Mitochondrial injuries in rat lungs preserved for 17 h: An ultrastructuralstudy

Citation
M. Ueda et al., Mitochondrial injuries in rat lungs preserved for 17 h: An ultrastructuralstudy, EUR SURG RE, 31(2), 1999, pp. 162-172
Citations number
35
Language
INGLESE
art.tipo
Article
Categorie Soggetti
Surgery,"Medical Research Diagnosis & Treatment
Journal title
EUROPEAN SURGICAL RESEARCH
ISSN journal
0014-312X → ACNP
Volume
31
Issue
2
Year of publication
1999
Pages
162 - 172
Database
ISI
SICI code
0014-312X(199903/04)31:2<162:MIIRLP>2.0.ZU;2-V
Abstract
Mitochondria of the small vasculature endothelial cells were examined in pr eserved rat lungs before and after reperfusion, and the ultrastructural cha nges were correlated with pulmonary function after reperfusion. Rat lungs w ere flushed with perfusate and prostaglandin El and divided into five group s (n = 5 in each group): group A, normal control group; group B, University of Wisconsin solution; group C, Euro-Collins solution; group D, ET-Kyoto s olution, and group E, new ET-Kyoto solution. After preservation at 4 degree s C for 17 h, the left lungs were reperfused at 37 degrees C for 60 min. Ti ssue was sampled and mitochondria of the small vasculature endothelial ce I ls were ultrastructurally analyzed by transmission electron microscopy befo re and after reperfusion. The ultrastructure of the mitochondria was well m aintained in groups A, B and E before and after reperfusion. In group C, th e number of severely degenerated mitochondria in the sectional area of 100 mu m(2) before reperfusion was 18.0 +/- 3.9, which was significantly larger than in the other groups (p < 0.01), and the total number of mitochondria significantly decreased with reperfusion (from 24.8 +/- 3.5 to 8.2 +/- 2.4, p < 0.05). In group C, the shunt fraction, mean pulmonary arterial pressur e and the wet-dry ratio of the lung tissue after reperfusion C were signifi cantly higher than in the other groups (p < 0.05; 76.3 +/- 1.5%, 54.8 +/- 4 .2 mm Hg, and 20.6 +/- 2.5, respectively). A positive correlation was found between the percentage of the mitochondrial degeneration before reperfusio n and the physiological parameters after reperfusion. Mitochondrial damage associated with cold ischemia is probably involved in lung injury caused by cold preservation and reperfusion.