The effect of right paralumbar fossa exploratory celiotomy and omentopexy on peritoneal fluid constituents was studied in 22 adult dairy cows. Six cows were eliminated on the basis of physical examination findings (n = 2), surgical findings (n = 2), or inability to obtain a sufficient volume of peritoneal fluid (n = 2). Sixteen cattle had normal results of Csc and serum biochemical analysis, and a minimum of 1 ml of peritoneal fluid was obtained by abdominocentesis. Abdominocentesis was repeated on days 1, 2, and 6 after surgery. Statistical analysis for repeated measures was performed, using a significance level of P < 0.05. Stage of gestation was evaluated for interaction with time. Mean total nucleated cell count was 3,200 cells/1 before surgery, was significantly increased 2 days after surgery (16,336 cells/microliter), and continued to increase through day 6 (20,542 cells/microliter). Mean polymorphonuclear cell count was 1,312 cells/microliter before surgery and was significantly higher at 2 (11,043 cells/microliter) and 6 (10,619 cells/microliter) days after surgery. Mean lymphocyte count was 254 cells/microliter before surgery and was significantly increased 2 days (1,911 cells/microliter) after surgery. By day 6, lymphocyte numbers were similar to preoperative values. Mean mononuclear cell count was 770 cells/microliter before surgery and was significantly increased on days 1 (3,084 cells/microliter), 2 (3,285 cells/microliter and 6 (2,349 cells/microliter) after surgery. Mean eosinophil numbers were 1,388 cells/microliter before surgery and were significantly increased on day 6 (6,347 cells/microliter) only. Interaction between time and stage of gestation was found only for specific gravity and total protein concentration. In general, specific gravity and total protein concentration increased after surgery (mean before surgery, 1.016 and 3.6 g/dl; mean after surgery, 1.021 and 5.6 g/dl). Left paralumbar fossa celiotomy performed 7 days after surgery did not reveal complications of repeated abdominocentesis, and pregnancy status was unchanged. Peritoneal fluid constituents are highly variable after exploratory celiotomy and omentopexy in cattle. However, results of this study may provide a reference for interpretation of postoperative peritoneal fluid sample findings in cattle.

Ursodeoxycholic acid (UDCA; 10 mg/kg of body weight) was administered orally to 5 healthy cats for 3 months. Signs of illness were not apparent in any cat during treatment with UDCA. Results of monthly CBC, serum biochemical analysis, and urinalysis were unchanged during drug administration. There was a decrease in serum cholesterol concentration in 4 cats. Total postprandial serum bile acids (PPSBA) concentration was significantly (P = 0.0003) increased over total preprandial serum bile acids (PRSBA) concentration at all sample collection periods. The PRSBA and PPSBA concentrations were significantly (P < 0.05) increased at all sample collection periods after administration of UDCA, compared with baseline values. Ursodeoxycholic and tauroursodeoxycholic acids were not detected in serum prior to initiating administration of UDCA. Both bile acids were detected in the serum of all cats 1 and 2 months after UDCA administration and were detected in the serum of 2 cats 3 months after initiating UCDA administration. Hepatic ultrasonographic findings were normal before and after completion of UDCA administration. A mild, focal lymphocytic infiltrate was observed in 3 cats 3 months after initiating UDCA administration. Results of the study indicate that UDCA is absorbed into the systemic circulation of cats after oral administration, undergoes hepatic conjugation, and appears to be safe.

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.

4-Methylpyrazole (4-MP), an alcohol dehydrogenase inhibitor, was administered to dogs to treat ethylene glycol (EG) intoxication. Eleven dogs were given 10.6 g of EG/kg of body weight; 5 dogs were treated with 4-MP 5 hours after EG ingestion and 6 dogs were treated with 4-MP 8 hours after EG ingestion. 4-Methylpyrazole was administered IV as a 50-mg/dl solution in 50% polyethylene glycol: initial dose, 20 mg/kg; at 12 hours after initial dose, 15 mg/ kg; at 24 hours after initial dose, 10 mg/kg, and at 30 hours after initial dose, 5 mg/kg. Physical, biochemical, hematologic, blood gas, serum and urine EG concentrations, and urinalysis findings were evaluated at 0, 1, 3, 6, 9, 12, 24, 48, 72 hours, and at 1 week and 2 weeks after EG ingestion. Dogs of both groups developed clinicopathologic signs associated with EG intoxication, including CNS depression, hyperosmolality, high anion gap metabolic acidosis, polydipsia, polyuria, calcium oxalate monohydrate and dihydrate crystalluria, and isosthenuria. Fractional excretion of sodium was increased in all dogs between 1 and 9 hours after EG ingestion, but remained increased beyond 24 hours only in the 2 dogs treated at 8 hours after EG ingestion that developed acute renal failure. All dogs treated 5 hours after EG ingestion recovered without morphologic, biochemical, or clinical evidence of renal impairment. Of the 6 dogs treated 8 hours after EG ingestion, 2 developed acute renal failure. One of the dogs treated 8 hours after EG ingestion remained isosthenuric for 2 months, but did not manifest any other signs of renal impairment. Of the dogs treated 8 hours after EG ingestion, 3 recovered without morphologic, biochemical, or clinical evidence of renal impairment. Serum half-life of EG was prolonged in the dogs treated 8 hours after EG ingestion. Percentage of EG excreted unchanged was 84 +/- 2% in the dogs treated 5 hours after EG ingestion, and was 40 +/- 10% in the dogs treated 8 hours after EG ingestion. 4-Methylpyrazole was effective in preventing renal failure in all dogs given 10.6 g of EG/kg when treatment was initiated by 5 hours after EG ingestion, and in 4 of 6 dogs when treatment was initiated by 8 hours after EG ingestion.

