Objective—To determine the effects of protamine sulfate on clot formation time and clot strength thromboelastography variables for canine whole blood samples. Animals—Blood samples obtained from 11 healthy dogs. Procedures—Blood samples were collected from jugular veins of dogs into syringes with 3.2% sodium citrate (blood to citrate ratio, 9:1). Blood samples were divided into aliquots, and protamine sulfate was added to various concentrations (0 [control], 22, 44, and 66 μg/mL). Prepared samples were activated with kaolin (n = 8) or not activated (8), CaCl2 was added, and thromboelastography was performed. Reaction time (R), clot formation time (K), rate of clot formation (α angle), and maximum amplitude (MA) were measured. Results—For kaolin-activated and nonactivated blood samples, protamine (66 μg/mL) significantly increased R and K and decreased α angle and MA, compared with values for control samples. Also, protamine (44 μg/mL) decreased MA in nonactivated blood samples and increased K and decreased α angle in kaolin-activated samples, compared with values for control samples. Conclusions and Clinical Relevance—Results indicated protamine prolonged clot formation time and decreased overall clot strength in a dose-dependent manner; such effects may contribute to a hypocoagulable state in dogs. Kaolin-activated and nonactivated blood samples were appropriate for measurement of the effects of protamine on coagulation. Administration of protamine to reverse the effects of heparin should be performed with caution.

The effects of heparin administration, by the oral route, were evaluated in dogs. In single and multiple dose studies (single 7.5 mg/kg, multiple 3 × 7.5 mg/kg per 48 h), plasma, urine, and fecal samples were collected at various times up to 120 h after oral administration of unfractionated heparin. Changes in plasma and urine anti-Xa activity, plasma and urine anti-IIa activity, plasma activated partial thromboplastin time (APTT) and antithrombin (ATIII), and chemical heparin in urine and feces were examined with time. There was support for heparin absorption, with significant differences in APTT, heparin in plasma as determined by anti-Xa activity (Heptest) in the single dose study and plasma anti-Xa activity, anti-IIa activity and ATIII; and chemical heparin in urine in the multiple dose study. No clinical evidence of bleeding was detected in any dog during the studies. Oral heparin therapy may be applicable for thromboembolic disease in animals. Further studies are warranted to determine the effects of oral heparin at the endothelial level in the dog.

Objective—To determine dose dependency of tranexamic acid–induced emesis and the time course of the antifibrinolytic potency of tranexamic acid in dogs. Animals—10 Beagles. Procedures—In a dose-escalating experiment, ascending doses of tranexamic acid (10, 20, and 30 mg/kg, IV) were administered at 5-minute intervals until vomiting was observed. In a separate single-dose experiment, ascending doses of tranexamic acid (20, 30, 40, and 50 mg/kg, IV) were administered at 1-week intervals until vomiting was observed. Time to onset of vomiting and number of vomiting episodes were measured in both experiments. In a coagulation experiment, a single 50 mg/kg bolus of tranexamic acid was administered, and blood was obtained 1 hour before and 20 minutes, 3 hours, and 24 hours after administration. Antifibrinolytic potency of tranexamic acid was evaluated by use of a modified rotational thromboelastography method. Results—Tranexamic acid induced vomiting in a dose-dependent manner. Vomiting frequency was < 2 episodes, and vomiting concluded < 250 seconds after administration. Antifibrinolytic potency of tranexamic acid was significantly higher at 20 minutes following administration, but not different by 24 hours, when compared with the potency measured before administration. No adverse effects were observed in any experiment. Conclusions and Clinical Relevance—IV administration of tranexamic acid induced emesis in a dose-dependent manner. The antifibrinolytic potency of tranexamic acid decreased in a time-dependent manner and was resolved < 24 hours after administration. Further studies are warranted to investigate the emetic and other adverse effects of tranexamic acid in dogs of various breeds and ages.