Evaluation of a point-of-care coagulation analyzer (Abaxis VSPro) for identification of coagulopathies in dogs.

OBJECTIVE: To evaluate the ability of the Abaxis VSPro, a point-of-care analyzer that measures prothrombin time (PT) and activated partial thromboplastin time (aPTT), to identify dogs with coagulopathies caused by administration of anticoagulants. SETTING: Veterinary teaching hospital. ANIMALS: Six healthy adult dogs that are part of a preexisting research colony. One dog was not included in the warfarin portion of the study. MEASUREMENTS AND MAIN RESULTS: Unfractionated heparin (UFH, 50 U/kg i.v. once then 300 U/kg s.q. q 8 h) was administered to prolong aPTT. Citrated whole blood was used for PT and aPTT analyses with the VSPro and were run in duplicate. The VSPro results were compared to PT and aPTT measured in plasma with a standard benchtop coagulometer (AMAX Destiny). A washout period of at least 24 hours followed. Once dogs had normal PT and aPTT values, warfarin was administered (0.25-0.30 mg/kg p.o.) once then (0.15 mg/kg p.o.) as needed up to every 12 hours to prolong PT values. Seventy separate samples were evaluated for PT and 73 samples for aPTT. Pearson correlation coefficients (PCC) for replicate VSPro measures of PT and aPTT were 0.941 and 0.891, respectively (P < 0.001). The PCC between VSPro and AMAX was 0.578 for PT and of 0.865 for PTT (P < 0.001). Receiver operating characteristic (ROC) analysis indicated a maximum sensitivity and specificity for diagnosis of coagulopathy (by AMAX) at VSPro PT value of 21.6 seconds (sensitivity 72%, specificity 86%) and a maximum sensitivity and specificity at VSPro aPTT of 105.3 seconds (sensitivity 93%, specificity 89%). The positive predictive value for PT and aPTT were 84% and 89%, respectively. CONCLUSIONS: The Abaxis VSPro showed acceptable correlation with clinical laboratory tests, and is a useful POC device for identification of animals with abnormalities in PT or aPTT.

Lack of inhibitory effect of acetylsalicylic acid and meloxicam on whole blood platelet aggregation in cats.

OBJECTIVE: To determine the effects of acetylsalicylic acid (ASA) and meloxicam on feline platelet aggregation and associated platelet thromboxane production and serotonin release. DESIGN: Prospective interventional study. SETTING: University research facility. ANIMALS: Eight healthy male castrated domestic short hair cats from a research colony. INTERVENTIONS: Oral medications were administered to 8 cats for 14 days in a randomized, placebo-controlled, crossover design. Treatment groups included: aspirin (ASA) (5 mg/kg q 48 h), meloxicam (0.05 mg/kg q 24 h), and placebo (0.5 mL of water q 24 h). Thromboxane assays (TXB(2) ) and whole blood (impedance) aggregometry (WBA) were performed on samples collected before drug administration, and on days 7, 15, and 17, using adenosine diphosphate (ADP; 10 µM) and collagen (5 µg/mL) as agonists for WBA. Serotonin release was assayed on postaggregation plasma. Oral mucosal bleeding time (OMBT) and complete blood cell counts were measured on days 0 and 15. MEASUREMENTS AND MAIN RESULTS: Neither medication affected WBA at any time point. OMBT decreased in the ASA group relative to baseline. No differences were detected in WBA and OMBT baseline between any groups. No difference was detected in serotonin secretion at any time point. TXB(2) was significantly decreased in the ASA group at all times after initiation of treatment but no change was noted in the meloxicam or placebo groups. CONCLUSIONS: At the doses studied, neither meloxicam nor ASA had an inhibitory effect on WBA or OMBT in cats. Thromboxane concentrations were significantly decreased with ASA treatment.

Efficacy of ABT-116, an antagonist of transient receptor potential vanilloid type 1, in providing analgesia for dogs with chemically induced synovitis.

OBJECTIVE: To investigate the ability of ABT-116 (a proprietary antagonist of transient receptor potential vanilloid type 1) administered at 2 doses to attenuate lameness in dogs with experimentally induced urate synovitis. ANIMALS: 8 purpose-bred mixed-breed dogs. PROCEDURES: In a 4-way crossover study, dogs orally received each of low-dose ABT-116 treatment (LDA; 10 mg/kg), high-dose ABT-116 treatment (HDA; 30 mg/kg), firocoxib (5 mg/kg), and no treatment (nontreatment) once a day for 2 days, in a randomly assigned order. Synovitis was induced on the second day of each treatment period by intra-articular injection of either stifle joint with sodium urate, alternating between joints for each treatment period, beginning with the left stifle joint. Ground reaction forces, clinical lameness scores, and rectal temperature were assessed before the injection (baseline) and at various points afterward. RESULTS: Lameness scores at the 2-, 6-, and 12-hour assessment points were higher than baseline scores for HDA and nontreatment, whereas scores at the 2- and 6-hour points were higher than baseline scores for LDA. For firocoxib, there was no difference from baseline scores in lameness scores at any point. Compared with baseline values, peak vertical force and vertical impulse were lower at 2 and 6 hours for HDA and nontreatment and at 2 hours for LDA. No changes in these values were evident for firocoxib. The HDA or LDA resulted in higher rectal temperatures than did treatment with firocoxib or nothing, but those temperatures did not differ among treatments. CONCLUSIONS AND CLINICAL RELEVANCE: HDA had no apparent effect on sodium urate-induced lameness; LDA did attenuate the lameness but not as completely as firocoxib treatment. High rectal temperature is an adverse effect of oral ABT-116 administration that may be of clinical concern.

Effect of perzinfotel and a proprietary phospholipase A(2) inhibitor on kinetic gait and subjective lameness scores in dogs with sodium urate-induced synovitis.

OBJECTIVE: To investigate the ability of perzinfotel (an N-methyl-d-aspartate receptor antagonist) and a proprietary phospholipase A(2) (PLA(2)) inhibitor to attenuate lameness in dogs with sodium urate (SU)-induced synovitis. ANIMALS: 8 adult dogs. PROCEDURES: A blinded 4-way crossover study was performed. Dogs received perzinfotel (10 mg/kg), a proprietary PLA(2) inhibitor (10 mg/kg), carprofen (4.4 mg/kg; positive control treatment), or no treatment (negative control treatment). On the fourth day after initiation of treatment, synovitis was induced via intra-articular injection of SU 1 hour before administration of the last treatment dose. Ground reaction forces were measured and clinical lameness evaluations were performed before (baseline [time 0]) and 2, 4, 6, 8, 12, and 25 hours after SU injection. There was a 21-day washout period between subsequent treatments. Data were analyzed via repeated-measures ANOVAs. RESULTS: Peak vertical force (PVF) and vertical impulse (VI) values for negative control and perzinfotel treatments were significantly lower at 2 and 4 hours, compared with baseline values. Values for PVF and VI for the PLA(2) inhibitor and positive control treatments did not differ from baseline values at any time points. Between-treatment comparisons revealed significantly higher PVF and VI values for the positive control treatment than for the negative control and perzinfotel treatments at 2 and 4 hours. Values for VI were higher for PLA(2) inhibitor treatment than for negative control treatment at 2 hours. CONCLUSIONS AND CLINICAL RELEVANCE: Perzinfotel did not significantly alter SU-induced lameness. The proprietary PLA(2) inhibitor attenuated lameness but not as completely as did carprofen.