PATHOPHYSIOLOGY OF BLEEDING IN HEAT-STRESS - AN EXPERIMENTAL-STUDY INSHEEP

Widespread hemorrhagic manifestations commonly occur in patients with severe heat stroke. The pathogenesis of hemostatic disorders in these patients is not fully understood, although it is believed to be multif actorial in origin. The present investigation was designed to study th e changes in blood platelets caused by heat stress in an experimental model of five merino sheep. The experiments were performed in two grou ps of five merino sheep each. In one group the sheep were subjected to a combination of heat (elevated environmental temperature) and exerti onal stress, and allowed to proceed throughout the experiment until a state of near collapse was reached (Task A). In the other group (Task B) the animals were heated in the same manner as those in Task A and a lso subjected to exertional heat; however, when the temperature reache d 43.6 +/- 0.2 degrees C, the critical core temperature (CCT), they we re subjected to evaporative cooling in a climatic chamber. Serial chan ges in the platelet counts and platelet functions were measured throug hout the duration of the experiments. At the core temperature (CT) of 42.1 degrees C and above there was a significant impairment of adhesio n of platelets to glass beads. During the early phases of elevation of CT, platelets showed hyperaggregation in the presence of different ag onists (such as, collagen, ADP, ristocetin); this was followed by hypo aggregation when the CCT was raised above 43.6 +/- 0.2 degrees C. Howe ver, these impairments of platelet functions occurring at elevated CT and CCT were found to reverse to normal within 24 hours after the anim als were cooled to 39 degrees C. It was also found that the hyperaggre gation of platelets to different agonists induced by raised CT could b e partially prevented by prior in vitro treatment of platelets with ap yrase, a known enzyme destroying of ADP. The results of these experime nts indicate that heat stress induced by exposing merino sheep to elev ated controlled temperature directly activates the platelets. This may be an important contributing factor in causing altered hemostasis in heat stroke activated directly by heat. This mechanism may be operatin g in altered hemostasis in heat stroke.