A relation exists between colloid osmotic pressure and serum total protein concentration; equations describing this relation have been used to determine a calculated value for colloid osmotic pressure. However, the relation between total protein concentration and colloid osmotic pressure is altered by the method used to measure protein and by changes in the ratio of concentrations of albumin (A) to globulin (G). We developed nomograms for estimating colloid osmotic pressure from A and G concentrations, using samples obtained from clinically normal animals and compared the accuracy of these nomograms with that of previously described equations relating colloid osmotic pressure to total protein concentration. For comparison, serum samples from canine (n = 106), equine (n = 79), feline (n = 24), and bovine (n = 27) patients admitted to the University of Georgia Veterinary Medical Teaching Hospital were used. Results indicated that nomograms based on protein concentration estimated by a refractometer generally were the least reliable. Although predictive nomograms, using total protein concentration determined by the biuret method, provided better results for serum samples, there was considerable variation between measured and calculated values for colloid osmotic pressure in all species studied. Calculated values for colloid osmotic pressure derived from A and G concentrations were most closely related to measured values for colloid osmotic pressure in dogs, horses, and cats. However, calculated values for colloid osmotic pressure differed from measured values by as much as 5 mm of Hg for some samples by each of the methods of estimation. These results indicate that, although calculated values for colloid osmotic pressure may be most accurate when variations in the A-to-G ratio are accounted for in the nomogram, none of the calculation methods provided a consistently accurate estimate of colloid osmotic pressure.

Serum C-reactive protein (CRP) concentration was measured, using an automated immunoturbidimetric assay, in 44 clinically normal dogs and 67 dogs with band neutrophil count greater than or equal to 10(9) cells/L, and values were found to be significantly (P less than or equal to 0.05) different. Correlation of serum CRP concentration and band neutrophil count in the 67 dogs with greater than or equal to 10(9) band neutrophils/L resulted in a statistically significant P less than or equal to 0.05), but low correlation coefficient of 0.34. Serum CRP concentration and CBC values were determined for 6 clinically normal dogs undergoing anesthesia (controls) and 6 clinically normal dogs undergoing anesthesia and ovariohysterectomy. Significant alterations in CBC results and serum CRP concentration, compared with baseline values, were lacking in dogs of the control group. Serum CRP concentration was significantly (P less than or equal to 0.05) increased above baseline values in dogs undergoing surgery and was significantly (P less than or equal to 0.05) increased, compared with values in control dogs by 12 hours after surgery. In dogs undergoing surgery, serum CRP concentration was also significantly (P less than or equal to 0.05) different from values in control dogs at 28 and 36 hours, but not at the 76- and 124-hour sample collection times. Alterations in CBC values compatible with possible or convincing inflammation were detected in 83% of the dogs undergoing surgery at the 8- and 12-hour postsurgery sample collection times, 100% of dogs at 16, 22, 28, and 36 hours after surgery, 83% of dogs at 52 and 76 hours after surgery, 67% of dogs at 100 hours after surgery, and 0% of dogs at 124 hours after surgery It was concluded that significant increases in CRP, concentration in dogs with surgical trauma were not detected earlier than CBC alterations compatible with possible or convincing inflammation.

Effects of dietary ochratoxin A (OA) and T-2 toxin, fed singly and in combination, were evaluated in growing crossbred pigs. Thirty-six barrows (3 replicates of 3 for each of 4 treatment groups, mean body weight, 18.0 kg) were fed: 0 mg of OA and 0 mg of T-2/kg of feed (control); 2.5 mg of OA/kg of feed; 8.0 mg of T-2/kg of feed; or 2.5 mg of OA plus 8.0 mg of T-2/kg of feed for 30 days. Production performance, serum biochemical, hematologic, immunologic, and pathologic evaluations were made. Body weight and body weight gain were decreased by all toxin treatments, but the combination toxin treatment reduced weight gain more than did either of the toxins administered singly and could be considered additive. Liver weight was decreased by combination treatment, whereas kidney weight was increased by OA treatment. Ochratoxin decreased serum cholesterol, inorganic phosphorus, and alkaline phosphatase values; reduced mean cell volume, hemoglobin concentration, and macrophage phagocytosis; and increased creatinine and total protein values. Consumption of T-2 toxin reduced hemoglobin and serum alkaline phosphatase values. The combination treatment decreased serum cholesterol, gamma-glutamyltransferase, alkaline phosphatase, mean cell volume, hematocrit, and hemoglobin values, as well as lymphoblastogenesis and phagocytosis, and increased serum nine concentration. We concluded that OA and T-2, singly or in combination, can affect clinical performance, serum biochemical, hematologic, and immunologic values, and organ weights of growing barrows. Although some analytes were affected more by the combination than by either toxin alone, the interactions could best be described as additive, not synergistic.

