This work was an attempt to develop an in vitro adherence model for Mycoplasma hyopneumoniae, using monolayers of human and porcine lung fibroblasts and porcine kidney cells. Mycoplasma hyopneumoniae grown in Friis mycoplasma broth was radiolabeled with 35[S]-methionine, washed, concentrated, and inoculated on the monolayers. After 15 minutes of centrifugation to facilitate adherence, monolayers were washed 3 times, dissolved with 0.1N NaOH, and suspended in scintillation liquid, and the radioactivity was determined in a liquid scintillation counter. Adherence, measured as a percentage of counts added, varied according to the mycoplasma strain and the cell line used. Comparison of strains J, 144L, and 232 of M hyopneumoniae revealed 7.5 +/- 5.9, 31.9 +/- 13, and 9.6 +/- 5% adherence to porcine kidney cells, respectively. Slightly different, but proportionally the same relationships were obtained with swine or human fibroblasts. Adherence was decreased slightly by repeated washings of the mycoplasma-treated cell monolayers; however, a plateau was reached, indicating irreversibility of the adherence process. Pretreatment of cell monolayers with nonlabeled organisms substantially blocked adherence by labeled organisms. Dilution of labeled organisms resulted in an increased proportion adhering. Therefore, it appears that the adherence was a receptor-dependent event. Treatment of the mycoplasmas with trypsin prior to the inoculation of monolayers resulted in a marked reduction in adherence. Treatment of the mycoplasmas with hyperimmune swine serum against M hyopneumoniae or normal swine serum resulted in 80 to 90% reduction of adherence; however, no inhibition occurred when mycoplasmas were treated with purified IgG from the hyperimmune serum.

Aminoglycoside nephrotoxicosis (AGNT) was induced in ewes by daily SC administration of gentamicin. Changes in urinary indices of renal function during the development of AGNT are reported. Measurements from timed, volume-measured urine samples were made on days 0, 7, and 8 and included creatinine clearance, total excretion (TE) rates of electrolytes (Na, K, Cl, P) and urine volume. Measurements from free-catch urine samples (without volume measurement) were made daily and included fractional excretion (FE) rate of electrolytes, urine osmolality, and urine-to-serum osmolality and urine-to-serum creatinine ratios. With the onset of AGNT, FE rates of Na, K, Cl, and P increased many fold above baseline values (200 X, 4 to 5 X, 6 to 9 X, and 70 to 95 X, respectively, on days 7 and 8), indicating decreased tubular reabsorption or increased tubular secretion. The increased FE rates were not representative of increases in total electrolyte excretion rates. The total excretion of Na (TE(Na)) was mildly increased, TE(K) was decreased, TE(Cl) was unchanged, and TE(P) was significantly increased on days 7 and 8. Abnormal urinalysis results, glucosuria, and increased FE(P) preceded appreciable increase in serum creatinine concentration. Other abnormal urinary indices of renal function coincided with or followed the increase in serum creatinine concentration. Urinary indices may help characterize renal function associated with the disease state, but did not provide early indication of AGNT.

Cardiopulmonary effects of IV administered butorphanol tartrate (BUT) were assessed in 7 yearling steers medicated with atropine and anesthetized with guaifenesin, thiamylal sodium, and isoflurane in O2 for surgical placement of duodenal cannulae. Heart rate, respiratory rate, arterial blood pressures, pHa, PaCO2, PaO2, arterial [HCO3-], esophageal temperature, and end-tidal isoflurane concentrations were measured before and after IV administration of BUT (10 mg). Mean respiratory rate increased significantly (P < 0.05) only at 45 and 60 minutes after BUT administration. Mean respiratory rate was 26 +/- 6.3 breaths/min before BUT administration and 46 +/- 12.1 breaths/min 60 minutes after BUT administration. Arterial blood pressures were increased significantly (P < 0.05) at all times, except 5 minutes after BUT administration. The mean value for mean arterial pressure was 76 +/- 9.6 mm of Hg before BUT injection and 117 +/- 12.6 mm of Hg 60 minutes after BUT injection. Mean values for pHa and arterial [HCO3-] were significantly (P < 0.05) higher at 60 minutes after BUT administration (baseline, pH = 7.25 +/- 0.04 and [HCO3-] = 29.9 +/- 3.5 mEq/L; 60 minutes after BUT, pH = 7.28 +/- 0.03 and [HCO3-] = 33.0 +/- 1.8 mEq/L). Although some statistically significant changes were recorded, IV administration of BUT to these steers did not have a marked effect on the cardiopulmonary variables measured.

