Cardiac thrombosis normally occurs in old Syrian hamsters and according to the research it has a higher incidence rate in females than males. The most frequent site of thrombus formation has been reported to be the left atrium and it usually occurs secondary to degenerative cardiomyopathy and amyloidosis. In this study during a period of 2 years, 22 pet Syrian hamsters aged between 1-3 years-old with signs of cardiovascular disease and referred to the small animal Veterinary Teaching Hospital of University of Tehran were examined in order to evaluate for cardiac diseases as well as atrial thrombosis. During the examinations and observations clinical signs such as lethargy, anorexia, hyperpnoea, reduced daily activity, tachycardia, cyanosis, and vaginal discharge were observed. Based on the clinical sings, the initial diagnosis of cardiac disease was made and for more accurate evaluation of cardiac disease, the cases were referred to the radiology department. For detection of specific signs of cardiac disease echocardiography was performed on all patients. in some cases, sampling of vaginal discharge was taken as well and transferred to the lab for bacterial culture. Cardiac thrombosis and especially atrial thrombosis in all cases were diagnosed by echocardiography so that 9 cases showed pyometra concurrently.

Prothrombotic changes occurring in the prodromal stages of carbohydrate-induced laminitis were investigated. Hemostatic alterations were evaluated by determining platelet counts, platelet survival, activated partial thromboplastin time, one-stage prothrombin time, and monocyte procoagulant activity. Thrombosis of vessels in the hoof wall was evaluated by contrast arteriography and histologic examination. Of 5 horses, 4 became lame between 28 and 52 hours after carbohydrate administration. Mean platelet count in laminitis-affected horses was lower throughout the prodromal stages of laminitis, compared with that in control horses, but differences were not statistically significant. However, survival of indium-111-labeled platelets was less than the value in control horses by 6 hours after carbohydrate administration. Arteriography of disarticulated feet revealed marked reduction in blood supply to hooves in laminitis-affected horses. Histologic examination of the laminar dermis disclosed microthrombi in venules of the laminar dermis in 2 of 4 affected horses. Statistically significant changes in prothrombin time were not observed, and changes in activated partial thromboplastin time were slight and occurred only at the onset of lameness. Statistically significant changes in monocyte procoagulant activity were not observed. Plasma endotoxin-like activity was not detected in laminitis-affected horses. These data indicate that platelet survival was decreased within the first 6 hours after induction of carbohydrate-induced laminitis, but systemic activation of the coagulation system was not detected.

Chromobacterium violaceum is a facultative anaerobic, gram-negative rodshaped bacteria normally found in soil and stagnant water of tropical and subtropical countries. Infections of Chromobacterium violaceum are rare among mammals, but the first human infection were reported in Malaysia in 1927. This clinical case reports two separate cases of Chromobacterium violaceum infection in two sub-adult male Black-handed Gibbon (Hylobates agilis). Both animals were presented with the history of diarrhea, pyrexia and inappetance. From the physical examination, the findings were high body temperature, dull, inactive, soft fecal stained at the rectum and small open wound at lower limb of one of the case. The treatment given was antipyretic and multivitamin. Unfortunately, due to poor prognosis both patients died within 48 hours after presentation and treatment. Autopsy examinations wereperformed to find out the cause of death. Post mortem examination findings revealed hepatomegaly with multiple size whitish-yellow spots on the liver surface, congestion and enlargement of spleen and lymph node, congestion of lung and loss of demarcation between renal cortex and medulla of the kidney. The cellular changes via histopathological findings of kidney, spleen, lung and liver were suggestive of septicaemia. The gross and histopathologicalfindings were supported by the isolation of Chromobacterium violaceum via bacterial isolation and identification from lung, liver, spleen and kidney. Thus, the cause of death of the two sub-adult male Black-handed gibbon in this case are due to septicaemiadue to Chromobacterium violaceum infection.

Although the effects of the rice bran have recently been investigated, there is no information regarding platelet physiology available. However, it is well known that fermented natural plants have a beneficial effect on cardiovascular diseases. Therefore, this study was conducted to investigate whether fermented rice bran extract (FRBE) with several plants (Artemisia princeps, Angelica Gigantis Radix, Cnidium officinale, and Camellia sinensis) affected agonist - induced platelet aggregation, and if so, what the underlying mechanism of its activity was. We performed several experiments, including in vitro platelet aggregation, intracellular calcium concentration and adenosine triphosphate release. In addition, the activation of integrin alpha IIb beta3 was determined using fibrinogen binding. Thrombus formation was also evaluated in vivo using an arterio-venous shunt model. The FRBE inhibited collagen-induced platelet aggregation in a concentrationdependent manner. FRBE significantly and dose dependently attenuated thrombus formation using rat arterio-venous shunt. FRBE suppressed the intracellular calcium mobilization in collagen-stimulated platelets. We also found that FRBE inhibited extracellular stimuli-responsive kinase 1/2, p38-mitogen - activated protein kinases and c-Jun N-terminal kinase phosphorylation. These results suggested that FRBE inhibited collagen-induced platelet aggregation, which was mediated by modulation of downstream signaling molecules. In conclusion, FRBE could be developed as a functional food against aberrant platelet activation-related cardiovascular diseases.

