Abstract
This chapter discusses the role of platelet activating factor (PAF) as a mediator of allergic disease and in cellular responses. The use of antagonists, in determining the biological significance of PAF, has also been discussed in the chapter with particular emphasis on asthma and ischemic states. The functional consequences of PAF antiagonist interaction with PAF receptors has been evaluated in various cell types and isolated tissues in vitro and in several organ systems in vivo . The efficacy of PAF antagonists in a variety of animal models, in which endogenous mediators are released, supports a major contributory role for PAF in several inflammatory and allergic pathophysiological conditions. Delayed bronchospasm, bronchial hyperreactivity, shock syndromes, ischemia and reperfusion injury, and transplant rejection has been discussed in the chapter. PAF can induce several functional responses in a variety of inflammatory cells. The pyridoquinazoline carboxamide inhibits both the acute bronchospasm and hypotension induced by intravenous PAF. There is much evidence supporting a role of PAF in models of several shock syndromes. In contrast to heart and lung, PAF-induced increases in vascular permeability of isolated rat kidney. The contribution of endogenous PAF to the damage caused by ischemia and reperfusion in several vascular beds has been discussed. PAF antagonists protect several specific organ systems from a variety of insults.
Published Version
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
