Platelet Function In Dogs Research Articles

PB0902 The Effect of Hypercortisolism on Platelet Function in Dogs with Cushing's Syndrome

PB0902 The Effect of Hypercortisolism on Platelet Function in Dogs with Cushing's Syndrome

Platelet function in dogs with chronic liver disease.

To assess platelet function, buccal mucosal bleeding time and plasma von Willebrand factor concentration in dogs with chronic inflammatory and/or fibrotic liver disease and to compare results with those obtained in healthy dogs. Preliminary study including 18 dogs with chronic inflammatory and/or fibrotic liver disease undergoing liver biopsy and 18 healthy age-matched control dogs. Platelet function was assessed by measuring closure time with the PFA-100® analyser using adenosine diphosphate (ADP) as an agonist. Buccal mucosal bleeding time, closure time and plasma von Willebrand factor antigen were measured in dogs in both groups. After undergoing ultrasound-guided needle biopsy, dogs were monitored for haemorrhage to determine if there was an association of any measurement with post-biopsy bleeding. The closure time was not different between the liver disease group (median 76.3; range 53 to 118.5seconds) and control group (72.8; 57 to 89.5seconds). The buccal mucosal bleeding time was longer in the liver disease group (median 138; range 95 to 229 seconds) than the control group (103; 63 to 200 seconds). The plasma von Willebrand factor antigen concentration was not different between the liver disease group (median 203; range 109 to 351%) and control group (165.5; 63 to 246%). In this study, dogs with chronic necroinflammatory and/or fibrotic liver disease did not have overt, clinically relevant derangements in platelet function as assessed by buccal mucosal bleeding time, closure time and von Willebrand factor analysis. In addition, none of the dogs undergoing percutaneous ultrasound-guided biopsy in the study exhibited bleeding complications post-biopsy procedure.

In vivo effects of aspirin and cyclosporine on regulatory T cells and T-cell cytokine production in healthy dogs

Cyclosporine and aspirin are routinely used in combination to treat immune-mediated hemolytic anemia (IMHA) in dogs. Cyclosporine is a potent immunosuppressive agent that targets T cell production of the cytokines IL-2 and IFN-γ. Low-dose aspirin is often used to inhibit platelet function in dogs with IMHA, since these animals are prone to life-threatening thromboembolic disease. In rodents and humans, aspirin and cyclosporine have both been shown to variably affect T cell cytokine production, and also numbers of circulating regulatory T cells (Tregs). In dogs, it has not yet been determined if concurrent aspirin alters the effects of cyclosporine on T-cell cytokine expression, or if either drug influences Treg numbers.In a crossover study, seven healthy young adult dogs were given either oral high-dose cyclosporine (10 mg/kg Q12 h), oral low-dose aspirin (1 mg/kg Q24 h), oral high-dose aspirin (10 mg/kg Q12 h), or combined low-dose aspirin with cyclosporine, each for 8 days, with a washout of at least 2 weeks after each treatment. Activated T cell cytokine expression (IL-2 & IFN-γ) and percent CD4 + CD25 + FOXP3+ Tregs were evaluated using flow cytometry, both prior to and on the last day of treatment. The difference between pre- and post-treatment values for each group, as well as the difference between treatment groups, was evaluated.Cyclosporine significantly decreased IL-2 and IFN-γ expression when used alone or in combination with low-dose aspirin. High-dose aspirin, but not low-dose aspirin, also significantly decreased IL-2 expression, although the decrease was not as marked as that seen with cyclosporine alone or in combination with aspirin. Neither low-dose nor high-dose aspirin significantly affected IFN-γ expression. No drug or drug combination affected Treg numbers.Low-dose aspirin given with cyclosporine creates the same degree of T-cell cytokine suppression as does cyclosporine alone, suggesting that the two drugs can be used concurrently without significantly altering the immunosuppressive mechanism of action of cyclosporine.

Effects of aspirin dose escalation on platelet function and urinary thromboxane and prostacyclin levels in normal dogs.

