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.

A protocol was developed for preparation of platelet concentrates (PC) to support thrombocytopenic dogs. Four clinically normal dogs with platelet counts that ranged from 200 to 330 X 10(9) platelets/L were used as donors. One unit (450 ml) of blood was collected by venipuncture into a double blood bag. Whole blood (WB) was centrifuged for 4 minutes at 1,000 X g (braking time = 2 minutes, 30 seconds) to prepare platelet-rich plasma (PRP). The PRP was expressed into the satellite bag and was centrifuged for 10 minutes at 2,000 X g (braking time = 2 minutes, 36 seconds). The platelet-poor plasma was expressed, leaving 40 to 70 ml of plasma and the pelleted platelets in the satellite bag. The resulting PC was left undisturbed for 60 minutes to promote disaggregation, and the platelets were then resuspended by gentle manual agitation. Forty-eight PC were prepared. Mean (+/- SD) platelet yield from WB to PRP was 78 +/- 13)% (range, 35 to 97%); yield from PRP to PC was 94 (+/- 6) % (range, 75 to 100%); and overall yield (PC from WB) was 74 (+/- 13) % (range, 36 to 91%). Mean PC platelet count was 8.0 (+/- 3.0) X 10(10) platelets/PC (range, 2.3 to 13.4 X 10(10) platelets/PC). The WBC content was 0.1 to 2.3 X 10(9) platelets/PC, representing 3 to 74% of WBC in the WB. Hematocrit was 0.1 to 26.2%. Results of bacterial and fungal culturing were negative.

A cerebrovascular accident or stroke is a rare condition in dogs, but previous studies suggest that it is now increasingly being recognised. Platelets and fibrin networks are involved in haemostasis,which is disrupted during a thrombotic event. In this study we investigate the ultrastructure of the fibrin networks of a dog that had suffered ischaemic stroke, following suspected thromboembolism from clots that became dislodged during catheter maintenance (flushing with heparinised saline) 2 days after carotid artery catheter insertion. Fibrin networks of blood samples that were collected immediately after the stroke, 15 min after treatment with streptokinase and 24 h after treatment, were studied. The results were compared to those of two control dogs. During a stroke, fibrin morphology changes to form a thick, matted layer.Post-treatment ultrastructure shows that the fibrin morphology returns to that comparable to controls. Our results show that during thrombotic risk, fibrin network morphology changes visibly and reduces the fibrinolytic activity of the coagulation system.

Due to logistical problems in obtaining sufficient blood samples from apparently healthy animals in the wild in order to establish normal haematological reference values, only limited information regarding the blood platelet count and morphology of free-living lions (Panthera leo) is available. This study provides information on platelet counts and describes their morphology with particular reference to size in two normal, healthy and free-ranging lion populations. Blood samples were collected from a total of 16 lions. Platelet counts, determined manually, ranged between 218 and 358 x 10(9)/l. Light microscopy showed mostly activated platelets of various sizes with prominent granules. At the ultrastructural level the platelets revealed typical mammalian platelet morphology. However, morphometric analysis revealed a significant difference (P < 0.001) in platelet size between the two groups of animals. Basic haematological information obtained in this study may be helpful in future comparative studies between animals of the same species as well as in other felids.

A cerebrovascular accident or stroke is a rare condition in dogs, but previous studies suggest that it is now increasingly being recognised. Platelets and fibrin networks are involved in haemostasis, which is disrupted during a thrombotic event. In this study we investigate the ultrastructure of the fibrin networks of a dog that had suffered ischaemic stroke, following suspected thrombo-embolism from clots that became dislodged during catheter maintenance (flushing with heparinised saline) 2 days after carotid artery catheter insertion. Fibrin networks of blood samples that were collected immediately after the stroke, 15 min after treatment with streptokinase and 24 h after treatment, were studied. The results were compared to those of two control dogs. During a stroke, fibrin morphology changes to form a thick, matted layer. Post-treatment ultrastructure shows that the fibrin morphology returns to that comparable to controls. Our results show that during thrombotic risk, fibrin network morphology changes visibly and reduces the fibrinolytic activity of the coagulation system.

This study was performed to investigate the effects of calcium administration on the blood coagulation mechanism through APTT in the calf. Five male calves (70~90 kg) were used in this experiment. In the control group, heparinized normal saline (1 IU/kg/min) had been infusing into the jugular vein for 100 minutes. For the analysis of calcium effects on the APTT, the same solutions had been infusing during the first 40 minutes, subsequently the solution including calcium gluconate (3.3 mg/ml/min) had been infusing for 60 minutes.