Abnormal function and thromboxane release from platelets of dogs with cyclic hematopoiesis.
Investigation of platelet function in dogs with cyclic hematopoiesis (CH) revealed a platelet aggregation disorder. Collagen-induced aggregation of CH dog platelets was significantly abnormal, although normal aggregation in response to ADP was observed. Aggregation was particularly defective on days 2-4 and 14 of the 14-day neutrophil cycle that is typical of CH dogs. The lack of response to collagen suggested a defect in the arachidonic acid pathway of platelet metabolism, since platelet-generated thromboxane-B2 levels were about 30% (p less than 0.0005) of control values. Platelets from dogs heterozygous for CH demonstrated moderately depressed responses to collagen that were intermediate between the values found for platelets from CH dogs and platelets from normal, mixed-breed dogs. Not only does this work indicate a platelet defect in CH dogs, but this phenomenon may be useful as a genetic marker for identification of dogs heterozygous for the CH gene.
D000244:Adenosine Diphosphate / Q000494:pharmacology; D000818:Animals; D001792:Blood Platelets / Q000378:metabolism / Q000503:physiopathology*; D003094:Collagen / Q000494:pharmacology; D004283:Dog Diseases / Q000235:genetics / Q000503:physiopathology*; D004285:Dogs; D005260:Female; D006413:Hematopoietic System / Q000502:physiology*; D006579:Heterozygote; D008297:Male; D009503:Neutropenia / Q000150:complications; D010974:Platelet Aggregation / Q000187:drug effects; D013931:Thromboxanes / Q000097:blood*
D013931:Thromboxanes; D000244:Adenosine Diphosphate; D003094:Collagen