Direct activation of platelets by heat is the possible trigger of the coagulopathy of heat stroke

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Abstract
The trigger of the coagulopathy that complicates heat stroke is obscure, but direct platelet activation by heat is a possibility we set out to study. Platelet rich plasma (PRP), prepared from blood donors, was incubated at increasing temperatures (38-45.degree. C) and then platelet aggregation was undertaken in response to decreasing low doses of ADP (>2.0 .mu.mol/l). Hyperaggregability was manifested when the incubation temperature reached 43.degree. C and was maximum at 44.degree.C before complete inhibition of responses at 45.degree. C. The platelet hyperactivity induced by heating at 44.degree. C persisted after reincubating PRP samples at 37.degree. C. These platelet responses could not be triggered in PRP samples prepared from subjects after the overnight ingestion of aspirin or after the addition of aspirin to PRP before starting the heating procedure. However, aspirin was less effective when added to PRP after the appearance of the heat-induced hyperaggregability. In conclusion, these results indicate that platelets can be activated directly by heat. This mechanism which may be operational in heat stroke, is unaffected by cooling (body cooling being basic in the management of heat stroke) but can be prevented by the early administration of aspirin.