Ischemic-reperfused isolated working mouse hearts: membrane damage and type IIA phospholipase A2

• Published in: American journal of physiology. Heart and circulatory physiology 2001-06, Vol.280 (6), p.H2572-H2580
• Main Authors: De Windt, Leon J, Willems, Jodil, Roemen, Theo H. M, Coumans, Will A, Reneman, Robert S, Van Der Vusse, Ger J, Van Bilsen, Marc
• Format: Article
• Language: English
• Subjects: Adenine Nucleotides - metabolism; Adenosine Triphosphate - metabolism; Animals; Cardiac Output; Cell Membrane - metabolism; Fatty Acids - metabolism; Female; Group II Phospholipases A2; Hemodynamics; In Vitro Techniques; Lactic Acid - metabolism; Male; Mice; Mice, Inbred C57BL; Myocardial Ischemia - metabolism; Myocardial Ischemia - physiopathology; Myocardial Reperfusion - methods; Myocardial Reperfusion Injury - genetics; Myocardial Reperfusion Injury - metabolism; Myocardial Reperfusion Injury - physiopathology; Phospholipases A - deficiency; Phospholipases A - genetics; Phospholipases A - metabolism; Phospholipases A2; Phospholipids - metabolism; Recovery of Function; Time Factors; Triglycerides - metabolism
• ISSN: 0363-6135; 1522-1539
• DOI: 10.1152/ajpheart.2001.280.6.h2572

Department of Physiology, Cardiovascular Research Institute Maastricht, Maastricht University, 6200 MD Maastricht, The Netherlands For the murine heart the relationships between ischemia-reperfusion-induced loss of cardiac function, enzyme release, high-energy phosphate (HEP), and membrane phospholipid metabolism are ill-defined. Accordingly, isolated ejecting murine hearts were subjected to varying periods of ischemia, whether or not followed by reperfusion. On reperfusion, hemodynamic function was almost completely restored after 10 min of ischemia [83 ± 14% recovery of cardiac output (CO)], but was severely depressed after 15 and 20 min of ischemia (40 ± 24 and 31 ± 24% recovery of CO, respectively). Reperfusion was associated with partial recovery of HEP stores and enhanced degradation of phospholipids as indicated by the accumulation of fatty acids (FA). Myocardial FA content and enzyme release during reperfusion were correlated ( r  = 0.70), suggesting that membrane phospholipid degradation and cellular damage are closely related phenomena. To investigate the role of type IIA secretory phospholipase A 2 (sPLA 2 ) in this process, hearts from wild-type and sPLA 2 -deficient mice were subjected to ischemia-reperfusion. Postischemic functional recovery, ATP depletion, enzyme release, and FA accumulation were not significantly different between wild-type and sPLA 2 - deficient hearts. These findings argue against a prominent role of type IIA sPLA 2 in the development of irreversible cell damage in the ischemic-reperfused murine myocardium. cardiac function; ischemic; reperfusion; fatty acids; phospholipids; adenine nucleotides;