Objective—To determine whether incubation of cruciate ligament cells with acetylsalicylic acid, carprofen, meloxicam, or robenacoxib provides protection against apoptosis induced by sodium nitroprusside (SNP).
Sample—Explants of cranial (CCL) and caudal (CaCL) cruciate ligaments from eight 1-day-old Beagles.
Procedures—Primary cultures of CCL and CaCL cells were created via enzymatic dissociation of cruciate explants. Purified cell cultures were incubated for 2 hours without (controls) or with 1 of 3 concentrations of 1 of 4 NSAIDs (10, 100, or 200 μg of acetylsalicylic acid/mL; 0.1, 1, or 10 μg of carprofen/mL; 0.1, 1, or 10 μg of meloxicam/mL; or 0.1, 1, or 10 μg of robenacoxib/mL) and subsequently incubated for 18 hours with 1 of 3 concentrations of SNP in an attempt to induce mild, moderate, or severe cytotoxic effects. Cell viability and apoptosis were analyzed via a cell proliferation assay and flow cytometry, respectively. Prostaglandin E2 concentrations were measured via an ELISA.
Results—Cytoprotective effects of NSAIDs were dependent on the extent of SNP-induced apoptosis and were greatest in CCL and CaCL cell cultures with moderate SNP-induced cytotoxic effects. Preincubation with an NSAID improved cell viability by 15% to 45% when CCL and CaCL cells were subsequently incubated with SNP. Carprofen (10 μg/mL) had the greatest cytoprotective effects for CCL and CaCL cells. Incubation with NSAIDs resulted in a nonsignificant decrease in PGE2 production from SNP-damaged cells.
Conclusions and Clinical Relevance—Results indicated that carprofen, meloxicam, and robenacoxib may reduce apoptosis in cells originating from canine cruciate ligaments.
Objective—To determine plasma and urine concentrations
of retinol, retinyl esters, retinol-binding protein
(RBP), and Tamm-Horsfall protein (THP) in dogs
with chronic renal disease (CRD).
Animals—17 dogs with naturally developing CRD and
21 healthy control dogs.
Procedure—A diagnosis of CRD was established on
the basis of clinical signs, plasma concentrations of
creatinine and urea, and results of urinalysis.
Concentrations of retinol and retinyl esters were measured
by use of reverse-phase high-performance liquid
chromatography. Concentrations of RBP and THP
were measured by use of sensitive ELISA systems.
Results—Dogs with CRD had higher plasma concentrations
of retinol, which were not paralleled by differences
in plasma concentrations of RBP. Calculated
ratio of urinary total vitamin A (sum of concentrations
of retinol and retinyl esters to creatinine concentration)
and ratio of the concentration of urinary retinyl esters
to creatinine concentration did not differ between
groups. However, we detected a significantly higher
retinol-to-creatinine ratio in the urine of dogs with
CRD, which was paralleled by a higher urinary RBP-to-creatinine
ratio. Thus, in dogs with CRD, the estimated
fractional clearance of total vitamin A, retinol, and RBP
was increased. Furthermore, dogs with CRD had a
reduced urinary THP-to-creatinine ratio.
Conclusions and Clinical Relevance—Results of
this study documented that CRD affects the concentrations
of retinol in plasma and urine of dogs.
Analysis of the data indicates that measurement of
urinary RBP and urinary THP concentrations provides
valuable information that can be helpful in follow-up
monitoring of dogs with CRD. (Am J Vet Res 2003:64:874–879)