(Stroke. 1996;27:514-519.)
© 1996 American Heart Association, Inc.
Articles |
From the Section on Analytical Biochemistry, Laboratory of Clinical Science, National Institute of Mental Health, Bethesda, Md.
Correspondence to Sanford P. Markey, PhD, Section on Analytical Biochemistry, Laboratory of Clinical Science, National Institute of Mental Health, Bldg 10, Room 3D40, 10 Center Dr MSC 1262, Bethesda, MD 20892-1262. E-mail s_markey@codon.nih.gov.
Background and Purpose Platelet-activating factor (PAF) has been reported to be an active mediator in ischemic brain damage on the basis of indirect pharmacological data from PAF antagonists. The direct measurement of PAF in neuronal tissues has not been reported previously in analogous animal models. We have examined regional brain PAF concentration changes during the reperfusion period after ischemia in gerbils to obtain direct evidence for the involvement of PAF with ischemic brain damage and reported gas chromatography/mass spectrometry (GC/MS) methods of PAF quantitative analysis in brain tissues.
Methods After transient (10 minutes) ischemia followed by controlled periods (0 to 96 hours) of reperfusion and recovery, regional PAF concentrations were determined in gerbil brain tissue. Quantitative analysis of PAF in brain regions is performed using an electron-capture negative chemical ionization GC/MS method, modified for brain tissue.
Results The level of PAF was increased significantly and maximally in hippocampus (211%), cortex (168%), and thalamus (169%) after 1 hour of reperfusion. In contrast, there were no significant changes of PAF in any brain region from 6 hours to 96 hours after reperfusion.
Conclusions PAF is increased in gerbil brain in response to ischemia at early stages of reperfusion. PAF increases could contribute to the onset and progress of ischemic neuropathology.
Key Words: platelet-activating factor spectrum analysis, mass gerbils
This article has been cited by other articles:
![]() |
A. Bouayad, J.-C. Fouron, X. Hou, M. Beauchamp, C. Quiniou, D. Abran, K. Peri, R. I. Clyman, D. R. Varma, and S. Chemtob Developmental regulation of prostaglandin E2 synthase in porcine ductus arteriosus Am J Physiol Regulatory Integrative Comp Physiol, May 1, 2004; 286(5): R903 - R909. [Abstract] [Full Text] [PDF] |
||||
![]() |
A. M. Marrache, F. Gobeil Jr., S. G. Bernier, J. Stankova, M. Rola-Pleszczynski, S. Choufani, G. Bkaily, A. Bourdeau, M. G. Sirois, A. Vazquez-Tello, et al. Proinflammatory Gene Induction by Platelet-Activating Factor Mediated Via Its Cognate Nuclear Receptor J. Immunol., December 1, 2002; 169(11): 6474 - 6481. [Abstract] [Full Text] [PDF] |
||||
![]() |
G. J. del Zoppo, K. J. Becker, and J. M. Hallenbeck Inflammation After Stroke: Is It Harmful? Arch Neurol, April 1, 2001; 58(4): 669 - 672. [Full Text] [PDF] |
||||
![]() |
C. Chen, J. C. Magee, V. Marcheselli, M. Hardy, and N. G. Bazan Attenuated LTP in Hippocampal Dentate Gyrus Neurons of Mice Deficient in the PAF Receptor J Neurophysiol, January 1, 2001; 85(1): 384 - 390. [Abstract] [Full Text] [PDF] |
||||
![]() |
P. K. Mukherjee, M. A. DeCoster, F. Z. Campbell, R. J. Davis, and N. G. Bazan Glutamate Receptor Signaling Interplay Modulates Stress-sensitive Mitogen-activated Protein Kinases and Neuronal Cell Death J. Biol. Chem., March 5, 1999; 274(10): 6493 - 6498. [Abstract] [Full Text] [PDF] |
||||
|
Stroke Home | Subscriptions | Archives | Feedback | Authors | Help | AHA Journals Home | Search Copyright © 1996 American Heart Association, Inc. All rights reserved. Unauthorized use prohibited. |