Đang chuẩn bị nút TẢI XUỐNG, xin hãy chờ
Tải xuống
Tuyển tập báo cáo các nghiên cứu khoa học quốc tế ngành y học dành cho các bạn tham khảo đề tài: Early Changes in ion transport in inflammatory disease. | Journal of Inflammation BioMed Central Review Changes in ion transport in inflammatory disease Michael Eisenhut Address Institute of Child Health University of Liverpool Eaton Road Liverpool L12 2AP UK Email Michael Eisenhut - michael.eisenhut@talk21.com Corresponding author Open Access Published 29 March 2006 Received 18 January 2006 Accepted 29 March 2006 Journal of Inflammation 2006 3 5 doi l0.ll86 l476-9255-3-5 This article is available from http www.journal-inflammation.cOm content 3 1 5 2006 Eisenhut licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License http creativecommons.org licenses by 2.0 which permits unrestricted use distribution and reproduction in any medium provided the original work is properly cited. Abstract Ion transport is essential for maintenance of transmembranous and transcellular electric potential fluid transport and cellular volume. Disturbance of ion transport has been associated with cellular dysfunction intra and extracellular edema and abnormalities of epithelial surface liquid volume. There is increasing evidence that conditions characterized by an intense local or systemic inflammatory response are associated with abnormal ion transport. This abnormal ion transport has been involved in the pathogenesis of conditions like hypovolemia due to fluid losses hyponatremia and hypokalemia in diarrhoeal diseases electrolyte abnormalites in pyelonephritis of early infancy septicemia induced pulmonary edema and in hypersecretion and edema induced by inflammatory reactions of the mucosa of the upper respiratory tract. Components of membranous ion transport systems which have been shown to undergo a change in function during an inflammatory response include the sodium potassium ATPase the epithelial sodium channel the Cystic Fibrosis Transmembrane Conductance Regulator and calcium activated chloride channels and the sodium potassium chloride co-transporter. .