Interrelationship between cellular calcium homeostasis and free radical generation in myocardial reperfusion injury

Chem Biol Interact. 1997 May 2;104(2-3):65-85. doi: 10.1016/s0009-2797(97)03766-6.

Abstract

This review describes the interrelationship between two important biological factors, intracellular calcium overloading and oxygen-derived free radicals, which play a crucial role in the pathogenesis of myocardial ischemic reperfusion injury. Free radicals are generated during the reperfusion of ischemic myocardium, and polyunsaturated fatty acids in the membrane phospholipids are the likely targets of the free radical attack. On the other hand, activation of phospholipases can provoke the breakdown of membrane phospholipids which results in the activation of arachidonate cascade leading to the generation of prostaglandins, and oxygen free radicals can be produced during the interconversion of the prostaglandins. In conclusion, it has been emphasized that the two seemingly different causative factors of reperfusion injury, intracellular calcium overloading and free radical generation are, in fact, highly interrelated.

Publication types

  • Research Support, U.S. Gov't, P.H.S.
  • Review

MeSH terms

  • Calcium / metabolism*
  • Calcium Channel Blockers / pharmacology
  • Calcium Channel Blockers / therapeutic use
  • Cell Membrane / metabolism
  • Clinical Trials as Topic
  • Electrophysiology
  • Fatty Acids, Unsaturated / chemistry
  • Fatty Acids, Unsaturated / metabolism
  • Homeostasis / drug effects
  • Homeostasis / physiology*
  • Humans
  • Hydrogen-Ion Concentration
  • Myocardial Reperfusion Injury / drug therapy
  • Myocardial Reperfusion Injury / metabolism
  • Myocardial Reperfusion Injury / physiopathology*
  • Neutrophils / cytology
  • Neutrophils / metabolism
  • Patient Care Planning / standards
  • Phospholipids / metabolism
  • Phospholipids / physiology
  • Reperfusion Injury / drug therapy
  • Reperfusion Injury / metabolism
  • Reperfusion Injury / physiopathology
  • Superoxides / metabolism*

Substances

  • Calcium Channel Blockers
  • Fatty Acids, Unsaturated
  • Phospholipids
  • Superoxides
  • Calcium