Objective—To evaluate markers of in vivo platelet function (urinary 11-dehydro-thromboxane B2 [11-dehydroTXB2] and 2,3-dinorTXB2) and assess their response to administration of 2 commonly used dosages of aspirin in healthy dogs. Animals—20 healthy dogs. Procedures—Urine was collected prior to aspirin administration and on the morning following the last evening administration. Twenty dogs received aspirin (1 mg/kg, PO, q 24 h) for 7 consecutive doses. After a washout period of 5 months, 10 dogs received a single dose of aspirin (10 mg/kg, PO). Concentrations of urinary thromboxane metabolites 11-dehydroTXB2 and 2,3-dinorTXB2 were measured via ELISA, and values were normalized to urine creatinine concentration. Results—Median baseline 11-dehydroTXB2 concentrations were 0.38 ng/mg of creatinine (range, 0.15 to 1.13 ng/mg). Mean ± SD baseline 2 at a 3-dinorTXB2 concentrations were 6.75 ± 2.77 ng/mg of creatinine. Administration of aspirin at a dosage of 1 mg/kg, PO, every 24 hours for 7 days did not significantly decrease urinary 11-dehydroTXB2 concentration, but administration of the single aspirin dose of 10 mg/kg did significantly decrease 11-dehydroTXB2 concentration by a median of 45.5% (range, 28.2% to 671%). Administration of the 1 mg/kg aspirin dosage significantly decreased urinary 2,3-dinorTXB2 concentration by a mean ± SD of 33.0 ± 23.7%. Administration of the single aspirin dose of 10 mg/kg also significantly decreased 2,3-dinorTXB2 concentration by a mean ± SD of 46.7 ± 12.6%. Conclusions and Clinical Relevance—Aspirin administration (1 mg/kg/d) may be insufficient for reliable platelet inhibition in healthy dogs.

Objective-To determine the effects of once-daily oral administration of N-acetyl-d-glucosamine (NAG) on plasma and urine glycosaminoglycan (GAG) concentrations in cats with idiopathic cystitis (IC). Animals-19 cats with IC and 10 clinically normal cats. Procedures-Cats with IC were randomly assigned to receive 250 mg of NAG in capsule form orally once daily for 28 days (n = 12) or a placebo (capsule containing cellulose) orally once daily for the same period (7). In cats with IC, plasma and urine GAG concentrations and urine creatinine concentration were measured on days 0 (immediately before first dose), 7, 14, 21, 28, and 56. For purposes of comparison, those variables were measured in 10 clinically normal cats on day 0. Results-Mean +/- SEM urine GAG-to-creatinine concentration ratios (day 0 data) for cats with IC and clinically normal cats differed significantly (3.11 +/- 0.62 μg/mL and 14.23 +/- 3.47 μg/mL, respectively). For cats with IC, mean plasma GAG concentration in NAG-treated cats (39.96 +/- 5.34 micrograms/mL) was higher than that in placebo-treated cats (24.20 +/- 3.35 micrograms/mL) on day 21. In the NAG-treated cats, plasma GAG concentration on days 21 (39.96 +/- 5.34 micrograms/mL) and 28 (39.91 +/- 6.74 micrograms/mL) differed significantly from the day 0 concentration (27.46 +/- 3.90 micrograms/mL). Conclusions and Clinical Relevance-Cats with IC have lower urinary GAG-to-creatinine concentration ratios than did clinically normal cats. Administration of NAG (250 mg, PO, q 24 h) significantly increased plasma GAG concentrations in cats with IC after 21 days of treatment.