Staphylococcal antigens and immune complexes (IC) prepared from antigen and hyperimmune canine serum were tested for their effects on certain functions of mononuclear (MN) and polymorphonuclear (PMN) leukocytes (cells) obtained from healthy dogs. The effect on MN cells was studied by determining the ability of antigen or IC to augment or inhibit mitogenesis induced by phytohemagglutinin (PHA). The effect of antigen or IC on PHA cells was studied by measurement of H2O2 production as an indicator of respiratory burst. Neither the antigen nor the IC, when cultured with MN cells, was mitogenic. Coincubation of antigen or IC with MN cells and PHA resulted in a concentration-dependent decrease in mitogenesis. The decreased mitogenesis could not be overcome by addition of excess PHA, and may in part have been related to toxic effects of the antigen or IC on MN cells. When MN cells were instead preincubated with antigen or IC, then washed and stimulated with PHA, there was still a concentration-dependent inhibition of mitogenesis, although toxicity to the cells was not observed. Low concentrations of staphylococcal antigen or IC stimulated slight H2O2 production by PHA cells. When PHA cells were coincubated with IC and another stimulus (opsonized zymosan or phorbol myristate acetate), IC appeared to augment phorbol myristate acetate-, but not zymosan-induced stimulation. These results suggest that staphylococcal antigens, either alone or complexed with antibody, have the ability to stimulate PMN cells and inhibit MN cell function. Such actions may have a role in the pathogenesis of recurrent staphylococcal infection in canine patients.

The effect of topically applied 2% pilocarpine and 0.25% demecarium bromide on aqueous humor flare was evaluated while treating normal eyes of dogs 3 times daily for 8 days. Fifteen clinically normal Beagles were allotted to 2 drug treatment groups, and flare was measured, using laser flaremetry. Pilocarpine caused an increase of flare to 167 photon counts (pc)/ms at 7 hours, compared with the nontreated control eye mean value 3.7 pc/ms. By 31 hours, flare had decreased to 70 pc/ms with 3 daily topical treatments. By 55 hours, the flare measurement was in the normal range. Intraocular pressure (IOP) decreased in the treated eyes, compared with the nontreated eyes, and maximal decrease in IOP was observed at the same time as maximal flare. Demecarium induced a similar increase in flare and decrease in IOP, with peak effect seen at 31 hours. At that time, the flaremetry result was 28 pc/ms, compared with 3.4 pc/ms in the nontreated control eyes. After 8 days of 3 times daily treatment, flare values had returned to normal in eyes of dogs in both treatment groups. The transient increase in aqueous humor protein concentration did not result in ocular or visual damage, and long-term changes were not seen. The amount of flare increase attributable to topical application of pilocarpine was greater than the increase in human eyes when measured by use of laser flaremetry.

The efficacy of 4-methylpyrazole (4-MP) and ethanol as treatment for ethylene glycol (EG) intoxication in cats was compared. Twenty-two cats were assigned at random to 6 experimental groups. Cats of 1 experimental group were given only 4-MP; those of another experimental group were given only EG. Cats of 3 experimental groups were intoxicated with EG and given 4-MP at 0 hour or 2 or 3 hours after EG ingestion, and those of 1 experimental group were given EG and treated with ethanol 3 hours after EG ingestion. Physical, biochemical, hematologic, blood gas, serum and urine EG concentrations, and urinalysis findings were evaluated at 0, 1, 3, 6, 9, 12, 24, 48, and 72 hours, 1 week, and 2 weeks after EG ingestion, or 4-MP treatment in cats of the 4-MP only group. The half-life of EG and percentage of ingested EG excreted unchanged were determined for each group. 4-Methylpyrazole treatment at 0 hour was most effective at preventing metabolism of EG. 4-Methylpyrazole was not effective in preventing development of renal failure when given 2 or 3 hours after EG ingestion. Ethanol given 3 hours after EG ingestion was successful in preventing development of renal dysfunction in 2 of the 6 cats treated 3 hours after EG ingestion. Of the remaining 4 cats treated with ethanol, 2 developed transient renal dysfunction and 2 developed acute oliguric renal failure and were euthanatized. 4-Methylpyrazol given 2 or 3 hours after EG ingestion was less effective in preventing EG metabolism than was ethanol given 3 hours after EG ingestion. Therefore 4-MP, at the dose found to be effective in dogs, cannot be recommended as an alternative to ethanol for treatment of EG intoxication in cats.

