We investigated the influence of parasympathetic tone on the arrhythmogenicity of graded dobutamine infusions in horses anesthetized under clinical conditions. Six horses were used in 9 trials. Two consecutive series of graded dobutamine infusions were given IV; each continuous graded dobutamine infusion was administered for 20 minutes. The dobutamine infusion dosage (5, 10, 15, and 20 microgram/kg of body weight/min) was increased at 5-minute intervals. Isovolumetric saline solution vehicle (v) or atropine (A; 0.04 mg(kg) was administered IV, or bilateral vagotomy (VG) was performed as a treatment before the second series of dobutamine infusions. Treatment was not administered prior to the first dobutamine infusion. Significant interaction between treatment and dosage of dobutamine infusion existed for differences from baseline for mean arterial pressure, systolic arterial pressure, diastolic arterial pressure, heart rate, and cardiac index at dosages of 5 and 10 micrograms of dobutamine/kg/min, given IV and for heart rate at dosage of 15 micrograms of dobutamine/kg/min, given IV. Results for group-V horses were different from those for group-A and group-VG horses, but were not different between group-A and group-VG horses in all aforementioned cases, except for heart rate and cardiac index at dosage of 5 micrograms of dobutamine/kg/min, given IV. Normal sinus rhythm, second-degree atrioventricular block, and bradyarrhythmias predominated during low dobutamine infusion rates during the first infusion series (nontreated horses) and in group-V horses during the second infusion series. Only tachyarrhythmias were observed during the second infusion series in the horses of the A and VG groups. The modulating influence of parasympathetic nervous system activity on hemodynamics and development of arrhythmia was conspicuous during low dobutamine infusion rates. Significant differences were not observed in hemodynamic responses to dobutamine, with respect to parasympathetic influence at high dobutamine infusion rates.

Ovine progressive pneumonia (OPP) is a lentivirus-induced disease of sheep in the United States that is similar, if not identical, to maedi/visna in many other countries. Prevalence estimates of seropositivity to this virus in sheep in the United States have been confined to limited groups or flocks of sheep and have varied from 1 to 90%. In this study of detection of antibodies against OPP virus, we found a lower general prevalence of antibodies to OPP virus in sheep than was previously reported. Of 16,827 sheep from 29 states in the United States, 26% were seropositive and 48% of 164 flocks that were tested had 1 or more seropositive sheep. Seropositivity to OPP virus for sheep within special categories was determined, although nonrandom samples that were available may have biased the results. Within regions of the United States, prevalence was highest in the Rocky Mountain region at 49% and lowest in the northern Atlantic region at 9%. Seropositive sheep were not evenly distributed among flocks, but were clustered in a few flocks of sheep. A high number of flocks had no or few seropositive sheep. Prevalence increased with age from 4% at < 1 year to a plateau of 34% at 4 years. Seropositivity was variable among breeds and was not associated with sex, wool class, or place of origin of ancestors.

Six nontrained mares were subjected to steady-state, submaximal treadmill exercise to examine the effect of exercise on the plasma concentration of atrial natriuretic peptide (ANP) in arterial, compared with mixed venous, blood. Horses ran on a treadmill up a 6 degree grade for 20 minutes at a speed calculated to require a power equivalent to 80% of maximal oxygen uptake. Arterial and mixed venous blood samples were collected simultaneously from the carotid and pulmonary arteries of horses at rest and at 10 and 20 minutes of exercise. Plasma was stored at -80 degrees C and was later thawed; ANP was extracted, and its concentration was determined by radioimmunoassay. Exercise caused significant (P < 0.05) increases in arterial and venous plasma ANP concentrations. Mean +/- SEM arterial ANP concentration increased from 25.2 +/- 4.4 pg/ml at rest to 52.7 +/- 5.2 pg/ml at 10 minutes of exercise and 62.5 +/- 5.2 pg/ml at 20 minutes of exercise. Mean venous ANP concentration increased from 24.8 +/- 4.3 pg/ml at rest to 67.2 +/- 14.5 pg/ml at 10 minutes of exercise and 65.3 +/- 13.5 pg/ml at 20 minutes of exercise. Significant differences were not evident between arterial or mixed venous ANP concentration at rest or during exercise, indicating that ANP either is not metabolized in the lungs or is released from the left atrium at a rate matching that of pulmonary metabolism.

