A novel model of senile lung: senescence-accelerated mouse (SAM)

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)