Established "low" aspirin dosages inconsistently inhibit platelet function in dogs. Higher aspirin dosages consistently inhibit platelet function, but are associated with adverse effects. The objectives of this study were to use an escalation in dosage to determine the lowest aspirin dosage that consistently inhibited platelet function without inhibiting prostacyclin synthesis. Eight dogs were treated with five aspirin dosages: 0.5mg/kg q24h, 1mg/kg q24h, 2mg/kg q24h, 4mg/kg q24h and 10mg/kg q12h for 7days. Utilizing aggregometry and a whole-blood platelet function analyzer (PFA-100), platelet function was evaluated before and after treatment. Urine 11-dehydro-thromboxane-B2 (11-dTXB2 ) and 6-keto-prostaglandin-F1α (6-keto-PGF1α ), were measured. Compared to pretreatment, there were significant post-treatment decreases in the maximum aggregometry amplitude and increases in the PFA-100 closure times for all dosages expect 0.5mg/kg q24h. There was no difference in amplitude or closure time among the 2mg/kg q24h, 4mg/kg q24h, and 10mg/kg q12h dosages. Compared to pretreatment values, there was a significant decrease in urinary 11-dTXB2 -to-creatinine and 6-keto-PGF1α -to-creatinine ratios, but there was no dose-dependent decrease for either metabolite. An aspirin dosage of 2mg/kg q24h consistently inhibits platelet function without decreasing prostacyclin synthesis significantly more than lower aspirin dosages.

Comparison of the effects of 7.2% hypertonic saline and 20% mannitol on whole blood coagulation and platelet function in dogs with suspected intracranial hypertension - a pilot study

BackgroundHyperosmolar therapy with either mannitol or hypertonic saline (HTS) is commonly used in the treatment of intracranial hypertension (ICH). In vitro data indicate that both mannitol and HTS affect coagulation and platelet function in dogs. The aim of this study was to compare the effects of 20% mannitol and 7.2% HTS on whole blood coagulation using rotational thromboelastometry (ROTEM®) and platelet function using a platelet function analyzer (PFA®) in dogs with suspected ICH. Thirty client-owned dogs with suspected ICH needing osmotherapy were randomized to receive either 20% mannitol (5 ml/kg IV over 15 min) or 7.2% HTS (4 ml/kg IV over 5 min). ROTEM® (EXTEM® and FIBTEM® assays) and PFA® analyses (collagen/ADP cartridges) were performed before (T0), as well as 5 (T5), 60 (T60) and 120 (T120) minutes after administration of HTS or mannitol. Data at T5, T60 and T120 were analyzed as a percentage of values at T0 for comparison between groups, and as absolute values for comparison between time points, respectively.ResultsNo significant difference was found between the groups for the percentage change of any parameter at any time point except for FIBTEM® clotting time. Within each group, no significant difference was found between time points for any parameter except for FIBTEM® clotting time in the HTS group, and EXTEM® and FIBTEM® maximum clot firmness in the mannitol group. Median ROTEM® values lay within institutional reference intervals in both groups at all time points, whereas median PFA® values were above the reference intervals at T5 (both groups) and T60 (HTS group).ConclusionsUsing currently recommended doses, mannitol and HTS do not differ in their effects on whole blood coagulation and platelet function in dogs with suspected ICH. Moreover, no relevant impairment of whole blood coagulation was found following treatment with either solution, whereas a short-lived impairment of platelet function was found after both solutions.

Effects of acepromazine maleate on platelet function assessed by use of adenosine diphosphate activated– and arachidonic acid– activated modified thromboelastography in healthy dogs