Specific contrast ultrasound is widely applied in diagnostic procedures on humans but remains underused in veterinary medicine. The objective of this study was to evaluate the use of microbubble-based contrast for rapid ultrasonographic diagnosis of thrombosis in small animals, using male New Zealand white rabbits (average weight about 3.5 kg) as a model. It was hypothesized that the use of microbubble-based contrast agents will result in a faster and more precise diagnosis in our model of thrombosis. A pro-coagulant environment had been previously established by combining endothelial denudation and external vessel wall damage. Visualization of thrombi was achieved by application of contrast microbubbles [sterically stabilized, phospholipid-based microbubbles filled with sulfur hexafluoride (SF6) gas] and ultrasonography. As a result, rapid and clear diagnosis of thrombi in aorta abdominalis was achieved within 10 to 30 s (mean: 17.3 s) by applying microbubbles as an ultrasound contrast medium. In the control group, diagnosis was not possible or took 90 to 180 s. Therefore, sterically stabilized microbubbles were found to be a suitable contrast agent for the rapid diagnosis of thrombi in an experimental model in rabbits. This contrast agent could be of practical importance in small animal practice for rapid diagnosis of thrombosis.

The effect of aspirin on bovine platelet function and thromboxane A2 (TXA2) production in stimulated platelets was evaluated. A single dose of aspirin (100 mg/kg of body weight) was administered orally to Holstein cows, and blood samples were obtained before and at regular intervals for 7 days after treatment. The production of TXA2 was assessed by measuring the stable metabolite thromboxane B2, using a specific radioimmunoassay. Within 4 hours of aspirin administration, the production of TXA2 was significantly (P less than 0.05) decreased, irrespective of whether collagen, adenosine diphosphate, or platelet activating factor was used to initiate platelet aggregation. Despite the inhibition of TXA2 release from the stimulated platelets, platelet function, assessed by initial rate of aggregate formation and extent of aggregation, was unaffected by aspirin administration. The extent of aggregate formation in response to collagen, adenosine diphosphate, or platelet activating factor was independent of the amount of TXA2 released from platelets before and after aspirin treatment. The results suggested that TXA2 formation is not the primary biochemical pathway involved in the aggregation of stimulated bovine platelets.

Cats with cardiomyopathy, especially dilated cardiomyopathy associated with taurine deficiency, often develop systemic thrombi. To investigate the relation of taurine deficiency to formation and persistence of thrombi, cats were made taurine-deficient by consumption of a casein-based taurine-deficient diet, then were evaluated for anticoagulant and pro-fibrinolytic activities and platelet function. The cats served as their own controls in the taurine-replete state; then, values were compared for the taurine-deficient state. Plasma (P < 0.01), blood (P < 0.05), and platelet (P < 0.05) taurine concentrations were decreased markedly after cats consumed the taurine-deficient diet for 6 weeks, compared with baseline concentrations before diet. Compared with the taurine-replete state, taurine deficiency induced significantly (P < 0.05) increased mean antithrombin III activity, no significant change in plasminogen and fibrinolytic activities, and similar clot retraction/lysis test results. Decreased (P < 0.01) adenosine diphosphate (ADP)-induced platelet aggregation and [14C]serotonin release, and slightly increased (P < 0.05) collagen-induced platelet [14C]serotonin release, but unchanged collagen-induced platelet aggregation were observed in taurine-deficient cats, compared with taurine-replete cats. Changes in antithrombin III activity most likely reflected hepatocellular acute-phase reaction, which indicates that taurine deficiency may induce a stress-responsive state. Results of platelet function testing indicate that taurine may modulate platelet responsiveness to physiologic agonists, but not in a consistent manner. That platelets from the taurine-deficient cats had decreased responsiveness to ADP, but increased responsiveness to collagen is surprising, because irreversible aggregation is mediated by release of granule-associated ADP after sufficient initial stimulus. All cats had normal clot retraction in dilute blood, which indicated adequate platelet numbers and function; however, clots failed to lyse in vitro. To the authors knowledge, this observation, at present, lacks adequate explanation. Development of marked taurine deficiency and altered in vitro results of anticoagulant activities and some platelet function tests did not result in clinical manifestations in our cats. Results of our study do not conclusively document a pathophysiologic role of taurine depletion in the formation or persistence of thrombi.

