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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
12
|
| pubmed:dateCreated |
1986-12-18
|
| pubmed:abstractText |
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.
|
| pubmed:grant | |
| pubmed:language |
eng
|
| pubmed:journal | |
| pubmed:citationSubset |
AIM
|
| pubmed:status |
MEDLINE
|
| pubmed:month |
Dec
|
| pubmed:issn |
0196-0644
|
| pubmed:author | |
| pubmed:issnType |
Print
|
| pubmed:volume |
15
|
| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
|
| pubmed:pagination |
1397-400
|
| pubmed:dateRevised |
2010-11-18
|
| pubmed:meshHeading | |
| pubmed:year |
1986
|
| pubmed:articleTitle |
Renal response to shock.
|
| pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, U.S. Gov't, Non-P.H.S.,
Research Support, Non-U.S. Gov't
|