To evaluate the effect of acepromazine maleate administered IV on platelet function assessed in healthy dogs by use of a modified thromboelastography assay. 6 healthy adult mixed-breed dogs. Dogs received each of 3 treatments (saline [0.9% NaCl] solution [1 to 2 mL, IV] and acepromazine maleate [0.05 and 0.1 mg/kg, IV]) in a randomized crossover study with a minimum 3-day washout period between treatments. From each dog, blood samples were collected via jugular venipuncture immediately before and 30 and 240 minutes after administration of each treatment. A modified thromboelastography assay, consisting of citrated kaolin-activated (baseline assessment), reptilase-ADP-activated (ADP-activated), and reptilase-arachidonic acid (AA)-activated (AA-activated) thromboelastography, was performed for each sample. Platelet inhibition was evaluated by assessing the percentage change in maximum amplitude for ADP-activated or AA-activated samples, compared with baseline values. Percentage change in maximum amplitude was analyzed by use of Skillings-Mack tests with significance accepted at a family-wise error rate of P < 0.05 by use of Bonferroni corrections for multiple comparisons. No significant differences were found in the percentage change of maximum amplitude from baseline for ADP-activated or AA-activated samples among treatments at any time. Platelet function in dogs, as assessed by use of a modified thromboelastography assay, was not inhibited by acepromazine at doses of 0.05 or 0.1 mg/kg, IV. This was in contrast to previous reports in which it was suggested that acepromazine may alter platelet function via inhibition of ADP and AA.

Effects of carprofen, meloxicam and deracoxib on platelet function in dogs

ObjectiveTo determine effects of anti-inflammatory doses of COX-2 selective NSAIDs carprofen, meloxicam, and deracoxib on platelet function in dogs and urine 11-dehydro-thromboxane B2. Study designRandomized, blocked, crossover design with a 14-day washout period. AnimalsHealthy intact female Walker Hounds aged 1–6 years and weighing 20.5–24.2 kg. MethodsDogs were given NSAIDs for 7 days at recommended doses: carprofen (2.2 mg kg−1, PO, every 12 hours), carprofen (4.4 mg kg−1, PO, every 24 hours), meloxicam (0.2 mg kg−1, PO, on the 1st day then 0.1 mg kg−1, PO, every 24 hours), and deracoxib (2 mg kg−1, PO, every 24 hours). Collagen/epinephrine and collagen/ADP PFA-100 cartridges were used to evaluate platelet function before and during and every other day after administration of each drug. Urine 11-dehydro-thromboxane B2 was also measured before and during administration of each drug. ResultsAll NSAIDs significantly prolonged PFA-100 closure times when measured with collagen/epinephrine cartridges, but not with collagen/ADP cartridges. The average duration from drug cessation until return of closure times (collagen/epinephrine cartridges) to baseline values was 11.6, 10.6, 11 and 10.6 days for carprofen (2.2 mg kg−1 every 12 hours), carprofen (4.4 mg kg−1 every 24 hours), meloxicam and deracoxib, respectively. Conclusions and clinical relevanceOral administration of some COX-2 selective NSAIDs causes detectable alterations in platelet function in dogs. As in humans, PFA-100 collagen/ADP cartridges do not reliably detect COX-mediated platelet dysfunction in dogs. Individual assessment of platelet function is advised when administering these drugs prior to surgery, particularly in the presence of other risk factors for bleeding.

Platelet function in dogs with congenital portosystemic shunt

The aim of this study was to examine the influence of congenital portosystemic shunts (CPSS) on primary haemostasis in dogs. Bleeding time, automated platelet function analysis (PFA 100 analyser), platelet count and platelet aggregation using different methods and agonists were measured in 10 dogs with untreated CPSS and in 10 healthy, age-matched controls. Bleeding time, platelet function analysis and platelet counts did not differ significantly between groups (P>0.05). Aggregation measured using the impedance method (area under the curve) was slightly to moderately reduced with high concentrations of collagen (e.g., 5μg/mL: 2948 ± 524 vs. 3472 ± 571 AU*Min) and arachidonic acid (e.g., 1mmol/L: 1006 ± 522 vs. 1963 ± 738 AU*Min) (P<0.05), but not with adenosine diphosphate. In contrast, collagen-induced turbidimetric aggregation revealed slightly higher maximum aggregation values in dogs with CPSS. Despite the moderately altered platelet aggregation, the lack of change in global primary haemostasis screening tests indicates that dogs with CPSS do not have regularly occurring clinically relevant disorders of primary haemostasis.

