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. 1994 Jul;150(1):238-44.
doi: 10.1164/ajrccm.150.1.8025756.

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

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

S Teramoto et al. Am J Respir Crit Care Med. 1994 Jul.

Abstract

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 VSports手机版. 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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