Mitochondrial free calcium regulation in hypoxia and reoxygenation: relation to cellular injury.
The role of mitochondria in myocardial ischemic and hypoxic injury is discussed. Increases in mitochondrial Ca content and ionized Ca2+ concentration are observed during and after ischemic and hypoxic exposure and have traditionally been considered to impair mitochondrial function. New data are discussed in which it is shown that increases in mitochondrial [Ca2+] do not necessarily reflect irreversible myocyte injury. Further, it is shown that irreversible cellular injury may occur in hypoxic myocytes in association with increases in mitochondrial [Ca2+] that would ordinarily be considered to fall within a physiologic range. The significance of these observations is considered in context with observations relating to the assessment of post-hypoxic mitochondrial function.
Silverman
H S
HS
Division of Cardiology, Johns Hopkins Medical Institutions, Baltimore, Maryland.
D000818:Animals; D002118:Calcium / Q000378:metabolism*; D000860:Hypoxia / Q000378:metabolism* / Q000473:pathology; D008722:Methods; D008929:Mitochondria, Heart / Q000378:metabolism* / Q000502:physiology; D017202:Myocardial Ischemia / Q000378:metabolism; D010100:Oxygen / Q000494:pharmacology*
D010100:Oxygen; D002118:Calcium