Role of phospholipases in myocardial ischemia: effect of cardioprotective agents on the phospholipases A of heart cytosol and sarcoplasmic reticulum in vitro.
Increased breakdown of myocardial phospholipids to fatty acids and lysophosphoglycerides is an early feature of myocardial ischemic injury and many investigators believe that enhanced phospholipase action is an important factor in the process. Several recent reports indicate that inhibitors of phospholipase A, such as mepacrine, chloroquine and chlorpromazine, can prevent heart phosphoglyceride breakdown in vivo. We isolated the phospholipases A from rat heart cytosol and sarcoplasmic reticulum and examined the effects of various cardioprotective substances on their activity. Most of the cardioprotective agents studied inhibited the heart phospholipases in vitro, providing further evidence that phospholipid degradation in ischemic myocardial injury may be modulated by pharmacologic agents.
Hostetler
K Y
KY
Department of Medicine, University of California, San Diego.
Jellison
E J
EJ
D000818:Animals; D002746:Chlorpromazine / Q000494:pharmacology; D003327:Coronary Disease / Q000188:drug therapy / Q000201:enzymology*; D003600:Cytosol / Q000201:enzymology; D066298:In Vitro Techniques; D008297:Male; D009206:Myocardium / Q000201:enzymology*; D010740:Phospholipases / Q000037:antagonists & inhibitors*; D010741:Phospholipases A / Q000037:antagonists & inhibitors* / Q000378:metabolism; D011796:Quinacrine / Q000494:pharmacology; D051381:Rats; D011919:Rats, Inbred Strains; D012519:Sarcoplasmic Reticulum / Q000201:enzymology; D014700:Verapamil / Q000494:pharmacology
D014700:Verapamil; D010740:Phospholipases; D010741:Phospholipases A; D011796:Quinacrine; D002746:Chlorpromazine