Renal response to shock

Détails

ID Serval
serval:BIB_B34614CB2033
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Institution
Titre
Renal response to shock
Périodique
Annals of Emergency Medicine
Auteur(s)
Burke  T. J., Burnier  M., Langberg  H., Shanley  P., Schrier  R. W.
ISSN
0196-0644 (Print)
Statut éditorial
Publié
Date de publication
12/1986
Volume
15
Numéro
12
Pages
1397-400
Notes
Journal Article
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, Non-P.H.S.
Research Support, U.S. Gov't, P.H.S. --- Old month value: Dec
Résumé
Renal hypoperfusion such as occurs in shock creates an environment in which cellular injury and organ dysfunction can occur during the episode of shock as well as during reoxygenation and reperfusion. A severe decrement in oxygen delivery compromises energy (adenosine triphosphate) production, leading to various degrees of cell injury ranging from cell swelling to acute cortical necrosis. These different responses of the kidney to shock explain the multiple clinical presentations varying from an isolated loss of concentrating ability to prolonged anuria. Many cellular events contribute to renal cell injury, including cellular ATP depletion, cellular and mitochondrial calcium overload, and activation of phospholipases and oxygen radical formation. Recent clinical and experimental studies suggest that ATP-MgCl2, free radical scavengers, diuretics, vasodilators, and calcium channel blockers appear to be beneficial in preventing acute tubular necrosis after anoxic or severe hypoxic insults. Thus these agents may be helpful in altering the course of acute renal failure in shock patients and may decrease their morbidity and mortality.
Mots-clé
Humans Kidney Failure, Acute/*etiology/physiopathology Shock/*complications
Pubmed
Web of science
Création de la notice
25/01/2008 12:55
Dernière modification de la notice
20/08/2019 15:21
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