Platelet aggregation and adenosine triphosphate (ATP) release were measured by use of the impedance method in blood samples obtained from 25 adult female Beagles before and after sedation with acepromazine (0.13 mg/kg of body weight) and atropine (0.05 mg/kg), and during general anesthesia. General anesthesia was induced by IV administration of thiamylal (average dosage, 2.1 mg/kg, range, 1.2 to 4.2 mg/kg) and was maintained with halothane in oxygen. Samples of jugular venous blood were obtained from each dog, using citrate as anticoagulant. Platelet count was done on each sample. Platelet aggregation and ATP released from the aggregating platelets were measured within 2.5 hours of sample collection, using a whole-blood aggregometer. Adenosine diphosphate (ADP) or collagen was used as aggregating agent. For each aggregating agent, platelet aggregation and ATP release were measured over 6 minutes. After sedation with acepromazine and atropine, significant (P < 0.01) reduction was observed in platelet count (from median values of 341,000 cells/microliter to 283,000 cells/microliter) and in the ability of platelets to aggregate in response to ADP (from 14.0 to 7.0 Ohms). During the same period, maximal release of ATP in response to collagen also was reduced (from 5.56 micromoles to 4.57 micromoles; P < 0.01); however, this difference ceased to be significant when ATP release was normalized for platelet count. During general anesthesia and surgery (200 minutes after sedation), platelet count and aggregation responses to ADP and collagen had returned to presedation values. None of the dogs in this study appeared to have hemostasis problems during surgery. In conclusion, sedation with acepromazine and atropine induces measurable inhibition of ADP-induced platelet aggregation that resolves during subsequent general anesthesia and surgery. Transient inhibition of platelet aggregation is not manifested by a change in gross hemostasis during surgery.

The biomechanical strength and stiffness of 3 fixation techniques used to repair acute slipped capital femoral epiphysis were evaluated in bone specimens from immature dogs. A servohydraulic testing machine was used to create slipped capital femoral epiphysis in 9 pairs of femurs by shearing the capital femoral epiphysis along the physis in a craniocaudal direction. The slip was reduced and repaired with 1, 2, or 3 double-pointed, 1.6-mm (0.062-inch) smooth pin(s) and retested. The strength and stiffness of each intact femur (which served as the control) and repaired femur were compared. Results of the study indicated that differences among the failure strengths of 1- and 2-pin fixations and their respective controls were not significant; however, the 3-pin fixation was 29% stronger than its control and was 60 and 45% stronger than the 1- and 2-pin fixations, respectively. One- and 2-pin fixations were 34 and 24% less stiff than their respective controls, whereas the stiffness of the 3-pin fixation was similar to its control. The 2- and 3-pin fixations were 48 and 76% stiffer, respectfully, than the 1-pin fixation, but were not significantly different, compared with each other.

Serum lipoprotein concentrations, routine serum biochemical values, and morphologic changes of the liver were evaluated in cats undergoing weight loss. Food was withheld from 6 obese and 6 control cats for 3 days (days 0 to 2), followed by feeding 50% of previous food intake for 26 days (days 3 to 28). Percutaneous liver biopsy specimens were obtained from all cats on days 0, 7, 14, and 28. Blood samples for serum biochemical analysis and lipoprotein profiles were obtained on days 0, 3, 7, 14, and 28. All cats lost weight throughout the study, and none developed signs of chemical illness, including those of idiopathic hepatic lipidosis syndrome. Serum total cholesterol concentrations decreased initially in all cats, but rapidly returned to normal after day 3 in obese cats, suggesting altered cholesterol metabolism during dietary restriction. Low-density lipoprotein concentrations decreased throughout the study in control cats, but were unchanged in obese cats. Examination of liver biopsy specimens from each cat revealed minimal lipid accumulation in all specimens, although some specimens contained hydropic degeneration.

Five cats were treated with an azathioprine suspension (2.2 mg/kg of body weight on alternate days) and 2 cats were given vehicle (controls) for 9 weeks. Complete blood and platelet counts and serum biochemistry variables were monitored weekly. Bone marrow aspirates were evaluated every 3 weeks, and core bone marrow biopsy was performed at the end of the study. Profound neutropenia (< 600 cells/microliter) was observed in all treated cats, and 1 cat developed pancytopenia. Treatment was discontinued if the WBC count was < 3,000 cells/microliter. Four weeks after discontinuation of azathioprine, 1 treated cat again was given azathioprine at a lower dosage (1.1 mg of azathioprine/kg on alternate days) and neutropenia recurred within 2 weeks. During treatment, 3 cats developed thrombocytosis, and 2 developed thrombocytopenia. In 4 of 5 cats, neutropenia and thrombocytopenia resolved when azathioprine was discontinued. Bone marrow cytologic examination during treatment revealed reduction of the neutrophil line, with relative increase in monocytes. Core bone marrow biopsy at the completion of the study revealed hypocellular marrow with marked decrease in the myeloid series in cats given azathioprine. One of the cats that was treated with azathioprine had a hyperceullar marrow with increased numbers of mature granulocytes and precursors; however, azathioprine had been discontinued 3 weeks prior to biopsy. Alterations in serum biochemical variables were not associated with azathioprine. Two cats that were treated with azathioprine developed respiratory tract infections, and 1 of them was euthanatized during the study.

