Cardiopulmonary effects of etomidate administration were studied in hypovolemic dogs. Baseline cardiopulmonary data were recorded from conscious dogs after instrumentation. Hypovolemia was induced by withdrawal of blood from dogs until mean arterial pressure of 60 mm of Hg was achieved. Blood pressure was maintained at 60 mm of Hg for 1 hour, by further removal or replacement of blood. One milligram of etomidate/kg of body weight was then administered IV to 7 dogs, and the cardiopulmonary effects were measured 3, 15, 30, and 60 minutes later. After blood withdrawal and prior to etomidate administration, heart rate, arterial oxygen tension, and oxygen utilization ratio increased. Compared with baseline values, the following variables were decreased: mean arterial pressure, mean pulmonary arterial pressure, central venous pressure, pulmonary wedge pressure, cardiac index, oxygen delivery, mixed venous oxygen tension, mixed venous oxygen content, and arterial carbon dioxide tension. Three minutes after etomidate administration, central venous pressure, mixed venous and arterial carbon dioxide tension, and venous admixture increased, and heart rate, arterial and venous pH, and arterial oxygen tension decreased, compared with values measured immediately prior to etomidate administration. Fifteen minutes after etomidate injection, arterial pH and heart rate remained decreased. At 30 minutes, only heart rate was decreased, and at 60 minutes, mean arterial pressure was increased, compared with values measured before etomidate administration. Results of this study indicate that etomidate induces minimal changes in cardiopulmonary function when administered to hypovolemic dogs.

The effect of feeding monensin, with or without dry hay plus wilted forage, on ruminal formation of 3-methylindole (3MI) was investigated in pastured cattle. Eighty-two cows were allotted to 3 groups. Cows of group-1 served as controls and were given a daily energy supplement (1 kg/head) without monensin for 1 day before and for 7 days after being allowed access to lush pasture. Cows of groups 2 and 3 were given the same daily energy supplement, which also contained monensin (200 mg/kg of supplement). Cows of group 3 also were fed dry hay for 5 days before the start of the study and continued to be given supplemental hay for 4 days after being allowed access to lush pasture containing a layer of wilted forage. Ruminal 3MI and indole concentrations increased on day 1 after all groups were allowed access to lush pasture. By day 7, 3MI concentration in all cows had decreased to pregrazing concentration. Indole concentration did not reach pregrazing concentration until day 10 for cows of groups 1 and 2. Group-3 cows had pregrazing indole concentration on day 7. Ruminal indole concentration did not differ (P > 0.05) between groups 1 and 2. Ruminal indole concentration was lower (P < 0.01) in group-3 cows on all sample collection days, except day 10, compared with that in the other groups. Monensin reduced (P < 0.01) 3MI formation on days 1 and 7 in group-2 cows, compared with group-1 cows. Group-3 cows had lower 3MI concentration than did group-1 cows (P < 0.01) on days -1, 1, 4, and 7. Monensin, when fed with dry hay and wilted forage, reduced (P < 0.01) 3MI formation on days 4 and 7 in group-3 cows, compared with cows that were only given monensin (group 2). Group-3 cows also had lower (P < 0.05) 3MI concentration, compared with group-2 cows on day 1. Results indicated that monensin reduced ruminal formation of 3MI. Feeding dry hay and wilted forage to cattle during the change to lush pasture resulted in further reduction in the amount of 3MI formed by ruminal microorganisms. To maximize the effectiveness of monensin in reducing 3MI formation, dry hay plus wilted forage should be fed to pastured cattle for at least 4 days after they are allowed access to lush pasture.

The effect of urine pH on plasma disposition of ampicillin sodium was evaluated. A single dose of 10 mg/kg of body weight was administered IV to Thoroughbreds with alkaline (pH > 8.0) or acidic (pH < 4.5) urine. Urine alkalinity was achieved and maintained by oral administration of up to 400 mg of sodium bicarbonate/kg/d, and acidity was achieved and maintained by oral administration of up to 400 mg of ammonium chloride/kg/d. Ampicillin sodium was measured in the plasma of horses by use of an agar diffusion microbiological assay with Bacillus subtilis as the test organism. The plasma disposition kinetics of ampicillin sodium best fitted a 2-exponential decay pattern, and statistically significant differences were not evident in elimination half-life, area under the plasma concentration time curve, volume of distribution, or body clearance rate between horses with alkaline or acidic urine. Results indicate that changes in urine pH over a range encountered in clinically normal horses are unlikely to affect plasma pharmacokinetic variables of ampicillin sodium after IV administration of the drug.

Viscosity of synovial fluid (SF) from 29 clinically normal horses was determined by use of a rotational cone and plate microviscosimeter. Total protein concentration in the SF of the 29 horses, as measured with a refractometer, was < 2.5 g/dl. When the Coomassie brilliant blue test was used to determine total protein concentration in SF for 15 horses, the mean value was 1,088 mg/dl. Viscosity values at 60, 30, 12, 6, 3, and 1.5 revolutions/min (rpm) spindle speed were 4.41 +/- 1.54 centipoise (cp), 5.29 +/- 1.94 cp, 6.76 +/- 2.76 cp, 8.52 +/- 4.27 cp, 10.41 +/- 6.30 cp, and 13.07 +/- 9.05 cp, respectively. Synovial fluid viscosity increased with decreasing rpm and shear rate, but the shape of the curve for each horse fitted the asymptotic curve. The rotational cone and plate microviscosimeter was an accurate instrument in measuring SF viscosity at multiple rpm or shear rates in horses. The values obtained on clinically normal horses in this study will serve as a baseline for comparison in the evaluation of horses with joint disease.

An ELISA was developed and tested to detect antibodies to Eperythrozoon suis in swine. Results were compare with those of the indirect hemagglutination (IHA) test. Antigen isolated from swine heavily infected with E suis was used for both tests. Comparison of the ELISA with the IHA test revealed a significant (P < 0.001) correlation between results. Of 114 samples obtained from 9 swine infected with E suis, 8 7.7% were seropositive (titer greater than or equal to 200) via the ELISA, and 80.7% were seropositive (titer greater than or equal to 20) via the IHA test. The sensitivity of the ELISA was greater than that of the IHA test. All blood samples obtained from specific-pathogen-free swine tested negative for E suis antibody. Cross-reactions were not observed between E suis antigen and antisera against various swine and cattle disease agents using ELISA. We concluded that the ELISA may be used for rapid and effective diagnosis of infection with E suis in swine.

Brain, spleen, and selected lymph nodes from sheep with clinical signs of scrapie were analyzed for presence of proteinase K-resistant protein (PrP-res). Diagnosis of scrapie on the basis of detection of PrP-res was compared with diagnosis on the basis of histologic evaluation of the brain from clinically affected or exposed sheep. Proteinase K-resistant protein was found in every brain that was histologically positive for scrapie, and in addition, was found in the brain of several clinically positive sheep that were not diagnosed as scrapie-positive by histologic evaluation. Proteinase K-resistant protein was also found in 87% of the spleens and lymph nodes from sheep that had PrP-res detected in brain homogenates. Therefore, analysis of sheep brain, spleen, or lymph nodes for PrP-res provided a diagnostic approach that was superior to histologic examination alone for detection of naturally scrapie agent-infected sheep.