Ironjustic
Mon, Mar-10-08, 17:16
"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. "SURFACTANT DYSFUNCTION IN LUNG CONTUSION" The
second article speaks to the fact iron released causes lung
problems. "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.
SURFACTANT DYSFUNCTION IN LUNG CONTUSION WITH AND WITHOUT
SUPERIMPOSED GASTRIC ASPIRATION IN A RAT MODEL. [JOURNAL
ARTICLE] 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 conditions.
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. Quinlan 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) feature 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 iron 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 prove of therapeutic benefit for
the treatment of SIRS and ALI.
systemic inflammatory response; hemolysis; oxidative stress
--------------------------------------------------------------
--------------= =AD-----
Address for reprint requests and other correspondence: G. J.
Quinlan, Dept. of Critical Care Medicine, Royal Brompton
Hospital, Sydney St., London SW3 6NP, UK (e-mail:
g.quin...@imperial.ac.uk) doi:10.1152/ajplung.00169.2007
1040-0605/08 $8.00
Who loves ya. Tom
Jesus Was A Vegetarian! http://jesuswasavegetarian.7h.com
Man Is A Herbivore! http://tinyurl.com/a3cc3
DEAD PEOPLE WALKING http://tinyurl.com/zk9fk
lung volumes".
When one looks at these two articles the first one shows lung
trauma causes a lack of surfactant / phosphatidylcholine in
the lung. "SURFACTANT DYSFUNCTION IN LUNG CONTUSION" The
second article speaks to the fact iron released causes lung
problems. "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.
SURFACTANT DYSFUNCTION IN LUNG CONTUSION WITH AND WITHOUT
SUPERIMPOSED GASTRIC ASPIRATION IN A RAT MODEL. [JOURNAL
ARTICLE] 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 conditions.
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. Quinlan 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) feature 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 iron 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 prove of therapeutic benefit for
the treatment of SIRS and ALI.
systemic inflammatory response; hemolysis; oxidative stress
--------------------------------------------------------------
--------------= =AD-----
Address for reprint requests and other correspondence: G. J.
Quinlan, Dept. of Critical Care Medicine, Royal Brompton
Hospital, Sydney St., London SW3 6NP, UK (e-mail:
g.quin...@imperial.ac.uk) doi:10.1152/ajplung.00169.2007
1040-0605/08 $8.00
Who loves ya. Tom
Jesus Was A Vegetarian! http://jesuswasavegetarian.7h.com
Man Is A Herbivore! http://tinyurl.com/a3cc3
DEAD PEOPLE WALKING http://tinyurl.com/zk9fk