Pulmonary bypass shunt reduces oxidative damage in the American alligator


Meeting Abstract

143.6  Monday, Jan. 7  Pulmonary bypass shunt reduces oxidative damage in the American alligator FELBINGER, K*; OWERKOWICZ, T; EME, J; SCHRINER, S/E; HICKS, J/W; California State University, San Bernardino; California State University, San Bernardino; University of North Texas, Denton; University of California, Irvine; University of California, Irvine kfelbing@hotmail.com

Various hypotheses have been proposed to explain the evolutionary persistence of cardiac shunting among the vertebrates. We hypothesised that the right-to-left (R-L) shunt acts to reduce oxidative stress in tissues, and offers protection during periods of atmospheric hyperoxia. In order to test this hypothesis, we eliminated R-L shunting ability by surgical ligation of the left aorta (LAo) in juveniles of the American alligator (Alligator mississippiensis), effectively converting their circulatory system from in-parallel to in-series. Experimental animals (no R-L shunt; n=8) and sham-operated controls (shunt intact; n=8) were exposed for 25 days to normoxia (21%O2) and hyperoxia (35%O2) at 30°C. Plasma samples collected after each exposure were assayed for lipid peroxidation and antioxidant activity. We found significantly higher (+13%) malondialdehyde concentrations in response to hyperoxia in experimental animals, and no differences in catalase concentration between treatment groups. This suggests alligators without shunting ability suffered increased oxidative damage, but were unable to mount sufficient antioxidant defences to protect against reactive oxygen species. We suggest the pulmonary bypass shunt, by admixture of deoxygenated and oxygenated blood, reduces blood oxygen tension and limits oxidative damage to systemic tissues. Palaeoatmospheric oxygen fluctuations would have had limited effect on contemporary vertebrate taxa with in-parallel circulation. Evolution of in-series circulation in ancestors of mammals and bird must have necessitated upregulation of antioxidant expression. Funded by NSF grants IOB 0445680 and IOS 922756 to JWH.

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