Lung Problems 
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 Lung Problems

"Surfactant replacement improved inflation/deflation lung volumes".

When one looks at these two articles the first one shows lung trauma
causes a lack of surfactant / phosphatidylcholine in the lung.
The second article speaks to the fact iron released causes lung
"Role of iron"
Now if one were to put the two together the one lung trauma reduces
lecithin and the other iron causes the problems.
Now since iron TARGETS phosphatidylcholine / lecithin .. then IS it
the .. iron in the first article .. which CAUSES the lack of
phosphatiodylcholine / lecithin .. ?

One must understand trauma causes bleeding though.

Shock 2008 Feb 21.
Raghavendran K, Davidson BA, Knight PR, Wang Z, Helinski J, Chess PR,
Notter RH

This study investigates surfactant dysfunction in rats with lung
contusion (LC) induced by blunt chest trauma. Rats at 24 h
postcontusion had a decreased percent content of large surfactant
aggregates in cell-free bronchoalveolar lavage (BAL) and altered large-
aggregate composition with decreased phosphatidylcholine (PC),
increased lyso-PC, and increased protein compared with uninjured
controls. The surface activity of large aggregates on a pulsating
bubble surfactometer was also severely impaired at 24 h postcontusion.
Decreases in large surfactant aggregate content and surface activity
were improved, but still apparent, at 48 and 72 h postcontusion
compared with uninjured control rats and returned to normal by 96 h
postcontusion. The functional importance of surfactant abnormalities
in LC injury was documented in pilot studies showing that exogenous
surfactant replacement at 24 h postcontusion improved inflation/
deflation lung volumes. Additional experiments investigated a
clinically relevant combination of LC plus gastric aspiration
(combined acid and small gastric">food particles) and found reductions
in large surfactant aggregates in BAL similar to those for LC.
However, rats given LC + combined acid and small gastric">food
particles versus LC had more severe surfactant dysfunction based on
decreases in surface activity and alterations in large aggregate
composition. Combined data for all animal groups had strong
statistical correlations between surfactant dysfunction (increased
minimum surface tension, decreased large aggregates in BAL, decreased
aggregate PC, and increased aggregate lyso-PC) and the severity of
inflammatory lung injury (increased total protein, albumin, protein/
phospholipid ratio, neutrophils, and erythrocytes in BAL plus
increased whole lung myeloperoxidase activity). These results show
that surfactant dysfunction is important in the pathophysiology of LC
with or without concurrent gastric aspiration and provides a rationale
for surfactant replacement therapy in these prevalent clinical

More from this journal
Shock (Augusta, Ga.) [Shock]

"Adverse aspects of altered iron handling"

Am J Physiol Lung Cell Mol Physiol 294: L161-L174, 2008. First
published November 30, 2007; INVITED REVIEW

Pathogenesis of the systemic inflammatory syndrome and acute lung
injury: role of iron mobilization and decompartmentalization
Anna L. Lagan, Daniel D. Melley, Timothy W. Evans, and Gregory J.
Department of Critical Care Medicine, Imperial College School of
Medicine, Royal Brompton Hospital, London, United Kingdom

Changes in iron homeostatic responses routinely accompany infectious
or proinflammatory insults. The systemic inflammatory response
syndrome (SIRS) and the development of acute lung injury (ALI)
pronounced systemic and lung-specific alterations in iron/heme
mobilization and decompartmentalization; such responses may be of
pathological significance for both the onset and progression of acute
inflammation. The potential for excessive iron-catalyzed oxidative
stress, altered proinflammatory redox signaling, and provision of
as a microbial growth factor represent obvious adverse aspects of
altered in vivo iron handling. The release of hemoglobin during
hemolytic disease or surgical procedures such as those utilizing
cardiopulmonary bypass procedures further impacts on iron
mobilization, turnover, and storage with associated implications.
Genetic predisposition may ultimately determine the extent to which
SIRS and related syndromes develop in response to such changes. The
design of specific therapeutic interventions based on endogenous
stratagems to limit adverse aspects of altered iron handling may
of therapeutic benefit for the treatment of SIRS and ALI.

systemic inflammatory response; hemolysis; oxidative stress


Address for reprint requests and other correspondence: G. J. Quinlan,
Dept. of Critical Care Medicine, Royal Brompton Hospital, Sydney St.,

1040-0605/08 $8.00

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Fri, 27 Aug 2010 20:11:41 GMT
 [ 1 post ] 

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