Sonographic observations were made of the image mean gray scale (MGS) of the flexor tendons and ligaments in the left and right metacarpal regions of each of 10 clinically normal horses. In images made in the dorsal and sagittal planes, the MGS was measured at multiple sites in the superficial digital flexor tendon (SDFT), deep digital flexor tendon (DDFT), accessory ligament (AL), and suspensory ligament (SL), and at single sites in the medial and lateral limbs of the SL, and the palmar ligament. Relative sonographic brightness of each tendon and ligament was calculated by dividing the value of its MGS by the mean value for the MGS of images of 3 soft tissue equivalent phantoms. When a multivariate repeated-measures of ANOVA of the relative brightness values was statistically significant (P < 0.05), Tukey's method of multiple comparisons was used to determine which values were significantly different from each other. In the dorsal plane, the SL was significantly brighter than the DDFT, SDFT, and AL; relative brightnesses of the DDFT and SDFT were similar, as were those of the SDFT and AL. In the sagittal plane, the SL again was the significantly brightest structure, followed by the Al, and similar brightnesses of the DDFT and SDFT. In dorsal images made 25 cm distal to the accessory carpal bone, relative brightnesses of the SDFT, DDFT, and the medial and lateral limbs of the SL were similar. In images made 30 cm distal to the accessory carpal bone, relative brightness of the palmar ligament was significantly (P < 0.05) less than that of the SDFT and DDFT in the dorsal plane, but not in the sagittal plane, where it was significantly greater. Relative brightness values represented a unique sonographic characteristic of each structure and, in the future, may provide further insights into tendon and ligament structure and function.

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.

Keratan sulfate (KS) is a glycosaminoglycan, distribution of which is confined mostly to hyaline cartilage. As such, it is a putative marker of hyaline cartilage catabolism. In experiment 1, a focal osteochondral defect was made arthroscopically in 1 radial carpal bone of 2 ponies, and in 2 other ponies, chymopapain was injected into the radiocarpal joint to induce cartilage catabolism. Sequential and concurrent plasma and synovial fluid concentrations of KS were measured, up to 13 months after induction of cartilage injury, to determine whether changes in KS concentrations reflected cartilage catabolism. In experiment 2, a large, bilateral osteochondral defect was made in the radial carpal bones of 18 ponies, which were subsequently given postoperative exercise and/or injected intra-articularly with 250 mg of polysulfated glycosaminoglycan (PSGAG). Medication was given at surgery, then weekly for 4 weeks. Blood samples were collected and synovial fluid was aspirated before surgery, when medication was given, and at postmortem examination (postoperative week 17). The KS concentration was measured in these fluids to determine whether changes in KS concentration indicated an effect of joint treatment. In experiment 1, the concentration of KS in synovial fluid was highest 1 day after joint injury, and the concentration in plasma peaked 2 days after joint injury. For ponies receiving chymopapain intra-articularly (generalized cartilage catabolism), a fivefold increase over baseline was observed in the concentration of KS in plasma (peak mean, 1.2 microgram/ml), and a tenfold increase over baseline in synovial fluid (peak mean, 2.0 mg/ml) was observed. On average, these maxima were threefold higher than values in fluids of ponies with osteochondral defects (focal cartilage disease). In experiment 2, nonexercised ponies had lower KS concentration (as a percentage of the preoperative concentration) in synovial fluid than did exercised ponies at all postoperative times, and.

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.