Why the study?
Does platelet-activating factor mediate leukocyte and platelet aggregation in patients with cerebral ischemia?
Does platelet-activating factor mediate leukocyte and platelet aggregation in patients with cerebral ischemia?
Platelets in ischemic stroke patients appear to be activated by PAF and leukotrienes released from hyperaggregable leukocytes, a process that is inhibited by ticlopidine but not aspirin.
Suggests PAF contributes to platelet hyperaggregability in stroke; hypothesis-generating and requires prospective confirmation before clinical consideration.
Leukocyte and platelet aggregation stimulated with formyl-methionyl-leucyl-phenylalanine (FMLP) was measured in 32 patients with cerebral ischemia and in 15 controls, using a whole blood aggregometer. The increases in impedance and the reductions in leukocyte and platelet counts were significantly greater in stroke patients than in controls. Aggregation was inhibited by oral ticlopidine, but not by oral aspirin. The effects were clearly counteracted by platelet-activating factor (PAF) antagonists, and counteracted in part by a 5-lipoxygenase inhibitor. The results suggest that platelets tend to be activated by PAF and leukotrienes liberated from hyperaggregable leukocytes in patients with ischemic stroke.
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Uchiyama et al. (1991) studied this question.
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