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.

The hypothesis that equine laminitis is caused by thrombosis of vessels in the laminar corium (dermis) was investigated. Hemostatic alterations were evaluated by determining platelet count, platelet survival, platelet adhesiveness to vascular subendothelium, activated clotting time, and whole blood recalcification time. Thrombosis of vessels in the hoof wall was evaluated by scintigraphic studies of the hoof wall after administration of indium-111 ((111)In)- labeled platelets, contrast arteriography, and histologic examination. Platelet count remained constant before and at the onset of lameness; however, survival of (111)In-labeled platelets was shortened. Scintigraphy of affected feet revealed accumulation of (111)In-labeled platelets distal to the coronary band. Arteriography of disarticulated saline-perfused feet revealed marked reduction in blood supply to affected hooves. Histologic examination of the laminar dermis disclosed variable numbers of microthrombi in dermal veins of affected feet from 3 of 4 ponies with laminitis. Whole blood recalcification time was shortened at 8 hours after administration of carbohydrate and was prolonged at the onset of laminitis. Activated clotting time was prolonged at 32 hours after carbohydrate administration and at the onset of lameness. Plasma endotoxin-like activity was detected in 1 of 4 affected ponies. These data confirm that microvascular thrombosis existed at the onset of lameness in ponies with carbohydrate-induced laminitis and indicate that systemic coagulopathy may have preceded development of thrombosis.

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.

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.

Platelet function, antithrombin and plasminogen activities, and fibrinolytic capabilities in 11 cats with acquired heart disease were compared with results in 4 healthy cats. Of 11 cats with heart disease, 9 had hyperthyroidism with secondary cardiac dysfunction. One cat with hyperthyroidism had renal disease and heart failure, and of 2 cats with idiopathic hypertrophic cardiomyopathy, 1 also had renal disease. At the time of testing, 3 cats had thromboembolic events associated with the disease. Compared with healthy cats, cats with acquired heart disease had increased activity of antithrombin III, a protein that behaves as an acute-phase reactant. Plasminogen activity was decreased, although not significantly, in cats with acquired heart disease, compared with results in healthy cats. In cats with left ventricular dysfunction, clot retraction was decreased (marginal significance, P = 0.058) and might be attributed, in some cases, to the medications received by the cats. Dilute whole blood clots from all cats failed to lyse in vitro. This observation, at present, lacks adequate explanation. Platelets from cats with acquired heart disease, compared with platelets from healthy cats, had decreased responsiveness (aggregation and [(14)C]serotonin release) to adenosine diphosphate and increased responsiveness to collagen. Hyperthyroid cats were receiving various drugs (propranolol, atenolol, or diltiazem) to empirically treat clinical signs of disease attributable to cardiac dysfunction. Although numbers of cats in each group were small, definite trends were observed in the results of tests. Platelets from cats receiving atenolol had decreased responsiveness to adenosine diphosphate and unaltered responsiveness to collagen, compared with platelets from healthy cats, and may have decreased risk of thrombus formation. Cats receiving propranolol and diltiazem had platelets with markedly increased responsiveness to collagen; however, these drugs appeared to provide sufficient cardioprotective benefits to counter the prothrombotic effects.

A semiquantitative heartworm test of antigen concentration was evaluated as a predictor of thromboembolism after adulticide treatment. Seventeen dogs with naturally acquired infections of Dirofilaria immitis (heartworms) were studied before and after thiacetarsamide treatment, using physical examinations, arterial blood gas analyses, thoracic radiography, and pulmonary hemodynamic and arteriographic tests. Eight dogs were considered to have a low burden of heartworms and 9 had a high burden. Dogs with a high worm burden had more severe pulmonary thromboembolism with pulmonary hypertension, dilated pulmonary arteries, flow obstruction of the caudal pulmonary arteries, and parenchymal lesions in the caudal lung lobes. Dogs with a low worm burden had minimal changes. Within each group of dogs, the severity of thromboembolism was less in some dogs in which all heartworms were not killed. Six of the 9 dogs with a high burden of heartworms had surviving heartworms, and 1 of these dogs had 38 live heartworms. Only 4 of the 8 low worm burden had complete heartworm mortality, but only 1 dog had more than 3 surviving heartworms. We concluded that dogs with a high worm burden were more likely to have pulmonary thromboembolism after thiacetarsamide treatment and that dogs with a low worm burden were more likely to have minimal changes. A semiquantitative heartworm test of antigen concentration is recommended as part of the pretreatment evaluation of dogs infected with heartworms.

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.