Platelet aggregates were induced in pial arterioles of the following strains of mice with a genetic predisposition for diabetes: ob/ob and db+/db+. Aggregation was compared with that in 6J+/+ mice, the nondiabetic controls for ob/ob animals, and in +m/+m as well as db+/+m, the nondiabetic controls for db/db+ mice. Aggregation was also induced within mesenteric arterioles of db+/db+ animals and compared with that in db+/+m mice. Aggregation was monitored microscopically, by measuring the time required for a noxious stimulus to initiate aggregation in an injured arteriole. Platelet aggregation was initiated with equal ease in the pial arterioles of ob/ob mice and their 6J/+ controls. However, the onset of aggregation in the pial arterioles of the db+/db+ group was significantly delayed when compared with the onset in either of the nondiabetic control groups, m/m or db/m. A similar prolongation in the time required to produce aggregation was also observed in the mesenteric arterioles of the db/db+ mice when compared with db/m controls. The basis for reduced platelet aggregation in the microcirculation of db+/db+ mice is not explained. The results differ from those showing enhanced aggregation in many in vitro studies of platelets from human diabetics and from those of in vivo studies of two other animal models described in the literature. However, not all published studies have reported enhanced aggregation. The delayed aggregation in the present study may provide a basis for analysis of factors that regulate platelet aggregation in diabetes.

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