Measurement of platelet function in dogs using a novel impedance aggregometer

The aim of this study was to optimise the technique and establish reference values for whole blood aggregometry in dogs using a novel multiplate analyser. Measurements were performed on the hirudin-anticoagulated blood of healthy dogs using a wide range of agonists. Optimal agonist concentrations were 10 micromol/L of adenosine diphosphate, 5 microg/mL of collagen and 1 mmol/L of arachidonic acid. Ristocetin (at 0.2 and 1 mg/mL) and thrombin receptor activating peptide (TRAP-6 at 32 and 160 micromol/L) did not consistently induce platelet aggregation. Coefficients of variance for within-run imprecision (n=10 repetitions) varied from 5% to 18%. Measurement signals were significantly higher when analyses were performed on standard samples (hirudin-anticoagulated blood) compared to citrated blood or blood samples anticoagulated with citrate buffer, regardless of whether or not re-calcification was performed (P<0.05). The findings indicate that the analyser is suitable for the investigation of platelet aggregation in dogs and analysis should be performed on hirudin-anticoagulated blood using optimised agonist concentrations.

Evaluation of platelet function in dogs with cardiac disease using the PFA‐100 platelet function analyzer

Cardiac disease has the potential to alter platelet function in dogs. Evaluation of platelet function using the PFA-100 analyzer in dogs of multiple breeds and with a broad range of cardiac conditions would help clarify the effect of cardiac disease on platelets. The objective of this study was to assess differences in closure time (CT) in dogs with cardiac disease associated with murmurs, when compared with that of healthy dogs. Thirty-nine dogs with cardiac murmurs and turbulent blood flow as determined echocardiographically were included in the study. The dogs represented 23 different breeds. Dogs with murmurs were further divided into those with atrioventricular valvular insufficiency (n=23) and subaortic stenosis (n=9). Fifty-eight clinically healthy dogs were used as controls. CTs were determined in duplicate on a PFA-100 analyzer using collagen/ADP cartridges. Compared with CTs in the control group (mean+/-SD, 57.6+/-5.9 seconds; median, 56.5 seconds; reference interval, 48.0-77.0 seconds), dogs with valvular insufficiency (mean+/-SD, 81.9+/-26.3 seconds; median, 78.0 seconds; range, 52.5-187 seconds), subaortic stenosis (71.4+/-16.5 seconds; median, 66.0 seconds; range, 51.5-95.0 seconds), and all dogs with murmurs combined (79.6+/-24.1 seconds; median, 74.0 seconds; range, 48.0-187 seconds) had significantly prolonged CTs (P<.01). The PFA-100 analyzer is useful in detecting platelet function defects in dogs with cardiac murmurs, most notably those caused by mitral and/or tricuspid valvular insufficiency or subaortic stenosis. The form of turbulent blood flow does not appear to be an important factor in platelet hypofunction in these forms of cardiac disease.

Platelet function in dogs: breed differences and effect of acetylsalicylic acid administration

Clinical studies investigating platelet function in dogs have had conflicting results that may be caused by normal physiologic variation in platelet response to agonists. The objective of this study was to investigate platelet function in clinically healthy dogs of 4 different breeds by whole-blood aggregometry and with a point-of-care platelet function analyzer (PFA-100), and to evaluate the effect of acetylsalicylic acid (ASA) administration on the results from both methods. Forty-five clinically healthy dogs (12 Cavalier King Charles Spaniels [CKCS], 12 Cairn Terriers, 10 Boxers, and 11 Labrador Retrievers) were included in the study. Platelet function was assessed by whole-blood aggregation with ADP (1, 5, 10, and 20 microM) as agonist and by PFA-100 using collagen and epinephrine (Col + Epi) and Col + ADP as agonists. Plasma thromboxane B(2) concentration was determined by an enzyme immunoassay. To investigate the effect of ASA, 10 dogs were dosed daily (75 or 250 mg ASA orally) for 4 consecutive days. A higher platelet aggregation response was found in CKCS compared to the other breeds. Longer PFA-100 closure time (Col + Epi) was found in Cairn Terriers compared to Boxers. Plasma thromboxane B(2) concentration was not statistically different between groups. Administration of ASA prolonged the PFA-100 closure times, using Col + Epi (but not Col + ADP) as agonists. Furthermore, ASA resulted in a decrease in whole-blood platelet aggregation. Platelet function is influenced by breed, depending upon the methodology applied. However, the importance of these breed differences remains to be investigated. The PFA-100 method with Col + Epi as agonists, and ADP-induced platelet aggregation appear to be sensitive to ASA in dogs.

