Minimal inhibitory concentration of 42 antimicrobial agents was determined against 57 field strains of Actinobacillus pleuropneumoniae isolated from pigs in Spain. Penicillins, aminoglycosides, and tetracyclines had irregular activity; ticarcillin, tobramycin, and doxycycline were the most active of each group, respectively. Macrolides, vancomycin, dapsone, and tiamulin, to which strains had high rate of resistance, were almost ineffective. Thiamphenicol, colistin, rifampin, fosfomycin, mupirocin, and metronidazole had good activity, with resistance ranging between 0 and 8.8%. Finally, cephalosporins (except cephalexin) and quinolones especially ciprofloxacin, enrofloxacin, and sparfloxacin) were the most active antibiotics against A pleuropneumoniae.

We investigated the influence of parasympathetic tone on the arrhythmogenic dose of dobutamine in horses premedicated with xylazine, anesthetized with guaifenesin and thiamylal, and maintained on halothane in oxygen. Six horses were used in 12 randomized trials. In each trial, after end-tidal halothane concentration was stabilized at 1.1% (1.25 times minimum alveolar concentration [MAC]) in oxygen, either saline solution (0.02 ml/kg of body weight) or atropine (0.04 mg/kg) was administered IV. Five minutes later, dobutamine infusion was started at dosage of 2.5 micrograms/kg/min, IV. The dobutamine infusion was continued for 10 minutes, or until 4 or more premature ventricular complexes occurred within 15 seconds, or sustained narrow-complex tachyarrhythmia clearly not sinus in nature occurred. If the criteria for termination were not met, dobutamine infusion was increased by 2.5 micrograms/kg/min, after the hemodynamic variables had returned to baseline. The horses were allowed to recover, and were rested for at least 1 week before the second trial. The arrhythmogenic dose of dobutamine was calculated by multiplying the infusion rate by the elapsed time into infusion when arrhythmia occurred. There was significant difference between the arrhythmogenic dose of dobutamine (ADD) in saline-treated horses (mean +/- SEM, ADD 105.6 +/- 16.3 micrograms/kg) and atropinized horses (ADD 36.2 +/- 8.7 micrograms/kg). There were no differences in the prearrhythmia or immediate postarrhythmia ventricular heart rate (HR) or systolic (SAP), diastolic (DAP), or mean (MAP) arterial pressures between treated and control groups. The change in hemodynamic variables from prearrhythmia to immediate postarrhythmia formation was not different between the 2 groups. Ventricular beats were clearly evident in 8 of the 12 arrhythmias meeting the criteria for establishing the ADD. These results indicate that atropine may lower the arrhythmogenic threshold.

Using catheter mounted microtip manometers, right atrial, pulmonary artery, and pulmonary artery wedge pressures were studied in 8 horses while they were standing quietly (rest), and during galloping at treadmill speeds of 8, 10, and 13 m/s. At rest, mean (+/- SEM) heart rate, mean right atrial pressure, mean pulmonary artery pressure, and mean pulmonary artery wedge pressure were 37 (+/- 2) beats/min, 8 (+/- 2) mm of Hg, 31 (+/- 2) mm of Hg, and 18 (+/- 2) mm of Hg, respectively. Exercise at treadmill belt speed of 8 m/s resulted in significant (P < 0.05) increments in heart rate, right atrial pressure, pulmonary artery systolic, mean, diastolic and pulse pressures, and pulmonary artery wedge pressure. All these variables registered further significant (P < 0.05) increments as work intensity increased to 10 m/s, and then to 13 m/s. Pulmonary artery diastolic pressure was, however, not different among the 3 work intensities. During exercise at belt speed of 13 m/s, heart rate, mean right atrial pressure, mean pulmonary artery pressure, pulmonary artery pulse pressure, and mean pulmonary artery wedge pressure were 213 (+/- 5) beats/min, 44 (+/- 4) mm of Hg, 89 (+/- 5) mm of Hg, 69 (+/- 4) mm of Hg, and 56 (+/- 4) mm of Hg, respectively. Assuming mean intravascular pulmonary capillary pressure to be halfway between the mean pulmonary arterial and venous pressures, its value during exercise at 13 m/s may have approached 72.5 mm of Hg. Transmural pressure (intravascular minus alveolar pressure) across pulmonary capillaries may be even higher because of the large negative pleural pressure swings in galloping horses. High transmural pressures may cause stress failure of pulmonary capillaries, resulting in exercise-induced pulmonary hemorrhage.

