Am. J. Respir. Crit. Care Med., Vol 150, No. 1, Jul 1994, 238-244.
A novel model of senile lung: senescence-accelerated mouse (SAM)
S Teramoto, Y Fukuchi, Y Uejima, K Teramoto, T Oka and H Orimo
Department of Geriatrics, Faculty of Medicine, University of Tokyo, Japan.
Senescence-accelerated mouse (SAM) has been characterized as a unique
animal model to investigate spontaneous aging as well as age-related
disorders. However, little is known about the properties of the lung. We
examined age-related morphologic and functional changes of the lung in SAM
P2, as the senescence-prone strain, and in SAM R1, as the
senescence-resistant strain. On morphologic examination, the earlier
(starting at 6 mo) and more severe change in airspace size (mean linear
intercept: MLI) was observed in SAM P2 (MLI [micron]; 3 mo: 72.1 +/- 2.4; 6
mo: 80.8 +/- 2.9; 12 mo: 91.1 +/- 3.1; 18 mo: 143.4 +/- 6.6), compared with
SAM R1 (MLI [micron]; 3 mo: 68.9 +/- 1.8; 6 mo: 70.8 +/- 2.6; 12 mo: 76.1
+/- 2.8; 18 mo: 101.2 +/- 4.7). The destructive index was not remarkably
changed through life in both strains, suggesting that the alveolar wall was
relatively intact in SAM. On functional examination, the left-sided shift
of the pressure-volume (P-V) curves observed in SAM P2 at an early stage of
aging (starting at 9 mo) compared with SAM R1. The shape constant (K)
obtained from the P-V curve was increased with aging in SAM P2 (K; 3 mo:
0.124 +/- 0.004; 9 mo: 0.142 +/- 0.003; 18 mo: 0.183 +/- 0.008), and also
increased at a late stage of aging in SAM R1 (K; 3 mo: 0.123 +/- 0.005; 9
mo: 0.135 +/- 0.004; 18 mo: 0.148 +/- 0.007). This study demonstrates that
SAM P2 manifested most of the characteristic changes in senile
lung.(ABSTRACT TRUNCATED AT 250 WORDS)
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Copyright © 1994 American Thoracic Society
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