Force plate gait analysis was used to study the effects of subject stance time and velocity on ground reaction forces in 6 adult Greyhounds at the trot. Data for 210 valid trials were obtained. Stance time negatively correlated with velocity (r = -0.85 for the forelimbs, r = -0.61 for the hind limbs), decreasing as velocity increased. Stance time in the forelimbs and hind limbs correlated more closely with changes in vertical peak force and impulse than did velocity. The trials were divided into 3 distinct velocity ranges (V1 = 1.5 to 1.8 m/s, V2 = 2.1 to 2.4 m/s, and V3 = 2.7 to 3.0 m/s), 3 distinct forelimb stance time ranges (FST1 = 0.144 to 0.176 second, FST2 = 0.185 to 0.217 second, and FST3 = 0.225 to 0.258 second), and 3 distinct hind limb stance time ranges (HST1 = 0.105 to 0.132 second, HST2 = 0.139 to 0.165 second, and HST3 = 0.172 to 0.198 second). Peak forces increased as velocity increased and decreased as stance time increased. Vertical impulse decreased as velocity increased and increased as stance time increased. The relation between stance time, subject velocity, and ground reaction forces was documented for clinically normal Greyhounds at the trot. Changes in stance time accurately reflected changes in subject velocity and ground reaction forces in clinically normal dogs and could be used to normalize trial data within a sampling period.

Packed cell volume and plasma total protein (TP), serum albumin (Alb) and globulin (Glb), and plasma ionized calcium (PCa) concentrations, blood viscosity (BV), and plasma viscosity (PV) were measured in 42 horses at rest and after the cross country jumping phase of a horse trial competition. The BV and Pv were determined at 6 shear rates (230, 115, 46, 23, 11.5, 5.75 s 1), using a digital rotational cone and plate microviscometer. A paired t-test was used to determine differences between PCV, TP, Alb, Glb and PCa values at rest and after exercise. The PCV, TP, Alb, and Glb values increased (P < 0.05) in horses after exercise. The PCa concentration decreased (P < 0.05) in horses after exercise. Mean BV and Pv in the 42 horses at rest and after exercise were fitted to an asymptotic function. Significant (P < 0.05) correlation at aH shear rates was seen between BV at rest and PCV, TP, Alb, Glb, and PCa values at rest; and between BV after exercise and PCV, TP, Alb, Glb, and PCa values after exercise. Significant correlation was not seen between PV at rest and TP, Alb, Glb, and PCa at rest, or between PV after exercise and TP, Alb, Glb, and PCa concentrations after exercise at any shear rate.

Parenchymal cells were isolated from the liver of male calves, and monolayer cultures formed were treated with glucocorticoids to examine whether haptoglobin, appearance of which is associated with hepatic lipidosis (fatty liver) in cattle, is induced by steroid hormones. Without addition of dexamethasone, only trace amounts of haptoglobin were detected in culture medium. With addition of dexamethasone (10(-12) to 10(-4)M), considerable amounts of haptoglobin were released into the medium. Maximal release was observed at concentrations of 10(-8) to 10(-6)M dexamethasone. Haptoglobin release was similarly induced by cortisol, although the effect was less potent than that of dexamethasone. Actinomycin D (a known protein synthesis inhibitor) dose-dependently reduced amounts of haptoglobin released in response to 10(-8)M dexamethasone. Dexamethazone also induced annexin I, which is known to be synthesized in response to glucocorticoids. Dexamethasone treatment resulted in reduced protein kinase C activity in the cell cytosol, which has been shown to be an early event in dexamethasone-treated cells. Other than glucocorticoids, estradiol induced haptoglobin release, whereas progesterone was less effective. The association of haptoglobin with hepatic lipidosis can be reasonably explained by the fact that haptoglobin production by the liver is induced by glucocorticoids and estradiol, and these steroid hormones are triggers for development of hepatic lipidosis in cattle.