A study was designed to compare use of an numerical rating scale (NRS) and a visual analogue scale (VAS) for subjective assessment of lameness, using sheep as a model. The NRS consisted of 5 divisions, 0, 1, 2, 3, and 4; 4 of these divisions (1-4) described lameness. The VAS used a 100-mm horizontal line with vertical bars at either end; one end was labeled 'sound' and the other was labeled 'could not be more lame.' Two independent observers graded lameness in 62 sheep, and between- and within-observer differences were assessed for each scoring system to compare the NRS with the VAS. Results indicated no significant differences between the 2 observers scoring lameness, using either the VAS or the NRS. The scores obtained, using the VAS, were not normally distributed, although differences between scores for the 2 observers were. The NRS scores followed a normal distribution pattern. Investigation of repeated measurement for the same sheep, using both scales, revealed no significant difference between either. A comparison of the NRS and VAS scores made by each observer indicated that although correlation was good (observer 1; r = 0.94; observer 2; r = 0.95), there was not perfect agreement. The maximal NRS score of 4 was associated with VAS values > 68 mm, indicating that the NRS divisions did not reflect equal increases in lameness. The VAS and NRS scores for each observer were highly reproducible, although they were more variable for sheep that were regarded as moderately lame. Results indicate that although the NRS and VAS compared favorably with respect to repeatability, reproducibility, and use by 2 observers, the VAS is inherently more sensitive. In addition, the NRS and VAS should not be used interchangeably.

Strength in bending was determined for inter. dental fixation apparatuses applied to hemimandibles obtained from 24 canine cadavers. Hemimandibles were osteotomized perpendicular to the long axis between the third and fourth premolars, and segments were stabilized with 1 of 5 interdental fixation apparatuses: Erich arch bar (EAB, n = 6); Stout loop (SL, n = 6); acrylic A, n = 6); Stout loop and acrylic (SLA, n = 24); and Erich arch bar and acrylic (EABA, n = 6). Ultimate strengths (mean +/- SEM) of EAB, SL, A, SLA, and EABA were 395 +/- 48; 523 t 57; 1,106 +/- 102; 1,306 +/- 156; and 2,707 +/- 504 N.m, respectively. Stiffness (mean +/- SEM) of EAB, SL, A, SLA, and EABA were 2,944 t 357; 6,322 +/- 2,201; 16,010 +/- 5,017; 15,777 +/- 1,026; and 27,079 +/- 5,576 N.m/ radian, respectively. Yield strengths (mean +/- SEM) Of EAB, SL, A, SIA, and EABA were 66 +/- 6; 264 +/- 19; 911 +/- 126; 1,114 +/- 159; and 1,855 +/- 401 N.m, respectively. There were no significant differences in acrylic weight, cross-sectional area of the acrylic, or area moment of inertia of acrylic at the osteotomy site among A, SIA, and EABA; and there were no significant differences in osteotomy surface area and area moment of inertia at the osteotomy site among all apparatuses (P > 0.05). The EABA apparatus had significantly higher mean ultimate strength, mean stiffness, and mean yield strength compared to other interdental fixation apparatuses. There were no significant differences in the mean ultimate strength, mean stiffness, or mean yield strength between EAB and SL (P > 0.05). Apparatuses that combine acrylic with metal reinforcement (SLA, EABA) were significantly stronger and stiffer than those that used metal alone (EAB, SL) or acrylic alone (A).

