Improved lung preservation relates to an increase in tubular myelin-associated surfactant protein A

doi:10.1186/1465-9921-6-60

Respiratory Research

Volume 6

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Fehrenbach H
Tews S
Fehrenbach A
Ochs M
Wittwer T
Wahlers T
Richter J

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Tews S
Fehrenbach A
Ochs M
Wittwer T
Wahlers T
Richter J
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Research

Improved lung preservation relates to an increase in tubular myelin-associated surfactant protein A

Heinz Fehrenbach² , Sebastian Tews¹ , Antonia Fehrenbach¹^,2 , Matthias Ochs¹^,4 , Thorsten Wittwer³ , Thorsten Wahlers³ and Joachim Richter¹

¹Division of Electron Microscopy, Centre of Anatomy, University of Göttingen, Kreuzbergring 36, D-37075 Göttingen, Germany

²Clinical Research Group "Chronic Airway Diseases", Department of Internal Medicine (Respiratory Medicine), Philipps-University, Baldingerstrasse, D-35043 Marburg, Germany

³Department of Cardiothoracic and Vascular Surgery, Friedrich Schiller University Jena, Bachstrasse 18, D-07740 Jena, Germany

⁴Institute of Anatomy, University of Bern, Baltzerstrasse 2, CH-3000 Bern 9, Switzerland

author email corresponding author email

Respiratory Research 2005, 6:60doi:10.1186/1465-9921-6-60


Published:	21 June 2005

Abstract

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.

Conclusion

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).