Abstract

After feeding, Burmese pythons (Python molurus bivittatus) undergo physiological cardiac remodeling associated with increased cardiac output. Because the left ventricle (LV) of the heart and aorta are anatomically and mechanically coupled, we tested the hypothesis that chronic overfeeding causes aortic remodeling. Nine‐month old snakes consumed 25% of their total body weight every 2 weeks (normal fed, NF, n=5) or once every 3 days (overfed, OF, n=7) for 12 weeks. Compared with NF, OF had a greater aortic lumen diameter (D, 2.42 ± 0.11 vs. 1.47 ± 0.04 mm, p<0.01) and total wall thickness (WT, 353 ± 12 vs. 227 ± 12 μm, p<0.001), with unchanged WT:D ratio (p=0.67). This remodeling was associated with increased intrinsic mechanical stiffening (elastic modulus: 6,457 ± 670 vs. 3,667 ± 501 kPa, p=0.01; stiffness: 18,811 ± 4,318 vs. 7,093 ± 1,187 kPa*m, p<0.05) and expression of collagen I (2.27 ± 0.34 vs. 1.00 ± 0.15 AU, p<0.05) and advanced glycation end‐products (1.84 ± 0.33 vs. 1.00 ± 0.35 AU, p<0.05). However, no difference in the oxidative stress marker nitrotyrosine was observed between groups, and OF actually had greater expression of the antioxidant enzyme CuZnSOD (2.45 ± 0.06 vs. 1.00 ± 0.25 AU, p=0.05). Chronic overfeeding induces a physiological remodeling of the aorta in Burmese pythons that is not mediated by oxidative stress, but may be an adaptive response to increased blood flow and cardiac remodeling.

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