Stress Induced Platelet Dysfunction in Rats with Folic Acid-Deficient Hyperhomocysteinemia

A rat model of experimental hyperhomocysteinemia (HHC) caused by chronic folic acid deficiency was used to study the impact of swimming stress on the values of agonist-induced platelet aggregation and ATP release. At week 8 of HHC development, platelet aggregability and ATP levels in response to tes...

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Bibliographic Details
Main Authors: S. V. Alisievitch, A. G. Dubichev, A. A. Levina, G. A. Nazarova, N. N. Zolotov, V. V, Krzhechkovskaya, N. N. Pavlova, E. P. Romanova, I. A. Rudko, K. A. Cherkasova, A. A. Kubatiev
Format: Article
Language:English
Published: Federal Research and Clinical Center of Intensive Care Medicine and Rehabilitology, Moscow, Russia 2006-12-01
Series:Общая реаниматология
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Online Access:https://www.reanimatology.com/rmt/article/view/1363
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Summary:A rat model of experimental hyperhomocysteinemia (HHC) caused by chronic folic acid deficiency was used to study the impact of swimming stress on the values of agonist-induced platelet aggregation and ATP release. At week 8 of HHC development, platelet aggregability and ATP levels in response to test inductors (ADP, thrombin, and collagen) moderately increased. After stress, the rate of platelet aggregation showed a more increase in rats with HHC; however, the increment was less pronounced than in the control group. The similar changes was observed in ATP, the release of which from dense platelet granules decreased in the experimental animals exposed to stress changes as compared to the controls. The experimental findings suggest that the stress potentiates platelet dysfunction in HHC.
ISSN:1813-9779
2411-7110