The effects of furosemide on the racing times of 79 horses without exercise-induced pulmonary hemorrhage (EIPH) and 52 horses with EIPH were investigated. Racing times were adjusted to 1-mile equivalent racing times by 2 speed handicapping methods, and analysis of covariance was used to adjust actual racing times by winning time and distance for each race. All 3 methods of determining racing time indicated that geldings without EIPH had significantly faster racing times (P < 0.05) when given furosemide before racing than when furosemide was not given before racing. Females and colts without EIPH were determined to have faster racing times when furosemide was given before racing, but the difference was not significant. Geldings with EIPH had significantly faster racing times (P = 0.0231) when given furosemide before racing, as determined by one of the speed handicapping methods. There was a strong correlation (range 0.9314 to 0.9751) between the 1-mile equivalent racing times, as determined by the 2 speed handicapping methods for horses with and without EIPH. Furosemide failed to prevent the development of EIPH in many horses that were previously considered to be EIPH-negative. When given furosemide, 62 (25.3%) of 235 EIPH-negative horses were EIPH-positive after racing. Furosemide had questionable efficacy for prevention of EIPH in known EIPH-positive horses. Thirty-two (61.5%) of 52 EIPH-positive horses given furosemide before a race remained EIPH-positive after that race.

To investigate the cardiopulmonary effects of positive end-expiratory pressure (PEEP), values of 10, 20, and 30 cm of H2O, were applied to anesthetized, dorsally recumbent, ventilated ponies. After IV induction of general anesthesia, PEEP was superimposed on controlled ventilation with 100% oxygen, and changes in gas exchange and cardiac function were measured. Increasing values of PEEP in these ponies caused a linear increase in the mean (+/- SEM) functional residual capacity, from a control value (zero end-expiratory pressure) of 1.7 +/- 0.24 L to 2.2 +/- 0.31, 2.9 +/- 0.32 and 3.4 +/- 0.3 L at PEEP of 10, 20, and 30 cm of H2O, respectively (P < 0.05). Paralleling these changes, intrapulmonary shunt fraction decreased significantly (P < 0.05) from a control value of 12.9 +/- 0.5%, to 7.5 +/- 1.1 and 2.1 +/- 0.6%, at PEEP of 20 and 30 cm of H2O, respectively. Cardiac output was decreased by increasing values of PEEP, from control value of 11.7 +/- 1.56 L/min to 9.9 +/- 1.51, 8.8 +/- 1.33 and 5.62 +/- 0.56 L/min at PEEP of 10, 20, and 30 cm of H2O, respectively. Related to decreasing cardiac output, tissue oxygen delivery also decreased as PEEP was increased, from control value of 2.0 +/- 0.09 L/min to 1.8 +/- 0.07, 1.6 +/- 0.06, and 1.03 +/- 0.04 L/min at PEEP of 10, 20, and 30 cm of H2O, respectively. Thus, the effects of increasing values of PEEP in these ponies included increased functional residual capacity and arterial oxygenation, but marked reduction in cardiac output, resulting in no improvement or decrease in total oxygen delivery. Although PEEP is useful for improving arterial oxygenation, the deleterious cardiovascular effects should be anticipated or ameliorated by use of volume loading and/or inotrope administration.

Opsonized Rhodococcus equi activated the respiratory burst of resident alveolar macrophages (AM) from adult horses in a logarithmic-linear, mass-related manner. The effect of R equi was not significantly different from that of equal masses of opsonized zymosan A. Therefore, R equi does not appear to attenuate the respiratory burst of equine AM. The stimulatory effect of R equi was not reflected by increased production of superoxide anion (O2-), but increased activity of the hexose monophosphate shunt was observed. These results suggest a similarity between the respiratory burst of Am from horses and that of AM from rabbits. We concluded that resident AM from adult horses do not produce O2- concurrently with an increase in activity of the hexose monophosphate shunt when stimulated with either opsonized zymosan A or opsonized R equi. This suggests that O2- is not an important component of the antibacterial defenses of equine AM. Whether equine AM are incapable of producing O2- or require different stimuli to produce it was not determined.