Transcutaneous oxygen (PO2.TC) monitoring is commonly used in human medicine for evaluating skin viability. The application of transcutaneous monitoring for evaluating skin viability in dogs was investigated. The changes in PO2-TC values were measured from 16 avascular skin flaps created along the lateral hemithoraces of 4 dogs. Transcutaneous oxygen values were serially recorded from the vascular base and avascular apex of each flap for 12 hours after surgery. A single transcutaneous measurement was obtained from each flap base and apex 24 hours after surgery. Serial arterial blood gas analyses were obtained to compare central oxygen values with PO2-TC values. Full-thickness skin biopsy specimens were harvested from the base and apex of each flap 24 hours after surgery. The flaps were observed for 4 days and then excised for histologic examination. A subjective grading scale was used to assess histologic changes. Throughout the 12-hour period and at 24 hours, a statistically significant difference was found between the PO2-TC values for apices and bases of the flaps. The mean PO2-TC for all bases was 90.9 mm of Hg +/- 3.3 SEM, and the mean PO2-TC for all apices was 21.2 mm of Hg +/- 1.8 SEM. The mean regional perfusion index (apex PO2.TC/base PO2-TC) was 0.23 +/- 0.02. The subjective numbers assigned to the biopsy specimens were statistically evaluated by using a paired Student's t test and a Wilcoxon signed-rank test. A significant difference was found between the numbers for the collective bases and apices with both tests. A statistically significant difference was found between the numbers for the apex biopsy specimens taken 24 hours after creation of the skin flap and those taken when the flap was excised, whereas no difference was found between the numbers for the base biopsy specimens. On the basis of our findings, PO2-TC monitoring is a useful technique for assessing skin viability in dogs.

The effect of hypercapnia on the arrhythmogenic dose of epinephrine (ADE) was investigated in 14 horses. Anesthesia was induced with guaifenesin and thiamylal sodium and was maintained at an end-tidal halothane concentration between 0.86 and 0.92%. Base-apex ECG, cardiac output, and facial artery blood pressure were measured and recorded. The ADE was determined at normocapnia (arterial partial pressure of carbon dioxide [Pa(CO2)] = 35 to 45 mm of Hg), at hypercapnia (Pa(CO2) = 70 to 80 mm of Hg), and after return to normocapnia. Epinephrine was infused at arithmetically spaced increasing rates (initial rate = 0.25 micrograms/kg of body weight/min) for a maximum of 10 minutes. The ADE was defined as the lowest epinephrine infusion rate, to the nearest 0.25 micrograms/kg/min, at which 4 premature ventricular complexes occurred in a 15-second period. The ADE (mean +/- SD) during hypercapnia (1.04 +/- 0.23 micrograms/kg/min) was significantly (P < 0.05) less than the ADE at normocapnia (1.35 +/- 0.38 micrograms/kg/min), whereas the ADE after return to normocapnia (1.17 +/- 0.22 micrograms/kg/min) was not significantly different from those during normocapnia or hypercapnia. Baseline systolic and diastolic arterial pressures and cardiac output decreased after return to normocapnia. Significant differences were not found in arterial partial pressure of O2 (Pa(O2)) or in base excess during the experiment. Two horses developed ventricular fibrillation and died during normocapnic determinations of ADE. Hypercapnia was associated with an increased risk of developing ventricular arrhythmias in horses anesthetized with guaifenesin, thiamylal sodium, and halothane.

We evaluated the biochemical and hemodynamic response to hypertonic saline solution plus dextran in isoflurane-anesthetized pigs infused IV with Escherichia coli endotoxin (5 micrograms/kg of body weight for 0 to 1 hour + 2 micrograms/kg for 1 to 4 hours). After 120 minutes of endotoxemia, pigs were treated with a bolus (4 ml/kg over 3 minutes) of either normal saline solution (NSS; 0.9% NaCl), or hypertonic saline solution plus dextran (HSSD; 7.5% NaCl + 6% dextran-70). Administration of HSSD significantly (P < 0.05) increased serum osmolality and concentrations of sodium and chloride for approximately 2 hours during endotoxemia. Plasma total protein concentration decreased significantly (P < 0.05) for 2 hours after treatment with HSSD, indicating hemodilution and increased plasma volume. Although HSSD transiently increased cardiac index (CI) for approximately 15 minutes, this effect was not sustained; however, the endotoxin-induced decrease in CI was ameliorated from 120 to 180 minutes. In pigs of the endotoxin + NSS group from 180 to 240 minutes, CI decreased significantly (P < 0.05), compared with baseline and control values. The endotoxin-induced increases in mean pulmonary arterial pressure and pulmonary vascular resistance were not attenuated by HSSD. At 135 minutes, total peripheral vascular resistance was transiently lower (for approx 15 minutes) in pigs treated with HSSD, compared with control pigs. The endotoxin-induced increase in plasma lactate concentration was not attenuated by HSSD, indicating continued peripheral O2 debt. We conclude that, despite sustained increases in serum osmolality and concentrations of sodium and chloride, HSSD has only transiently beneficial cardiopulmonary effects during endotoxemia in pigs.