Evaluation of the effect of ketoprofen and carprofen on platelet function in dogs studied by PFA-100 point-of-care analyser

The effect of two nonsteroidal anti-inflammatory drugs (carprofen and ketoprofen) on platelet adhesion and aggregation functions was evaluated by the PFA-100 analyser (Dade-Behring, CA, U.S.A.) using its collagen-adenosine diphosphate (ADP) and collagen-epinephrine (EPI) cartridges. The function of platelets was evaluated in 55 healthy dogs, in 7 dogs treated with ketoprofen and in 31 dogs treated with carprofen in a therapeutic dose for minimum 5 days. The therapeutic doses of carprofen had no effect on the closure time of PFA-100 (which is the marker of platelet function) but ketoprofen caused a significant increase when using collagen-EPI stimulation The closure times for both the healthy (control) and the treated dogs using EPI cartridges were often longer than the upper default cut-off point (300 sec) of the device. The PFA-100 analyser with collagen-ADP cartridges could be a useful tool for veterinary applications including the evaluation of platelet aggregation in dogs treated with NSAIDs. The upper cut-off point of PFA-100 might be extended.

In vitro comparison of the effects of two forms of hydroxyethyl starch solutions on platelet function in dogs

To evaluate the effect of 2 hydroxyethyl starch (HES) preparations (ie, HES solution with a molecular weight of 600 kd and a degree of substitution of 0.7 [HES 600/0.7] and a calcium-containing polyionic HES solution with a molecular weight of 670 kd and a degree of substitution of 0.75 [HES 670/0.75]) on canine platelet function. Blood samples from 10 healthy adult dogs. Dilution of citrated whole blood was performed with saline (0.9% NaCl) solution, HES 600/0.7, and HES 670/0.75 at ratios of 1:9 (ie, 1 part saline solution or colloid to 9 parts whole blood) and 1:3. Measurements of time to platelet plug formation in a capillary tube (ie, closure time) were made by use of a bench-top platelet function analyzer with collagen and ADP platelet agonists. Mean baseline closure time was 68.0 +/- 15.3 seconds. A 1:3 dilution of whole blood with saline solution, HES 600/0.7, and HES 670/0.75 resulted in mean closure times of 85.8 +/- 15.7 seconds, 100.6 +/- 18.6 seconds, and 101.6 +/- 16.2 seconds, respectively. Closure time following 1:3 dilution of whole blood with saline solution was significantly different from baseline and from 1:9 dilution with saline solution. Closure time following 1:3 dilution of whole blood with HES 670/0.75 was significantly different from baseline, 1:3 and 1:9 dilutions with saline solution, and 1:9 dilutions with HES 600/0.7 or HES 670/0.75. Saline solution, HES 600/0.7, and HES 670/0.75 affect canine platelet function by prolonging closure times; HES solutions prolonged closure time to a greater extent than saline solution.

Effects of 2 Concentrations of Sodium Citrate on Coagulation Test Results, von Willebrand Factor Concentration, and Platelet Function in Dogs

