Cardiac survival in anoxia-tolerant vertebrates: An electrophysiological perspective.
Certain vertebrates, such as freshwater turtles of the genus Chrysemys and Trachemys and crucian carp (Carassius carassius), have anoxia-tolerant hearts that continue to function throughout prolonged periods of anoxia (up to many months) due to successful balancing of cellular ATP supply and demand. In the present review, we summarize the current and limited understanding of the cellular mechanisms underlying this cardiac anoxia tolerance. What emerges is that cold temperature substantially modifies cardiac electrophysiology to precondition the heart for winter anoxia. Intrinsic heart rate is slowed and density of sarcolemmal ion currents substantially modified to alter cardiac action potential (AP) characteristics. These changes depress cardiac activity and reduce the energetic costs associated with ion pumping. In contrast, anoxia per se results in limited changes to cardiac AP shape or ion current densities in turtle and crucian carp, suggesting that anoxic modifications of cardiac electrophysiology to reduce ATP demand are not extensive. Additionally, as knowledge of cellular physiology in non-mammalian vertebrates is still in its infancy, we briefly discuss the cellular defense mechanisms towards the acidosis that accompanies anoxia as well as mammalian cardiac models of hypoxia/ischemia tolerance. By examining if fundamental cellular mechanisms have been conserved during the evolution of anoxia tolerance we hope to have provided a framework for the design of future experiments investigating cardiac cellular mechanisms of anoxia survival.
Stecyk
Jonathan A W
JA
Physiology Programme, Department of Molecular Biosciences, University of Oslo, PO Box 1041, N-0316, Oslo, Norway. jonathan.stecyk@imbv.uio.no
Galli
Gina L
GL
Shiels
Holly A
HA
Farrell
Anthony P
AP
D000200:Action Potentials; D000222:Adaptation, Physiological; D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D002347:Carps / Q000378:metabolism; D003080:Cold Temperature; D004734:Energy Metabolism; D006339:Heart Rate; D006439:Hemodynamics; D006863:Hydrogen-Ion Concentration; D000860:Hypoxia / Q000378:metabolism* / Q000503:physiopathology; D007473:Ion Channels / Q000378:metabolism; D009206:Myocardium / Q000378:metabolism*; D012508:Sarcolemma / Q000378:metabolism; D013997:Time Factors; D014426:Turtles / Q000378:metabolism
D007473:Ion Channels; D000255:Adenosine Triphosphate