Cardiorespiratory effects of abdominal insufflation were evaluated in 8 dogs during isoflurane anesthesia. Each dog was studied 3 times, in 1 of the following orders of insufflation pressures: 10-20-30, 20-30-10, 30-20-10, 10-30-20, 20-10-30, and 30-10-20 mm of Hg. Anesthesia was induced by use of a mask, dogs were intubated, and anesthesia was maintained by isoflurane in 100% oxygen. After instrumentation, baseline values were recorded (time 0), and the abdomen was insufflated with nitrous oxide. Data were recorded at 5, 10, 15, 20, 25, and 30 minutes after insufflation. The abdomen was then desufflated, with recording of data continuing at 35 and 40 minutes. Mean arterial pressure increased at 5 minutes during 20 mm of Hg insufflation pressure, and from 20 to 30 minutes during 30 mm of Hg pressure. Tidal volume decreased from 5 to 30 minutes during 10 and 20 mm of Hg pressures, and from 5 to 40 minutes during 30 mm of Hg pressure. Minute ventilation decreased at 10 and 20 minutes during 20 mm of Hg pressure. End-tidal CO2 concentration increased from 5 to 30 minutes during 20 and 30 mm of Hg pressure. The PaCO2 decreased at 40 minutes during 10 mm of Hg pressure, at 30 minutes during 20 mm of Hg pressure, and from 10 to 40 minutes during 30 mm of Hg pressure. Values for pH decreased from 10 to 30 minutes during 20 and 30 mm of Hg pressures. The PaO2 decreased from 20 to 40 minutes during 10 mm of Hg pressure, at 30 minutes during 20 mm of Hg pressure, and from 10 to 40 minutes during 30 mm of Hg pressure. Percentage decrease in tidal volume was greater at 5 and 15 minutes with 30 mm of Hg pressure. Differences in percentage increase in end tidal CO2 concentration were observed among the 3 pressures from 5 to 30 minutes. Although significant, these changes do not preclude use of laparoscopy if insufflation pressure > 20 mm of Hg is avoided.

A serologic survey was conducted to determine the prevalence and seroconversion rates for ovine adenovirus (OAV) serotypes 1-4 and bovine adenovirus (BAV) serotypes 2, 3, and 7 in sheep in Iowa and in surrounding states. For 2 consecutive years, paired serum samples were obtained from 1- to 2-month-old lambs as they entered a ram test station and, again, 2 months later. Sera were tested for adenovirus antibodies by use of a microtitration serum virus-neutralization test. At the time of entry, high prevalence of antibody (titer greater than or equal to 2) was detected to all tested adenoviruses except BAV-3. All adenoviruses were active in the ram test station both years, as indicated by greater than or equal to fourfold increase in adenovirus antibody titer (seroconversion) in some of the lambs. The prevalence and seroconversion rate for OAV-1 was 94.0 and 7.2%, respectively; for OAV-2, 98.6 and 15.1%; for OAV-3, 86.5 and 11.0%; for OAV-4, 98.4 and 13.2%; for BAV-2, 97.6 and 22.4%; for BAV-3, 11.4 and 3.8%; and for BAV-7, 81.6 and 4.5%. The results indicate that adenovirus infections were widespread in the sheep population and that the prevalence of active infection based on seroconversion rates was approximately 45%.