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This study investigates whether experimental diabetes alters the ease with which platelet aggregation can be initiated in pial and mesenteric microvessels of the mouse. Aggregation was elicited by exposing microvessels to radiant energy from a mercury lamp in the presence of sodium fluorescein. The time required for this noxious stimulus to initiate aggregation was similar in fed or fasted alloxan diabetics and their controls, and in fed streptozotocin diabetics and their controls, but was significantly shortened in streptozotocin mice fasted for 18 to 24 hours when these animals were compared with either fed or fasted controls. Aggregation was also elicited by puncture of microvessels or by micropunture plus locally applied adenosine 5'-diphosphate. No differences in aggregability were found between either fed or fasted diabetics and their respective controls. In the light plus dye model of injury, the capacity to enhance aggregation at will by fasting streptozotocin diabetics may provide a means by which some of the factors controlling aggregation in this model of diabetes can be identified, enhanced aggregation in other species or in other types of diabetes.

Proaggregatory effect of fasting on platelet aggregation in the microcirculation of mice with streptozotocin diabetes.