Stroke, Vol 22, 1448-1451, Copyright © 1991 by American Heart Association
R Joseph, C Tsering, S Grunfeld and KM Welch
BACKGROUND: We do not fully understand the mechanisms for neuronal damage
following cerebral arterial occlusion by a thrombus that consists mainly of
platelets. The view that certain endogenous substances, such as glutamate,
may also contribute to neuronal injury is now reasonably well established.
Blood platelets are known to contain and secrete a number of substances
that have been associated with neuronal dysfunction. Therefore, we
hypothesize that a high concentration (approximately several thousand-fold
higher than in plasma, in our estimation) of locally released platelet
secretory products derived from the causative thrombus may contribute to
neuronal injury and promote reactive gliosis. SUMMARY OF COMMENT: We have
recently been able to report some direct support for this concept. When
organotypic spinal cord cultures were exposed to platelet and platelet
products, a significant reduction in the number and the size of the
surviving neurons occurred in comparison with those in controls. We further
observed that serotonin, a major platelet product, has neurotoxic
properties. There may be other platelet components with similar effect.
CONCLUSIONS: The hypothesis of platelet-mediated neurotoxicity gains some
support from these recent in vitro findings. The concept could provide a
new area of research in stroke, both at the clinical and basic levels.
ARTICLES
Platelet secretory products may contribute to neuronal injury
Department of Neurology, Henry Ford Hospital and Health Sciences Center, Detroit, MI 48202.
This article has been cited by other articles:
![]() |
J. P. Mathew, H. M. Rinder, B. R. Smith, M. F. Newman, and C. S. Rinder Transcerebral Platelet Activation After Aortic Cross-Clamp Release is Linked to Neurocognitive Decline. Ann. Thorac. Surg., May 1, 2006; 81(5): 1644 - 1649. [Abstract] [Full Text] [PDF] |
||||
![]() |
L.-W. Fu and J. C. Longhurst Role of activated platelets in excitation of cardiac afferents during myocardial ischemia in cats Am J Physiol Heart Circ Physiol, January 1, 2002; 282(1): H100 - H109. [Abstract] [Full Text] [PDF] |
||||
|
Stroke Home | Subscriptions | Archives | Feedback | Authors | Help | AHA Journals Home | Search Copyright © 1991 American Heart Association, Inc. All rights reserved. Unauthorized use prohibited. |