Alloxan-induced hyperglycemia in rabbits and the response of platelets to aggregating agents in vitro and to exposed subendothelium in vivo.
Many patients with diabetes mellitus show increased platelet aggregation and prostaglandin synthesis in response to physiological agents such as ADP and collagen when their platelets are tested in platelet-rich plasma or washed platelet suspensions. However, the relationship between increased platelet aggregation in vitro and increased thrombosis in vivo is difficult to establish with certainty. We have developed an in vivo model system in rabbits which tests the response of platelets in circulating native blood to an arterial vessel wall with limited damage such as might occur in arteries of patients with diabetes mellitus. We have used this model system to investigate whether 5 to 9 weeks of alloxan-induced hyperglycemia increases platelet adhesion and aggregation on a damaged vessel wall in vivo as well as platelet aggregation in vitro. Our results show that rabbit platelet function is not affected by extreme hyperglycemia and suggest that alloxan-induced diabetes in the rabbit may not be a good model for human diabetes mellitus.
D000244:Adenosine Diphosphate / Q000494:pharmacology; D000496:Alloxan; D000818:Animals; D001158:Arteries / Q000473:pathology / Q000648:ultrastructure; D001792:Blood Platelets / Q000502:physiology*; D002448:Cell Adhesion; D003094:Collagen; D003921:Diabetes Mellitus, Experimental / Q000097:blood; D004195:Disease Models, Animal; D004727:Endothelium / Q000503:physiopathology* / Q000648:ultrastructure; D006943:Hyperglycemia / Q000097:blood* / Q000139:chemically induced; D008297:Male; D008855:Microscopy, Electron, Scanning; D010974:Platelet Aggregation / Q000187:drug effects*; D011817:Rabbits
D000244:Adenosine Diphosphate; D000496:Alloxan; D003094:Collagen