Background:Blood collection tubes containing 3.2% (0.109 M) sodium citrate, instead of 3.8% (0.129 M) sodium citrate, have recently become available in the United States. These tubes are visually indistinguishable from the traditional 3.8% sodium citrate tubes, except for wording on the label. Consequently, samples for hemostatic evaluation are frequently collected in tubes containing the lower concentration of sodium citrate.Hypothesis:Results of hemostasis assays are different in samples collected in 3.2% versus 3.8% sodium citrate.Animals:Twenty healthy dogs.Methods:This study aimed at determining whether results of standard coagulation tests, von Willebrand factor concentration (vWF:Ag), and platelet function with the platelet function analyzer PFA‐100a were affected by the different concentrations of sodium citrate. Blood samples were collected in tubes containing either 3.2% or 3.8% sodium citrate concentrations and processed routinely for coagulation assays (one‐stage prothrombin time [OSPT], activated partial thromboplastin time [aPTT], fibrinogen concentration, and platelet count), vWF:Ag, and platelet function assays with a PFA‐100.Results:There was no significant difference between samples collected in 3.2% versus those collected in 3.8% sodium citrate for OSPT, aPTT, fibrinogen concentration, platelet count, or vWF:Ag. The closure times with collagen/adenosine diphosphate were significantly shorter (66 ± 8.1 versus 74.8 ± 9.7 seconds; P &lt; .0001) with the 3.2% than with 3.8% sodium citrate concentration, and the hematocrit was significantly higher (47.9 ± 5.6 versus 46.0 ± 4.7 seconds; P= .03) in samples collected in 3.2% than in those collected in 3.8% sodium citrate.Conclusions and Clinical Importance: There is no clinically relevant effect of collection of blood into 3.2% or 3.8% sodium citrate.

Effects of 2 Concentrations of Sodium Citrate on Coagulation Test Results, von Willebrand Factor Concentration, and Platelet Function in Dogs

Blood collection tubes containing 3.2% (0.109 M) sodium citrate, instead of 3.8% (0.129 M) sodium citrate, have recently become available in the United States. These tubes are visually indistinguishable from the traditional 3.8% sodium citrate tubes, except for wording on the label. Consequently, samples for hemostatic evaluation are frequently collected in tubes containing the lower concentration of sodium citrate. Results of hemostasis assays are different in samples collected in 3.2% versus 3.8% sodium citrate. Twenty healthy dogs. This study aimed at determining whether results of standard coagulation tests, von Willebrand factor concentration (vWF:Ag), and platelet function with the platelet function analyzer PFA-100a were affected by the different concentrations of sodium citrate. Blood samples were collected in tubes containing either 3.2% or 3.8% sodium citrate concentrations and processed routinely for coagulation assays (one-stage prothrombin time [OSPT], activated partial thromboplastin time [aPTT], fibrinogen concentration, and platelet count), vWF:Ag, and platelet function assays with a PFA-100. There was no significant difference between samples collected in 3.2% versus those collected in 3.8% sodium citrate for OSPT, aPTT, fibrinogen concentration, platelet count, or vWF:Ag. The closure times with collagen/adenosine diphosphate were significantly shorter (66 +/- 8.1 versus 74.8 +/- 9.7 seconds; P < .0001) with the 3.2% than with 3.8% sodium citrate concentration, and the hematocrit was significantly higher (47.9 +/- 5.6 versus 46.0 +/- 4.7 seconds; P = .03) in samples collected in 3.2% than in those collected in 3.8% sodium citrate. There is no clinically relevant effect of collection of blood into 3.2% or 3.8% sodium citrate.

Inhibitory effects of cardiotonic pills on platelet function in dogs fed a high-fat diet

Insulin resistance and the consequent metabolic disorders are associated with a state of platelet hyperactivity. Oxidative stress is responsible for the persistent platelet activation. We sought to study the inhibitory effect of cardiotonic pills, an oral herbal component, on platelet function in a dog model with insulin resistance induced by high-fat feeding. We fed 18 dogs with a high-fat diet and six dogs with normal chow as control for 6 months. Then, six dogs were fed with a high-fat diet and received additional aspirin (250 mg/day), and another six dogs received additional cardiotonic pills (1,000 mg/day) for 4 months. Time-course changes in metabolic parameters and platelet function were detected. After high-fat feeding for 6 months, 18 dogs developed a series of metabolic disorders including obesity, dyslipidemia, oxidative stress and insulin resistance. In addition, a platelet hyperactivity state, characterized by increased agonist (arachidonic acid, ADP and collagen) induced platelet aggregation, platelet expression of adhesion molecules (P-selectin and GP IIb/IIIa), and platelet intracellular calcium concentration, was indicated. Cardiotonic pills showed a significant antioxidative activity by presenting an increase in plasma superoxide dismutase and decrease in erythrocyte glutathione, as well as a lipid-lowering effect (decrease in both plasma cholesterol and triglyceride). Either aspirin or cardiotonic pills could significantly reverse the platelet hypersensitivity and hyperfunction. Compared with aspirin, cardiotonic pills showed a more exaggerated inhibitory effect on platelet function (a significantly decreased collagen-stimulated platelet aggregation, and expression of adhesion molecules). In conclusion, cardiotonic pills inhibited platelet hyperfunction in dogs with insulin resistance. This inhibitory effect may mainly be explained by antioxidative activity and metabolic control.

