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

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.

• Authors: D Bagchi, G J Wetscher, M Bagchi, P R Hinder, G Perdikis, S J Stohs, R A Hinder, D K Das
• Journal: Chemico-biological interactions (Chem Biol Interact) Vol. 104 Issue 2-3 Pg. 65-85 (May 02 1997) ISSN: 0009-2797 [Print] Ireland
• PMID: 9212776 (Publication Type: Journal Article, Research Support, U.S. Gov't, P.H.S., Review)

Chemical References

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

Topics

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