In 8 Holstein cows, 50 colony-forming units (CFU) Of Escherichia coli was administered into 1 mammary gland. Infections were established in all inoculated glands. In 4 of the 8 cows, 500 mg of gentamicin sulfate was administered by intramammary infusion 14 hours after inoculation; the other 4 cows were untreated controls. Infusions of gentamicin also were given after each of the 3 successive milkings after the initial infusion, so that a total dose of 2 g of gentamicin was given to each of the treated cows. During the 33-hour treatment period and for the first milking after the last infusion of gentamicin, the treated cows had a mean gentamicin concentration of greater than or equal to 31.0 microgram/ml in milk samples that were collected from inoculated quarters immediately before each milking. Concentrations of 0.34 and 0.69 microgram of gentamicin were detected in milk from 2 cows at 8 days after inoculation with E coli. Mean serum concentrations of gentamicin were > 0.37 microgram/ml throughout the treatment period and the first 12 hours after the last infusion, with a mean peak concentration of 0.96 microgram/ml at 24.4 hours. The range of peak concentration of gentamicin detected in urine from all treated cows was 42 to 74.4 microgram/ml. Peak concentration of E coli in milk in the treated cows (6.08 +/- 1.02 log10 CFU/ml) did not significantly (P > 0.05) differ from that of the control cows (5.26 +/- 1.00 log10 CFU/ml). Similarly, mean duration of infection in the treated cows (54 hours) did not differ significantly from that of the control cows (48 hours). The treatment groups also did not differ significantly in peak concentrations of albumin or IgG1 in milk, although mean concentrations of albumin and IgG1 at 16 hours after inoculation, and of albumin at 20 hours, was significantly (P < 0.05) higher in the milk from control cows than from the treated cows. Mean values of peak rectal temperature and of mean rectal temperature throughout the trial did not differ between the groups. At the end of the 4-week trial, 1 of 4 inoculated glands in treated cows and 3 of 4 in control cows had somatic cell counts less than or equal to preinoculation concentrations (5.18 log10 cells/ml). Intramammary administration of gentamicin did not affect the duration or severity of experimentally induced E coli mastitis. In addition, substantial concentrations of gentamicin were detected in the serum of treated cows, suggesting that intramammary treatment may result in prolonged drug residues in tissue.

Glycoprotein I (gI) phenotypes and genotypes of 4 pseudorabies viral diagnostic isolates were evaluated by use of in vitro DNA amplification, monoclonal antibody binding, gI-specific serodiagnostic responses, and in vivo virulence approaches. Three viruses were avirulent and did not elicit gI-specific serologic responses, react with gI-specific monoclonal antibodies, or contain gI epitope-encoding DNA sequences. The fourth virus was virulent and did elicit a gI-specific serodiagnostic response. Compared with reference virulent pseudorabies viruses, however, the fourth isolate had reduced reactivity with a group of gI monoclonal antibodies and had a single nucleotide sequence substitution with a corresponding putative amino acid change in the epitopically dominant portion of the gI molecule. Presumably, the first 3 isolates represented diagnostic recoveries of viruses derived from gI-deleted modified-live pseudorabies viral vaccines, whereas the fourth isolate was a virulent but gI-aberrant wild-type virus. Thoroughly assessing the gI status of pseudorabies viral diagnostic isolates was considered to be essential in evaluating the epidemiologic importance of these viruses and in monitoring the validity of gI-based vaccine companion tests now used worldwide in pseudorabies control and eradication programs.

The effect of xylazine on the arrhythmogenic dose of epinephrine (ADE) was studied in 9 horses. Anesthesia was induced by administration of guaifenesin (50 mg/kg of body weight, IV) followed by thiamylal (4 to 6 mg/kg, IV) and was maintained at 1 minimal alveolar concentration MAC) of halothane (0.89%). Base apex ECG and facial artery pressure were recorded. Epinephrine was infused in a sequence of arithmetically spaced increasing rates (initial rate 0.25 (Lg/kg/min) for a maximum of 10 minutes. The ADE was defined as the lowest epinephrine infusion rate to the nearest 0.25 microgram/kg/min at which at least 4 premature ventricular depolarizations occurred in a 15-second period. Xylazine (1.1 mg/kg, IV) was administered after the control ADE was determined. Xylazine did not significantly alter the ADE (control, 1.12 +/- 0.38 microgram/kg/min; xylazine, 1.21 +/- 0.46 microgram/kg/min). Blood pressure increased transiently for 8 minutes after xylazine administration. Baseline systolic and diastolic arterial pressures and heart rate were not significantly different from control baseline pressures and heart rate 15 minutes after xylazine administration. Blood pressure and heart rate increased significantly during control and xylazine ADE determinations. Significant differences in pH, PaO2, PaCO2, or base excess were not observed between baseline and ADE in the control or xylazine groups. One horse developed atrial fibrillation, and 2 horses developed ventricular fibrillation during ADE determinations.