Hypoxia and Anoxia Tolerance of Vertebrate Hearts: An Evolutionary Perspective

Extreme changes in environmental oxygen (O2) is a constant issue that ecthotherm vertebrates have to deal with, whereas for endotherms severe hypoxia and reoxigenation are usually related to a pathological state. The physiological mechanisms of hypoxia tolerance in echtotherms are based on biochemic...

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Bibliographic Details
Published in:Antioxidants & Redox Signaling
Main Authors: Tota B, Angelone T, Cerra MC, MANCARDI, Daniele
Other Authors: Mancardi D
Format: Article in Journal/Newspaper
Language:English
Published: 2011
Subjects:
Online Access:http://hdl.handle.net/2318/74806
https://doi.org/10.1089/ars.2010.3310
Description
Summary:Extreme changes in environmental oxygen (O2) is a constant issue that ecthotherm vertebrates have to deal with, whereas for endotherms severe hypoxia and reoxigenation are usually related to a pathological state. The physiological mechanisms of hypoxia tolerance in echtotherms are based on biochemical evolutionary adaptations and may serve in understanding endogenous phenomena of protection against diminished O2 availability in the heart. In this review, we will, therefore, describe different species of fish, amphibian, and reptile that are well-known examples of cardiac tolerance to O2 deficiency. We will then focus on a subset of Antarctic fishes which have lost physiological transporters of O2 such as hemoglobin and myoglobin (Mb) and that have reached a surprising adaptation to this extreme environment. Moreover, we will concentrate on the cardio-protective effects of the interaction between Mb and nitric oxide with particular emphasis on the nitrite-reductase function of Mb. Finally, the role of a recently described gasotransmitter, the free diffusible hydrogen sulfide, will be briefly discussed in relation to hypoxia. This evolutionary and comparative perspective may provide a useful and heuristic stimulus for medically oriented research aimed at elucidating the environmental and genetic risk factors underlying the vulnerability of the human heart.