Beneficial effect of lung preservation is related to ultrastructural integrity of tubular myelin after experimental ischemia and reperfusion.
Ischemia/reperfusion (I/R) injury results in the impairment of surfactant activity. The hypothesis that the differences in lung preservation quality obtained by EuroCollins (EC) and Celsior (CE) solutions were related to surfactant alterations was tested. To avoid extensive structural damage and edema formation, which can secondarily affect the surfactant system, lungs were stored for a short ischemic period (2 h at 10 degrees C) and reperfused (50 min) in an isolated perfused rat lung model after preservation with either potassium-reduced (40 mmol) EC40 or with CE. Using a modified stereological approach ultrastructure, total amount and distribution of phospholipid membranes composing tubular myelin (tm) and small (s) and large (l) unilameliar vesicles (ul) were investigated in the organ in lungs fixed by vascular perfusion either in situ (controls) or after I/R (n = 5 per group). The total amount of intraalveolar surfactant was increased after I/R. However, a significant amount (p = 0.008) of tm was displaced into the alveolar lumen and showed wider meshes of the tm lattices than did the controls (p = 0.023) where almost all tm was epithelial. In lungs preserved with EC40, epithelial tm was significantly reduced (p = 0.018), resulting in a higher ratio (p = 0.034) of surface-inactive small ul (0.05 to 0.3 microm) to surface-active epithelial tm. In the CE group approximately 50% of the total tm pool was epithelial. This was accompanied by higher parenchymal air space and improved functional parameters. Epithelial and endothelial cell-specific immunostaining did not reveal any gross damage of the blood-gas barrier. In summary, improved lung function during reperfusion was associated with beneficial effects of lung preservation on tm integrity after I/R. These observations suggest that preservation solutions ameliorate events leading to surfactant disturbance even before extensive lung injury is manifested.
Fehrenbach
A
A
Division of Electron Microscopy, Center of Anatomy, University of Göttingen, Göttingen, Germany. afehren1@gwdg.de
Ochs
M
M
Warnecke
T
T
Wahlers
T
T
Wittwer
T
T
Schmiedl
A
A
Elki
S
S
Meyer
D
D
Richter
J
J
Fehrenbach
H
H
D000818:Animals; D001688:Biological Products; D004187:Disaccharides / Q000494:pharmacology; D004573:Electrolytes / Q000494:pharmacology; D005971:Glutamates / Q000494:pharmacology; D005978:Glutathione / Q000494:pharmacology; D006639:Histidine / Q000494:pharmacology; D006982:Hypertonic Solutions / Q000494:pharmacology; D007511:Ischemia / Q000473:pathology*; D008168:Lung / Q000098:blood supply* / Q000473:pathology; D008297:Male; D008353:Mannitol / Q000494:pharmacology; D009186:Myelin Sheath; D009926:Organ Preservation; D011506:Proteins; D011663:Pulmonary Surfactants / Q000648:ultrastructure*; D051381:Rats; D017207:Rats, Sprague-Dawley; D015427:Reperfusion Injury / Q000473:pathology*
D001688:Biological Products; C088453:Celsior; D004187:Disaccharides; D004573:Electrolytes; C037096:Euro-Collins' solution; D005971:Glutamates; D006982:Hypertonic Solutions; D011506:Proteins; D011663:Pulmonary Surfactants; C018167:tubular myelin; D008353:Mannitol; D006639:Histidine; D005978:Glutathione