 4) ng/ml, by use of a computer-controlled infusion system. Detomidine caused concentration-dependent sedation and somnolence. These effects were profound during infusions 3 and 4, in which marked head ptosis developed and all horses leaned heavily on the bars of the restraining stocks. Heart rate and cardiac index decreased from baseline measurements (42 +/- 7 beats/min, 65 +/- 11 ml.kg of body weight-1.min-1) in linear relationship with the logarithm of plasma detomidine concentration (ie, heart rate = -4.7 [log(e) detomidine concentration] + 44.3, P < 0.01; cardiac index = -10.5 [log(e) detomidine concentration] + 73.6, P < 0.01). Second-degree atrioventricular block developed in 5 of 7 horses during infusion 3, and in 6 of 7 horses during infusion 4. Mean arterial blood pressure increased significantly from 118 +/- 11 mm of Hg at baseline to 146 +/- 27 mm of Hg at infusion 4. Similar responses were observed for mean pulmonary artery and right atrial pressures. Systemic vascular resistance (baseline, 182 +/- 28 mm of Hg.ml-1.min-1.kg-1) increased significantly during infusions 3 and 4 (to 294 +/- 79 and 380 +/- 58, respectively). Plasma atrial natriuretic peptide concentration was significantly increased with increasing detomidine concentration (20.4 +/- 3.8 pg/ml at baseline to 33.5 +/- 9.1 at infusion 4). There were few significant changes in respiration rate and arterial blood gas and pH values. We conclude that maintenance of steady-state detomidine plasma concentrations resulted in cardiopulmonary changes that were quantitatively similar to those induced by detomidine bolus administration in horses.

Five healthy adult mares and 1 gelding were given a single dose (15 mg/kg of body weight) of metronidazole per rectum. After manual evacuation of feces from the rectum, a suspension of crushed tablets and water (40 ml) was administered via a 28-F catheter advanced 30 cm into the rectum. Blood samples were obtained by jugular venipuncture, and metronidazole concentration was measured serially for the 14 hours after drug administration. Mean serum concentration of metronidazole peaked at 4.5 micrograms/ml, 0.83 hour after administration, and decreased to 0.38 micrograms/ml, 14 hours after administration. Mean elimination rate constant was 0.23/h, and the harmonic mean elimination half-life was 3.04 hours. Further study is necessary to determine a therapeutic dose regimen for metronidazole administered per rectum.

Two cytopathic agents were isolated on porcine alveolar macrophages following inoculation with homogenates of lung tissues from pigs showing respiratory problems. These isolates were identified as porcine reproductive and respiratory syndrome (PRRS) virus isolates by indirect immunofluorescence using a PRRS virus (PRRSV) specific monoclonal antibody (MAb) and were designated as LHVA-92-1 and LHVA-92-2. Immunogold electron microscopy using a porcine PRRS positive serum pool and protein A-gold resulted in an intense labelling of aggregates of viral particles. Dark specific cytoplasmic staining of porcine alveolar macrophages infected with both virus isolates could be observed by immunogold silver staining (IGSS) using the specific MAb. This method proved effective in detecting PRRSV antigens in several ethanol-fixed tissues of piglets intranasally inoculated with the supernatants of macrophages infected with each isolate. Immunogold silver staining was also successfully used for the detection of PRRSV antigens on sections of formalin-fixed paraffin-embedded lung tissues and on frozen sections of lungs. The present results indicate that colloidal gold may be useful for the identification and immunohistochemical detection of PRRSV in tissues.

Five cows in the last month of gestation, provided with uterine electrodes and in which catheters had been chronically installed in the fetal aorta, were used to study patterns of fetal heart rate (FHR) and the influence of periods of myometrial electrical activity during gestation (contractures) on FHR. The FHR was calculated by counting the number of blood pressure pulses on the tracings during alternate periods of 12 seconds. Three 1-hour recordings without contractures and 10 recordings during the time of a contracture were randomly selected for each cow. The calculated data points were plotted on a graph to display FHR patterns. In 41 periods associated with single contractures, FHR data points were taken every 72 seconds. Changes in absolute and relative FHR in these periods were determined to analyze a possible effect of contractures on FHR. Three types of variation in FHR patterns could be distinguished: a short-term, low-amplitude variation of basal FHR; a second type in which the duration was < 4 minutes and the amplitude was greater than or equal to 15 beats/min; and prolonged periods with increased or decreased FHR values (> 4 minutes and greater than or equal to 15 beats/min). The relationship between these types of variation and fetal activity states remains to be established for cows. During the 60 hours of recordings that were analyzed, a period of several minutes during which FHR values were extremely high (> 180 beats/min) was found 3 times. There were no significant differences in absolute or relative FHR before, during, or after a contracture.

We evaluated the effects of clenbuterol HCl (0.8 micrograms/kg, of body weight, IV), a beta 2, agonist, on ventilation-perfusion matching and hemodynamic variables in anesthetized (by IV route), laterally recumbent horses. The multiple inert gas elimination technique was used to assess pulmonary gas exchange. Clenbuterol HCl induced a decrease in arterial oxygen tension (from 57.0 +/- 1.8 to 49.3 +/- 1.2 mm of Hg; mean +/- SEM) as a result of increased shunt fraction (from 6.6 +/- 2.1 to 14.4 +/- 3.1%) and ventilation to regions with high ventilation-perfusion ratios. In contrast, no changes in these variables were found in horses given sterile water. In horses given clenbuterol HCl, O2 consumption increased from 2.23 +/- 0.18 to 2.70 +/- 0.14 ml . min-1 . kg-1, and respiratory exchange ratio decreased from 0.80 +/- 0.02 to 0.72 +/- 0.01. Respiratory exchange ratio and O2 consumption were not significantly modified in sterile water-treated (control) horses. Clenbuterol HCl administration was associated with increased cardiac index (from 57.4 +/- 4.0 to 84.2 +/- 6.3 ml . min-1 . kg- 1), decreased total peripheral vascular resistance (from 108.3 +/- 9.3 to 47.6 +/- 2.8 mm of Hg . s . kg . ml-1), and decreased pulmonary vascular resistance (from 31.3 +/- 3.8 to 13.6 +/- 0.7 mm of Hg . s . kg . ml-1). Our findings indicated that clenbuterol HCl may potentiate hypoxemia as a result of increased shunt fraction in horses anesthetized by the IV route, and caused changes in hemodynamic variables that were consistent with its ability to stimulate beta 2-adrenergic receptors.