DENGUE FEVER ACTIVATES THE l-ARGININE-NITRIC OXIDE PATHWAY: AN EXPLANATION FOR REDUCED AGGREGATION OF HUMAN PLATELETS

SUMMARY 1 In patients with Dengue fever, a viral inflammatory syndrome, haemorrhage is a significant pathological feature, yet the underlying mechanisms remain unclear. Nitric oxide (NO) is an important regulator of platelet function, inhibiting aggregation, recruitment and adhesion to the vascular...

Full description

Saved in:
Bibliographic Details
Published in:Clinical and experimental pharmacology & physiology Vol. 35; no. 10; pp. 1143 - 1146
Main Authors: Mendes-Ribeiro, Antonio C, Moss, Monique B, Siqueira, Mariana AS, Moraes, Thalyta L, Ellory, J Clive, Mann, Giovanni E, Brunini, Tatiana MC
Format: Journal Article
Language:English
Published: Melbourne, Australia Blackwell Publishing Asia 01-10-2008
Subjects:
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:SUMMARY 1 In patients with Dengue fever, a viral inflammatory syndrome, haemorrhage is a significant pathological feature, yet the underlying mechanisms remain unclear. Nitric oxide (NO) is an important regulator of platelet function, inhibiting aggregation, recruitment and adhesion to the vascular endothelium. 2 We have investigated whether changes in the activity of the l‐arginine–NO pathway in human platelets may account for increased bleeding in patients with Dengue fever. A total of 16 patients with Dengue fever and 18 age‐matched healthy volunteers participated in the study. 3 Collagen induced platelet aggregation in a dose‐dependent manner in both Dengue patients and controls, but the degree of platelet aggregation was significantly reduced in the patient group. Elevated rates of l‐arginine transport in Dengue fever patients were associated with enhanced NO synthase activity and elevated plasma fibrinogen levels. 4 The present study provides the first evidence that Dengue fever is associated with increased l‐arginine transport and NO generation and reduced platelet aggregation.
Bibliography:istex:0D8E202369F7B642560E955BB8BE821488CDD5D7
ark:/67375/WNG-CW94FR93-6
ArticleID:CEP4970
ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 23
ISSN:0305-1870
1440-1681
DOI:10.1111/j.1440-1681.2008.04970.x