Improved lung preservation relates to an increase in tubular myelin-associated surfactant protein A.
BACKGROUND
Declining levels of surfactant protein A (SP-A) after lung transplantation are suggested to indicate progression of ischemia/reperfusion (IR) injury. We hypothesized that the previously described preservation-dependent improvement of alveolar surfactant integrity after IR was associated with alterations in intraalveolar SP-A levels.


METHODS
Using immuno electron microscopy and design-based stereology, amount and distribution of SP-A, and of intracellular surfactant phospholipids (lamellar bodies) as well as infiltration by polymorphonuclear leukocytes (PMNs) and alveolar macrophages were evaluated in rat lungs after IR and preservation with EuroCollins or Celsior.


RESULTS
After IR, labelling of tubular myelin for intraalveolar SP-A was significantly increased. In lungs preserved with EuroCollins, the total amount of intracellular surfactant phospholipid was reduced, and infiltration by PMNs and alveolar macrophages was significantly increased. With Celsior no changes in infiltration or intracellular surfactant phospholipid amount occurred. Here, an increase in the number of lamellar bodies per cell was associated with a shift towards smaller lamellar bodies. This accounts for preservation-dependent changes in the balance between surfactant phospholipid secretion and synthesis as well as in inflammatory cell infiltration.


CONCLUSIONS
We suggest that enhanced release of surfactant phospholipids and SP-A represents an early protective response that compensates in part for the inactivation of intraalveolar surfactant in the early phase of IR injury. This beneficial effect can be supported by adequate lung preservation, as e.g. with Celsior, maintaining surfactant integrity and reducing inflammation, either directly (via antioxidants) or indirectly (via improved surfactant integrity).
Fehrenbach
Heinz
H
Department of Internal Medicine (Respiratory Medicine), Philipps-University, Baldingerstrasse, D-35043 Marburg, Germany. fehrenba@med.uni-marburg.de
Tews
Sebastian
S
Fehrenbach
Antonia
A
Ochs
Matthias
M
Wittwer
Thorsten
T
Wahlers
Thorsten
T
Richter
Joachim
J
D000818:Animals; D004187:Disaccharides; D004573:Electrolytes; D005971:Glutamates; D005978:Glutathione; D006639:Histidine; D006982:Hypertonic Solutions; D066298:In Vitro Techniques; D008168:Lung; D016040:Lung Transplantation / Q000379:methods; D008297:Male; D008353:Mannitol; D009186:Myelin Sheath / Q000378:metabolism*; D019188:Organ Preservation Solutions; D011650:Pulmonary Alveoli / Q000378:metabolism* / Q000473:pathology*; D037662:Pulmonary Surfactant-Associated Protein A / Q000378:metabolism*; D051381:Rats; D017207:Rats, Sprague-Dawley; D015427:Reperfusion Injury / Q000378:metabolism / Q000473:pathology; D014021:Tissue Preservation / Q000379:methods*
C088453:Celsior; D004187:Disaccharides; D004573:Electrolytes; C037096:Euro-Collins' solution; D005971:Glutamates; D006982:Hypertonic Solutions; D019188:Organ Preservation Solutions; D037662:Pulmonary Surfactant-Associated Protein A; C018167:tubular myelin; D008353:Mannitol; D006639:Histidine; D005978:Glutathione