Evaluation of Platelet Aggregation Using a Point‐Of‐Care Instrument in Retired Racing Greyhounds

Veterinarians involved in Greyhound rescue have anecdotally observed that 10–15% of Greyhounds bleed profusely after simple surgical procedures. In most patients, platelet counts and hemostasis profiles are normal; therefore, it is possible that these dogs have platelet dysfunction. The PFA‐100a is a novel point‐of‐care platelet function analyzer that has recently been evaluated as a rapid method to assess platelet function in dogs. The objectives of this study were to characterize platelet function in a group of healthy Greyhounds by means of the PFA‐100. Blood samples were collected from the jugular vein from 30 healthy Greyhounds. CBC, biochemical profile, PFA‐100 assay with collagen/epinephrine (COL‐EPI) and collagen/ adenosindiphosphate (COL‐ADP), plasma von Willebrand factor antigen concentration (vWF: Ag), and vWF collagen‐binding assay (vWF:CBA) were performed. PFA‐100 closure times (CTs) with COL/ADP ranged from 63 to 92 seconds (mean ± SD, 74.7 ± 7.9 seconds) and with COL/EPI from 87 to 238 seconds (138 ± 41 seconds); vWF:Ag ranged from 22 to 120% (87.52 ± 25.5%) and vWF:CBA ranged from 36 to 102% (77.4 ± 17.3%); and platelet counts ranged from 147 to 265 ± 109/L (194.6 ± 31.64 ± 109/L). Greyhound CTs were significantly shorter than CTs in a mixed population of 50 healthy non‐Greyhound dogs, in which the COL/ADP CTs ranged from 61 to 172 seconds (mean ± SD, 87 ± 21.6 seconds), and the COL/ EPI CTs ranged from 81 to 300 seconds (mean ± SD, 183 ± 67.6 seconds; P= 0.005 for COL/ADP CT; P= 0.001 for COL/ EPI CT). Also, platelet counts were significantly lower (P= 0.001) and packed cell volume was significantly higher (P= 0.001) in the Greyhound than in the non‐Greyhound group. The PFA‐100 is a reproducible method that can be used in the clinical setting to assess platelet function in Greyhounds; however, normal CTs in healthy Greyhounds are shorter than in other breeds. The results obtained in this study will be used to screen for abnormal platelet function in Greyhounds with postoperative bleeding.

Evaluation of Platelet Aggregation Using a Point-Of-Care Instrument in Retired Racing Greyhounds

