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.

Venous access devices connected to jugular vein catheters were implanted SC in 2 groups of 6 White Carneau pigeons (Columba livia). Total parenteral nutrition (TPN), or a control solution (lactated Ringer's solution) was infused as a bolus 4 times daily. Physiologic, hematologic, and biochemical variables were monitored over 5 days. Complications in the TPN-treated pigeons included 8.7% weight loss during the 5-day trial, hyperglycemia for up to 90 minutes after infusion, and glucosuria after infusion. Control pigeons lost 1.3% of their body weight and did not become hyperglycemic or glucosuric after infusion. Hematocrit in both groups of pigeons decreased to a value slightly below published reference values for pigeons. Five pigeons developed venous thrombosis in the proximal part of the cranial vena cava. Results indicated that intermittent administration of TPN is possible in birds; however, further research is required to develop better techniques for administration of TPN solutions. Additionally, it is important to determine, more specifically, the caloric and nutrient requirements of pigeons under stress and receiving TPN.

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.