Ultrastructural alterations in intraalveolar surfactant subtypes after experimental ischemia and reperfusion.
Ischemia and reperfusion (I/R) result in surfactant dysfunction. Whether the impairment of surfactant is a consequence or a cause of intraalveolar edema formation is still unknown. The cumulative effects of lung perfusion, ischemic storage, and subsequent reperfusion on surfactant ultrastructure and pulmonary function were studied in a rat isolated perfused lung model. The left lungs were fixed for electron microscopy by vascular perfusion either immediately after excision (control; n = 5) or after perfusion with modified Euro-Collins solution (EC), storage for 2 h at 4 degrees C in EC, and reperfusion for 40 min (n = 5). A stereological approach was chosen to discriminate between intraalveolar surfactant subtypes of edematous regions and regions free of edema. Intraalveolar edema seen after I/R in the EC group occupied 36 +/- 6% (mean +/- SEM) of the gas exchange region as compared with control lungs (1 +/- 1%; p = 0.008). Relative intraalveolar surfactant composition showed a decrease in surface active tubular myelin (3 +/- 1 versus 12 +/- 0%; p = 0.008) and an increase in inactive unilamellar forms (83 +/- 2 versus 64 +/- 5%; p = 0.008) in the EC group. These changes occurred both in edematous (tubular myelin, 3 +/- 1%; unilamellar forms, 88 +/- 6%) and in nonedematous regions (tubular myelin, 4 +/- 3%; unilamellar forms, 77 +/- 5%). The ultrastructural changes in surfactant were associated with an increase in peak inspiratory pressure during reperfusion. In conclusion, surfactant alterations seen after I/R are not directly related to the presence of edema fluid in the alveoli. Disturbances in intraalveolar surfactant after I/R are not merely the result of inactivation due to plasma protein leakage but may instead be responsible for an increased permeability of the blood-air barrier, resulting in a vicious cycle of intraalveolar edema formation and progressing surfactant impairment.
Ochs
M
M
Division of Electron Microscopy, Department of Anatomy, University of Göttingen, Göttingen, Germany. mochs@gwdg.de
Nenadic
I
I
Fehrenbach
A
A
Albes
J M
JM
Wahlers
T
T
Richter
J
J
Fehrenbach
H
H
D000818:Animals; D015824:Blood-Air Barrier / Q000502:physiology; D002199:Capillary Permeability / Q000502:physiology; D007511:Ischemia / Q000473:pathology*; D008168:Lung / Q000098:blood supply* / Q000473:pathology; D008297:Male; D008854:Microscopy, Electron; D009926:Organ Preservation; D011650:Pulmonary Alveoli / Q000098:blood supply* / Q000473:pathology; D011654:Pulmonary Edema / Q000473:pathology; D011659:Pulmonary Gas Exchange / Q000502:physiology; D011663:Pulmonary Surfactants / Q000145:classification / Q000648:ultrastructure*; D051381:Rats; D017207:Rats, Sprague-Dawley; D015427:Reperfusion Injury / Q000473:pathology*
D011663:Pulmonary Surfactants