The metabolic responses of equine articular cartilage to incubation with bacterial lipopolysaccharide (LPS) were studied, using explant cultures of articular cartilage obtained from the metatarsophalangeal joints of 15 horses, age of which ranged from 3 months to 20 years. For comparison, explants were also established from the metatarsophalangeal joints of 3 calves. Explants were cultured for 3 days in medium containing various concentrations of LPS from 0 (control) to 100 microgram/ml. Glycosaminoglycan (GAG) released during the 3-day incubation was determined by a spectrophotometric assay, using the dye 1,9-dimethylmethylene blue. Newly synthesized GAG content was assayed by measuring [35S]sulfate incorporation during a 3-hour pulse labeling period. In addition, prostaglandin E2 (PGE2) synthesis was quantified, using a [3H]PGE2 radioimmunoassay kit and magnetic separation. Finally, explants from 3 animals were used to evaluate the effect of supplementing culture medium with 5% serum on the response of explants to LPS, and explants from 1 horse were used to compare responses to stimulation with LPS derived from 2 bacterial sources. Equine explants cultured with bacterial LPS had a dose-dependent decrease in synthesis and increase in release of GAG, and these responses were significantly (P < 0.0001) greater in explants from younger horses. In addition, equine explants had a significant (P = 0.0001) dose-dependent increase in concentration of PGE2 released into the culture medium in response to incubation with LPS. Comparison of data for GAG synthesis from equine and bovine explants revealed a significant (P = 0.025) difference in responsiveness to LPS between the 2 species. Equine explants tended to have a greater suppression of GAG synthesis in response to incubation with increasing concentrations of LPS than did age-corrected bovine samples. However, similar analysis of data on GAG release did not indicate any difference in sensitivity between the 2 species for this response. There was no evidence that the presence or absence of serum supplementation or the use of LPS derived from different bacterial sources made a significant difference in the response of explants to incubation with LPS.

High-intensity exercise results in a dramatic increase in mean pulmonary capillary blood pressure of horses, and administration of furosemide 4 hours before exertion significantly attenuates this exercise-induced increment. To test whether this effect of furosemide is mediated via release of prostaglandins, right atrial and pulmonary vascular pressures were measured in 8 healthy, sound, exercise-trained Thoroughbreds at rest and during incremental-step exercise on a treadmill. Horses were studied on 3 separate occasions: after IV administration of saline (0.9% NaCl) solution, after administration of furosemide (250 mg, iv, 4 hours before exercise) alone, and after administration of flunixin meglumine (1.1 mg/kg, IV, q 8 h for 3 days) and furosemide (250 mg, IV, 4 hours before exercise; last dose of flunixin meglumine was administered 90 seconds after furosemide injection). Experiments on each horse were separated by at least 7 days and were performed in random order. At rest and at the highest workload (14.5 m/s on a 5% uphill incline), mean pulmonary capillary blood pressure recorded after administration of furosemide alone was not significantly different from that recorded after administration of flunixin meglumine and furosemide. However, these values were significantly (P < 0.05) less than corresponding values of mean pulmonary capillary blood pressure recorded after administration of saline solution. Thus, it was concluded that furosemide-induced attenuation of the increment in pulmonary capillary blood pressure during strenuous exercise is probably not mediated via prostaglandin production.

To determine the effects of age on each analyte, CSF variables were evaluated in healthy foals from birth through 42 days of age. Cerebrospinal fluid was collected from 14 clinically normal, naturally delivered cross-bred foals and was analyzed for glucose, sodium, potassium, magnesium, and total protein concentrations, total and differential WBC counts, RbC count, and lactate dehydrogenase, aspartate transaminase, and creatine kinase activities. Samples were collected in 3 foals < 48 hours old, and at 11 to 14 days of age in 4 foals, 21 to 22 days of age in 3 foals, and 31 to 42 days of age in 4 foals. Each foal was tested only once, to avoid any effects of CSF sample collection on subsequent analysis. Regression analysis confirmed age-related effects on CSF glucose, protein, and magnesium concentrations, but did not indicate an effect of age on CSF sodium and potassium concentrations or cell counts. Results indicate that CSF glucose concentration decreases with age; foals < 2 days old had the highest CSF glucose values, 98.8 +/- 12.0 mg/dl (mean +/- 1 SD). In foals 10 to 14 days old, CSF glucose concentration was 67.3 +/- 12.0 mg/ dl, was 65.3 +/- 4.5 mg/dl in foals 21 to 22 days old, was 70.0 +/- 5.4 mg/dl in foals 31 to 42 days old, and was 51.1 +/- 2.5 mg/dl in adults. Protein values in CSF also decreased with age: 109.0 +/- 9.7 mg/dl in foals < 2 days old, 81.0 +/- 22.8 mg/dl in foals 10 to 14 days old, 60.5 +/- 22.4 mg/dl in foals 21 to 22 days old, and 58.5 +/- 17.0 mg/di in foals 31 to 42 days old. The CSF protein concentration was 60.3 +/- 10.8 mg/dl in adult horses. Magnesium concentration in CSF increased slightly with age, then decreased after 22 days of life. In foals < 2 days old, the value was 2.43 +/- 0.16 mg/dl. Values in older foals and horses were: 2.51 +/- 0.08 mg/dl in foals 10 to 14 days old, 2.65 +/- 0.05 mg/dl in 21- to 22-day-old foals, 2.55 +/- 0.05 mg/dl in 31- to 42-day-old foals, and 2.35 +/- 0.09 mg/dl in adult horses. Mean CSF sodium and potassium concentrations were 151.7 +/- 3.7 mmol/L and 3.14 +/- 0.54 mmol/L, respectively, for all ages. There was no effect of age on these analytes. Values for CSF enzymes were considered invalid for the assay technique used and were not further analyzed.