| Summary: | Low concentrations of endogenous carbon monoxide (CO), generated through catabolism of heme‐proteins, have been shown to protect tissues against inflammatory diseases, and ischemia‐reperfusion injuries. However, elevated carboxyhemoglobin (COHb) formed by CO binding to hemoglobin, prevents adequate O2 delivery to tissues by lowering arterial O2 content. Therefore there must be a balance in the level of endogenous CO which maximizes cytoprotective effects and minimizes inhibition of O2 delivery. The elevated heme‐protein concentrations as found in marine mammals, are likely associated with increased heme catabolism, and subsequently increased endogenous CO production and COHb values. We measured COHb in elephant seals, a species with exceptional blood volumes, hemoglobin concentrations and myoglobin content. The mean value in adult seals was 8.7 ± 0.3%, while juveniles and pups (with lower heme‐protein stores) had COHb values of 7.6 ± 0.2% and 7.1 ± 0.3%, respectively. Serial samples over several hours revealed little to no fluctuation in COHb values. This consistent elevation in COHb suggests the magnitude and/or rate of heme‐protein turnover, is higher than terrestrial mammals. While these COHb values decrease the O2 stores needed for diving, the constant presence of elevated CO in blood may provide protection against ischemia‐reperfusion events associated with breath‐holds in elephant seals. Grant Funding Source : Supported by National Institute of Health NHLBI RO1‐HL091767
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