Tuyển tập các báo cáo nghiên cứu về y học được đăng trên tạp chí y học 'Respiratory Research cung cấp cho các bạn kiến thức về ngành y đề tài: Role of free radicals in the pathogenesis of acute chest syndrome in sickle cell disease. | Available online http content 2 5 280 Review Role of free radicals in the pathogenesis of acute chest syndrome in sickle cell disease Elizabeth S Klings and Harrison W Farber The Pulmonary Center Boston University School of Medicine Boston Massachusetts USA Correspondence Elizabeth S Klings MD The Pulmonary Center R-304 Boston University School of Medicine 715 Albany Street Boston MA 02I18 USA. Tel 1 617 638 4860 fax 1 617 536 8093 e-mail eklings@ Received 6 February 2001 Revisions requested 26 February 2001 Revisions received 26 March 2001 Accepted 18 May 2001 Published 13 July 2001 Respir Res 2001 2 280-285 2001 BioMed Central Ltd Print ISSN 1465-9921 Online ISSN 1465-993X Abstract Acute chest syndrome ACS of sickle cell disease SCD is characterized pathologically by vasoocclusive processes that result from abnormal interactions between sickle red blood cells RBCs white blood cells WBCs and or platelets and the vascular endothelium. One potential mechanism of vascular damage in ACS is by generation of oxygen-related molecules such as superoxide O2- hydrogen peroxide H2O2 peroxynitrite ONOO- and the hydroxyl OH radical. The present review summarizes the evidence for alterations in oxidant stress during ACS of SCD and the potential contributions of RBCs WBCs and the vascular endothelium to this process. Keywords acute chest syndrome ACS endothelium hemoglobin nitric oxide NO oxidant stress Introduction ACS is an important cause of morbidity and mortality in SCD occurring in up to 45 of patients and recurring in up to 80 of those afflicted 1 2 . The hallmark pathologic event during ACS is vaso-occlusion the etiology of which is probably multifactorial. One of the mechanisms responsible for vaso-occlusion is abnormal adherence of sickle RBCs WBCs and or platelets to the vascular endothelium. Although the factors that lead to increased cellular adhesion and vascular damage are unclear one possible explanation is that during .
