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Studies On Alveolar Fluid Reabsorbed Mechanism In Alveolar Type Ⅱ Cells Of Neurogenic-ARDS Rats.

Posted on:2007-08-30Degree:DoctorType:Dissertation
Country:ChinaCandidate:T P LiFull Text:PDF
GTID:1104360185988556Subject:Neurology
Abstract/Summary:PDF Full Text Request
Objectives:Neurogenic Pulmonary Edema (NPE ) or called the centre pulmonary edema(CPN), or Neurogenic acute respiratory distress syndrome (N-ARDS ), it is a kind of serious complication with swift and violent oncoming force and developing rapidly , erupting simultaneously in early days , jeopardizing the life in short time. So serious central nervous system injuries is one of pulmonary edema's key factors. Common centre nervous diseases, for instance: brain injury, brain apoplexy, brain tumors, epilepsy, encephalitis and other intracranial infection.In traditional theory, development of pulmonary edema mainly as a result of the increase in hydrostatic pressure (cardiogenic edema) and capillary permeability (noncardiogenic edema).However, since Goodman found that alveolar epithelial cells could actively transport sodium ion, there were a lot of studies supported that the probable causes of lung edema included the dysfunction of alveolar epithelial cells who could actively transport sodium ions, except for the 2 reasons mentioned before. Namely, the probable mechanisms of lung edema include"2 for increase,1 for decrease ". The new mechanism which were found and validated to decrease lung liquid in order to maintain the balance of liquid across the alveolar epithelium will bring the traditional concept about origination of lung edema to a new milestone.
Keywords/Search Tags:Neurogenic pulmonary edema (NPE), Alveolar type II epithelial cells (AT-II), Acute respiratory distress syndrome(ARDS), Aquaporin1(AQP1), Sodium transport, Patch-clamp technique, Whole-cell recording mode
PDF Full Text Request
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