An integrated comparative physiology and molecular approach pinpoints mediators of breath-hold capacity in dolphins

作者: Douglas P Nowacek , Nicolas Devos , Andreas Fahlman , William C Eward , Ashley M Blawas

DOI: 10.1101/2021.01.20.425775

关键词: VasoconstrictionCause of deathIschemiaDownregulation and upregulationProgrammed cell deathPhysiologyComparative physiologyBiologyRodentHypoxia (medical)

摘要: Ischemic events, such as ischemic heart disease and stroke, are the number one cause of death globally. Ischemia prevents blood, carrying essential nutrients oxygen, from reaching tissues leading to cell death, tissue eventual organ failure. While humans relatively intolerant these other species, marine mammals, have evolved remarkable tolerance chronic ischemia/reperfusion during diving. Here we capitalized on unique adaptations bottlenose dolphins (Tursiops truncatus) a comparative model stress hypoxia identify molecular features associated with breath-holding. Using RNA-Seq observed time-dependent upregulation arachidonate 5-lipoxygenase (ALOX5) gene Consistent data, also increased ALOX5 enzymatic activity in serum undergoing breath-holds. has previously been shown be activated rodent models, its metabolites, leukotrienes, induce vasoconstriction. The occurred within estimated aerobic dive limit suggesting that may promote through sustained vasoconstriction These observations pinpoint potential mechanism by which dolphins, perhaps adapted prolonged breath-holds

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