The severity of pulmonary thromboembolism and pulmonary hypertension induced by heartworms dying after administration of 2 adulticides was evaluated. Because melarsomine dihydrochloride (RM340) has been shown to be more effective in killing Dirofilaria immitis (heartworms) than the traditional approved adulticide, thiacetarsamide, an attempt was made to determine whether this new adulticide induced more severe lung disease. Before adulticide treatment, 32 dogs with naturally acquired heartworm infections received physical examinations, semiquantitative antigen concentration tests, CBC, platelet counts, serum biochemistry analyses, arterial blood gas determinations, thoracic radiography, pulmonary arteriography, and pulmonary hemodynamic tests. Eight dogs with a low burden and 9 dogs with a high burden of heartworms were treated with thiacetarsamide, and 7 dogs with a low burden and 8 dogs with a high burden were treated with RM340. Except for the heartworm-burden test, tests were repeated at regular intervals during the first 7 weeks after treatment. None of the dogs coughed or had dyspnea after treatment. Six of 9 dogs with high worm burdens and 4 of 8 dogs with low worm burdens had surviving heartworms after thiacetarsamide treatment, in contrast to only 3 of 15 RM340-treated dogs. Differences between the 2 adulticide treatments were minimal as determined by thoracic radiography, pulmonary hemodynamic tests, clinical laboratory analyses, pulmonary arteriography, or necropsy. The RM340 treatment was a more effective adulticide, but it did not increase the severity of hypertension and thromboembolism.

Objective: To measure platelet membrane–derived microparticle (PMP) content and thrombin-generating capacity of canine plasma subjected to specific processing and storage conditions. Animals: 31 clinically normal dogs (19 males and 12 females). Procedures: Citrate-anticoagulated blood samples obtained from each dog were centrifuged at 2,500 × g to isolate platelet-poor plasma (PPP), then PPP was centrifuged at 21,000 × g to isolate microparticle-free plasma (MPF) and microparticle-enriched plasma (MPEP). Whole blood and paired samples of fresh and frozen-thawed PPP, MPF, and MPEP were dual labeled for flow cytometric detection of membrane CD61 (constitutive platelet antigen) and annexin V (indicating phosphatidylserine externalization). Platelets and PMPs were enumerated with fluorescent, size-calibrated beads. Thrombin generation in fresh and frozen-thawed PPP, MPF, and MPEP was measured via kinetic fluorometric assays configured with low tissue factor and low phospholipid concentrations. Results: Initial centrifugation yielded PPP with < 0.5% the platelets of whole blood, with median counts of 413 PMPs/μL for males and 711 PMPs/μL for females. Sequential centrifugation resulted in a 10-fold concentration of PMPs in MPEP and virtually depleted PMPs from MPF. Thrombin generation depended on PMP content, with median endogenous thrombin potential of 0, 893, and 3,650 nmol•min for MPF, PPP, and MPEP, respectively. Freeze-thaw cycling caused significant increases in PMP counts and phosphatidylserine externalization. Conclusions and Clinical Relevance: Canine PMPs were major determinants of thrombin-generating capacity; preanalytic variables influenced plasma PMP content. Processing conditions described here may provide a basis for characterization of PMPs in clinical studies of thrombosis in dogs.

Objective: To establish practical doses and administration frequencies of fondaparinux for cats that would approximate human therapeutic peak and trough plasma anti–factor Xa activities for thromboprophylaxis (TP) and thrombosis treatment (TT) protocols. Animals: 6 healthy adult purpose-bred cats. Procedures: Dosage protocols for TP and TT were selected on the basis of a single compartment pharmacokinetic model incorporating data from humans but modified to account for the higher body weight–normalized cardiac output of cats. Fondaparinux was administered at 0.06 mg/kg, SC, every 12 hours (TP) for 7 days in one session, and 0.20 mg/kg, SC, every 12 hours (TT) for 7 days in another, with a minimum of 1 week separating the sessions. Plasma anti–factor Xa activity was measured before fondaparinux administration (day 1) and at 2 (peak) and 12 (trough) hours after drug administration on days 1 and 7. Platelet aggregation and thromobelastographic (TEG) parameters were also measured 2 hours after drug administration on day 7. Results: Peak plasma anti–factor Xa activities on day 7 for TP (median, 0.59 mg/L; range, 0.36 to 0.77 mg/L) and TT (median, 1.66 mg/L; range, 1.52 to 2.00 mg/L) protocols were within therapeutic ranges for humans. However, only the TP protocol achieved trough anti–factor Xa activity considered therapeutic in humans (median, 0.19 mg/L; range, 0.00 to 0.37 mg/L) on day 7. There were significant changes in the TEG parameters at peak for the TT protocol, suggesting a hypocoagulable state. No significant changes in platelet aggregation were evident for either protocol. Conclusions and Clinical Relevance: A fondaparinux dosage of 0.06 or 0.20 mg/kg, SC, every 12 hours, was sufficient to achieve a peak plasma anti–factor Xa activity in cats that has been deemed therapeutic in humans. This study provided preliminary data necessary to perform fondaparinux dose-determination and clinical efficacy studies.