ANOXIA AND ISCHEMIA TOLERANCE IN TURTLE HEARTS

It has been known since ancient times that turtle hearts exhibit extra ordinary tolerance to anoxia or ischemia. The mechanisms by which they accomplish this remain obscure. The most important adaptation in anox ic turtles is a rapid and dramatic decrease in metabolic rate. Nuclear magnetic resonance measurements indicate that painted turtle (Chrysem ys Picta) hearts respond to anoxia with a rapid decrease in phosphocre atine (PCr; to 50% of control) after which PCr remains constant for at least 4 h. ATP is defended and does not decrease while intracellular pH (pHi) decreases by 0.2 pH units early in anoxia and is then maintai ned constant. Softshelled turtles (Trionyx spinifer) have been demonst rated to be far more sensitive than painted turtles to anoxia in vivo. However, isolated hearts from softshelled turtles appear to be as ano xia tolerant as those of Chrysemys. During ischemia there is also litt le difference in cardiac performance; high energy phosphates, or pHi b etween these two species. A peculiar feature of turtle hearts is an ex tremely high concentration of phosphodiesters (PDE). The role of cytos olic PDEs remains controversial but they may function as lysophospholi pase inhibitors and thereby limit phospholipid turnover (Burt CT and R ibolow H, Comparative Biochemistry and Physiology, 108B: 11-20, 1994). Whether PDEs promote anoxia/ischemia tolerance is unknown but these s tresses can result in membrane lipid dysfunction in mammals. Metabolic control, acid-base, and phospholipid homeostasis all play a role in a noxia and ischemia tolerance in turtle hearts. These physiologic proce sses are interdependent, and how they interact in these animals is unk nown, but they are experimentally accessible by modern analytical meth ods.