Abstract
Platelet-activating factor (PAF) is a phospholipid which acts as a mediator in inflammation and thrombosis (for review, see Braquet et al., 1987). A growing body of evidence supports the hypothesis that PAF may be a key mediator in neuroinjury (Frerichs and Feuerstein, 1990). Brain tissue and blood cells are able to synthesize PAF and this production may be enhanced during stroke and thrombosis. Locally increased levels of PAF during brain ischemia may be detrimental as PAF induces vasoconstriction and endothelial damage with consequent blood brain barrier damage and edema. In addition, high levels of PAF have been shown to be neurotoxic. Specific receptors are involved and have been demonstrated to be present in blood cells and brain tissue.
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© 1996 Plenum Press New York
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van Rossem, K., Vermariën, H., Decuyper, K., Bourgain, R. (1996). The Role of PAF and the Effect of a Specific PAF Antagonist on Local Tissue PO2 and Neuronal Integrity During and After Photothrombotic Brain Infarction in Unanesthetised Rabbits. In: Ince, C., Kesecioglu, J., Telci, L., Akpir, K. (eds) Oxygen Transport to Tissue XVII. Advances in Experimental Medicine and Biology, vol 388. Springer, Boston, MA. https://doi.org/10.1007/978-1-4613-0333-6_55
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DOI: https://doi.org/10.1007/978-1-4613-0333-6_55
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