Veterinarians involved in Greyhound rescue have anecdotally observed that 10-15% of Greyhounds bleed profusely after simple surgical procedures. In most patients, platelet counts and hemostasis profiles are normal; therefore, it is possible that these dogs have platelet dysfunction. The PFA-100 is a novel point-of-care platelet function analyzer that has recently been evaluated as a rapid method to assess platelet function in dogs. The objectives of this study were to characterize platelet function in a group of healthy Greyhounds by means of the PFA-100. Blood samples were collected from the jugular vein from 30 healthy Greyhounds. CBC, biochemical profile, PFA-100 assay with collagen/epinephrine (COL-EPI) and collagen/ adenosindiphosphate (COL-ADP), plasma von Willebrand factor antigen concentration (vWF:Ag), and vWF collagen-binding assay (vWF:CBA) were performed. PFA-100 closure times (CTs) with COL/ADP ranged from 63 to 92 seconds (mean +/- SD, 74.7 +/- 7.9 seconds) and with COL/EPI from 87 to 238 seconds (138 +/- 41 seconds); vWF: Ag ranged from 22 to 120% (87.52 +/- 25.5%) and vWF: CBA ranged from 36 to 102% (77.4 +/- 17.3%); and platelet counts ranged from 147 to 265 x 10(9)/L (194.6 +/- 31.64 x 10(9)/L). Greyhound CTs were significantly shorter than CTs in a mixed population of 50 healthy non-Greyhound dogs, in which the COL/ADP CTs ranged from 61 to 172 seconds (mean +/- SD, 87 +/- 21.6 seconds), and the COL/ EPI CTs ranged from 81 to 300 seconds (mean +/- SD, 183 +/- 67.6 seconds; P = 0.005 for COL/ADP CT; P = 0.001 for COL/ EPI CT). Also, platelet counts were significantly lower (P = 0.001) and packed cell volume was significantly higher (P = 0.001) in the Greyhound than in the non-Greyhound group. The PFA-100 is a reproducible method that can be used in the clinical setting to assess platelet function in Greyhounds; however, normal CTs in healthy Greyhounds are shorter than in other breeds. The results obtained in this study will be used to screen for abnormal platelet function in Greyhounds with postoperative bleeding.

Platelet Function in Dogs Treated for Lymphoma and Hemangiosarcoma and Supplemented with Dietaryn‐3 Fatty Acids

A prospective randomized, double‐blind clinical trial was performed to test the hypothesis that dogs with malignancies that are supplemented withn‐3 fatty acids do not have clinical or laboratory evidence of coagulation disorders or altered platelet function when compared with unsupplemented dogs with similar malignancies. Thirteen dogs with hemangiosarcoma and 66 dogs with lymphoma were evaluated. Coagulation status of the dogs with lymphoma and hemangiosarcoma was evaluated with prothombin time, partial thromboplastin time, platelet count, and in vitro platelet aggregometry using the whole‐blood method. These tests were performed at 5 time points: before beginning the diet (week 0), at weeks 3, 15, and 21, and at 1 year or when progressive disease was evident. Alterations in platelet function in dogs receiving a diet supplemented with dietaryn‐3 fatty acids were not identified when compared to dogs fed a control diet. Dietaryn‐3 fatty acid supplementation using this dosage and ratio in dogs with lymphoma or hemangiosarcoma did not induce clinically significant hemorrhage in these animals. Therefore, supplementation withn‐3 fatty acids did not result in clinical or laboratory evidence relating to uncontrolled hemorrhage in these dogs.

Platelet Function in Dogs Treated for Lymphoma and Hemangiosarcoma and Supplemented with Dietary n-3 Fatty Acids

A prospective randomized, double-blind clinical trial was performed to test the hypothesis that dogs with malignancies that are supplemented with n-3 fatty acids do not have clinical or laboratory evidence of coagulation disorders or altered platelet function when compared with unsupplemented dogs with similar malignancies. Thirteen dogs with hemangiosarcoma and 66 dogs with lymphoma were evaluated. Coagulation status of the dogs with lymphoma and hemangiosarcoma was evaluated with prothrombin time, partial thromboplastin time, platelet count, and in vitro platelet aggregometry using the whole-blood method. These tests were performed at 5 time points: before beginning the diet (week 0), at weeks 3, 15, and 21, and at 1 year or when progressive disease was evident. Alterations in platelet function in dogs receiving a diet supplemented with dietary n-3 fatty acids were not identified when compared to dogs fed a control diet. Dietary n-3 fatty acid supplementation using this dosage and ratio in dogs with lymphoma or hemangiosarcoma did not induce clinically significant hemorrhage in these animals. Therefore, supplementation with n-3 fatty acids did not result in clinical or laboratory evidence relating to uncontrolled hemorrhage in these dogs.