Samples of pleural fluid from 20 horses with effusive pleural diseases of various causes were evaluated; samples from 19 horses were used for the study. There were differences for pH (P = 0.001) and partial pressure of oxygen (P(O2)) between arterial blood and nonseptic pleural fluid (P = 0.0491), but there were no differences for pH, P(O2), partial pressure of carbon dioxide (P(CO2)) and concentrations of bicarbonate (HCO3-), lactate, and glucose between venous blood and nonseptic pleural fluid. Paired comparisons of venous blood and nonseptic pleural fluid from the same horse indicated no differences. There were differences (P = 0.0001, each) for pH, P(O2), P(CO2), and concentrations of HCO3- between arterial blood and septic pleural fluid. Differences also existed for pH (P = 0.0001), P(CO2) (P = 0.0003), and concentrations of HCO3- (P = 0.0001), lactate (P = 0.0051), and glucose (P = 0.0001) between venous blood and septic pleural fluid. Difference was not found for values of P(O2) between venous blood and septic pleural fluid, although 4 samples of septic pleural fluid contained virtually no oxygen. Paired comparisons of venous blood and septic pleural fluid from the same horse revealed differences (P < 0.05) for all values, except those for P(O2). These alterations suggested functional and physical compartmentalization that separated septic and healthy tissue. Compartmentalization and microenvironmental factors at the site of infection should be considered when developing therapeutic strategies for horses with septic pleural disease.

The size of the liver, as well as the situation and diameter of vessels in cattle were determined by use of ultrasonography. Ultrasonographic examinations of the liver were performed on 10 cows 10 times within 2 weeks, using a 3.5-MHz linear transducer on the right side in the 12th, 11th, and 10th intercostal spaces. Dorsal and ventral margin of the liver as well as localization and diameter of the caudal vena cava and the portal vein were determined in each intercostal space. Furthermore, the angle of the liver in the ventral area between the visceral surface and the diaphragmatic surface, the dorsal margin, and the circumference of the gall bladder were determined. The ultrasonographic values of liver size and localization in healthy cows can be used as reference values for the diagnosis of changes in liver size attributable to illness.

Cartilage retention strengths of laryngoplasty prostheses were compared in larynges of 2-, 3-, and 4-year-old horses, using doubled polyester and expanded polytetrafluoroethylene prostheses. Bilateral laryngoplasties were performed on each of 15 (seven 2-year-old, two 3-year-old, and six 4-year-old) larynges, which were collected at an abbatoir. Prostheses were secured to a mechanical testing machine, and tension causing arytenoid cartilage abduction was applied, until total failure of the cartilage or prosthesis resulted. Tension caused cricoid cartilage failure in 1 specimen, and muscular process cartilage failure in the remainder. There was no significant effect of age, prosthetic material, or side of prosthesis placement on cartilage retention of the prostheses. Additionally, frequency of multiple load-displacement peaks, indicating partial muscular process failure, was not affected by age or prosthetic material variables.

The influence of variable zinc content (29.1, 250, 1,000 and 2,000 mg/kg of dry weight) in a basic diet containing 7.7 mg of copper/kg on the ability of weanling foals to maintain normal copper balance was investigated. Serum copper and zinc concentrations were monitored, and terminal hepatic copper and zinc contents were measured in 4 weanling foals fed the basic diet containing 29.1 mg of zinc/kg and in 2 foals each fed the higher-zinc diets. Foals fed the lower-zinc diets (29.1 and 250 mg/kg) maintained normal serum copper and zinc concentrations for 14 to 15 weeks, whereas those fed the 2 higher-zinc diets became hypocupremic within 5 to 6 weeks and were lame within 6 weeks, owing to cartilaginous disease characteristic of osteochondritis dissecans. Serum zinc concentration in the foals fed the 2 higher-zinc diets increased to > 2 microgram/ml within 2 weeks. Foals fed the high-zinc diets became lame after serum copper concentration had remained at 0.3 microgram/ml for > 1 week. Serum copper concentration in these arthritic foals was less than or equal to 0.2 microgram/ml at the end of the study. In lame foals, fractures of the cartilage of the articular and growth physes occurred through the zone of hypertrophic cells, and varied from bilateral to unilateral and from small to large. Free masses and flaps of cartilage attached to one side were numerous.