To better characterize the idiopathic hyperlipoproteinemia of Miniature Schnauzer dogs, the plasma lipoproteins of 20 Miniature Schnauzers (MS) and 11 dogs of other breeds (DOB) were evaluated by ultracentrifugation, electrophoresis, and biochemical tests. Seventeen M S were healthy; 3 had diabetes mellitus. Plasma from 6 of 17 healthy and all 3 diabetic M S was visibly lipemic. Lipemia was slight to marked in healthy lipemic MS, and marked in diabetic ones. All DOB had clear plasma; 8 were healthy and 3 had diabetes. All healthy lipemic MS and diabetic lipemic M S had hypertriglyceridemia associated with excess very low density lipoproteins. Chylomicronemia was present in 4 of 6 healthy lipemic M S and all 3 diabetic lipemic MS. Lipoproteins with ultracentrifugal and electrophoretic characteristics of normal low density lipoprotein were lacking in 4 of 6 healthy lipemic MS. The lipoprotein patterns of 4 of 11 healthy nonlipemic M S were characterized by mild hypertriglyceridemia associated with increased very low density lipoproteins and a lack of lipoproteins with characteristics of normal low density lipoproteins. Lipoprotein patterns of diabetic DOB closely resembled those of healthy DOB those of diabetic lipemic M S resembled those of markedly lipemic healthy lipemic MS. In conclusion, the hyperlipoproteinemia of Miniature Schnauzers is characterized by increased very low density lipoproteins with or without accompanying chylomicronemia; some affected dogs may have decreased low There is evidence that primary hyperlipoproteinemias occur in dogs, but these disorders have not been well characterized, and their etiologies have not been established."6 In one report, primary hyperlipoproteinemia was believed to be the cause of the persistent fasting lipemia of five Miniature Schnauzers. Serum from these dogs formed cream layers on refrigeration, indicating the presence of chylomicrons. Triglyceride concentrations were moderately to markedly increased, and cholesterol concentrations were moderately increased. Lipoprotein electrophoresis showed lipoproteins that stayed at the origin (expected behavior of chylomicrons), and greater amounts of beta and alpha-2 migrating lipoproteins than were seen in healthy dogs.5Several hereditary disorders that cause fasting hypertriglyceridemia occur in people, and many of these are characterized by chylomicronemia. The hyperlipoproteinemias that involve chylomicronemia are often associated with abdominal pain and/or pancreatitis, and dia- 253
Hemostasis is a remarkable and a remarkably complex mechanism. It can maintain blood in a fluid state intravascularly but very quickly changes blood to a jellylike mass upon disruption of the vasculature. This review will give a synopsis of the 3 phases of hemostasis: platelet, vascular, and coagulation. Fibrinolysis and control mechanisms of hemostasis will also be covered. In addition, brief descriptions of the clinical and laboratory evaluation of patients and the diagnosis of bleeding disorders will be presented.
We have evaluated senescence related changes in canine red blood cells (RBCs) using the biotinylation system, where RBCs are labeled in vivo with biotin at the beginning of their life span, and retrieved from circulation on immobilized avidin at the end of their life span. This approach avoids the controversial use of density gradient centrifugation to collect presumably old RBCs. Furthermore, the dog is an appropriate model for human RBC senescence because it has a low degree of random RBC loss and a similarly long RBC life span (approximately 110 days). Two dogs had 97% to 100% of their circulating RBCs biotinylated by infusion of N-hydroxysuccinimido biotin (Clontech, Palo Alto, CA; Calbiochem, La Jolla, CA) dissolved in dimethyl sulfoxide. At postbiotinylation days 104 and 107 for one dog and day 110 for the other dog, biotinylated RBCs were isolated by magnetic cell sorting and analyzed for the presence of autologous IgG using 125I- labeled sheep-antidog IgG (SAD IgG). On all 3 days, there were at least three times more SAD IgG molecules per RBC on senescent biotinylated RBCs than on control (unfractionated) RBCs (day 104: 11,677 v 3,399; day 107: 6,710 v 2,115; day 110: 6,042 v 1,838 molecules of SAD IgG per senescent v control RBC). Furthermore, it is unlikely that an immune response to the conjugated biotin had been elicited, because fresh in vitro biotinylated RBCs that were incubated in autologous plasma (taken after exposure to circulating biotinylated RBCs for 113 days) and then exposed to the SAD IgG showed no increase in antibody binding over control (non-biotinylated) RBCs (1,431 v 1,378 cpm/10(8) biotinylated v control RBCs; P > .20). These results suggest that senescence of canine biotinylated RBCs is characterized by binding of autologous IgG and that antibiotin antibodies do not contribute to this process.
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