title: Ischemic-reperfused isolated working mouse hearts: membrane damage and type IIA phospholipase A2.
abstract: 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 A2 (sPLA2) in this process, hearts from wild-type and sPLA2-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 sPLA2- deficient hearts. These findings argue against a prominent role of type IIA sPLA2 in the development of irreversible cell damage in the ischemic-reperfused murine myocardium.
authors.affiliation: Department of Physiology, Cardiovascular Research Institute Maastricht, Maastricht University, 6200 MD Maastricht, The Netherlands.
authors.forename: L J
authors.initials: LJ
authors.lastname: De Windt
authors.forename: J
authors.initials: J
authors.lastname: Willems
authors.forename: T H
authors.initials: TH
authors.lastname: Roemen
authors.forename: W A
authors.initials: WA
authors.lastname: Coumans
authors.forename: R S
authors.initials: RS
authors.lastname: Reneman
authors.forename: G J
authors.initials: GJ
authors.lastname: Van Der Vusse
authors.forename: M
authors.initials: M
authors.lastname: Van Bilsen
mesh_terms: D000227:Adenine Nucleotides / Q000378:metabolism; D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D002302:Cardiac Output; D002462:Cell Membrane / Q000378:metabolism*; D005227:Fatty Acids / Q000378:metabolism; D005260:Female; D054501:Group II Phospholipases A2; D006439:Hemodynamics; D066298:In Vitro Techniques; D019344:Lactic Acid / Q000378:metabolism; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D017202:Myocardial Ischemia / Q000378:metabolism* / Q000503:physiopathology; D015425:Myocardial Reperfusion / Q000379:methods; D015428:Myocardial Reperfusion Injury / Q000235:genetics / Q000378:metabolism* / Q000503:physiopathology; D010741:Phospholipases A / Q000172:deficiency / Q000235:genetics / Q000378:metabolism*; D054467:Phospholipases A2; D010743:Phospholipids / Q000378:metabolism; D020127:Recovery of Function; D013997:Time Factors; D014280:Triglycerides / Q000378:metabolism
chemical_list: D000227:Adenine Nucleotides; D005227:Fatty Acids; D010743:Phospholipids; D014280:Triglycerides; D019344:Lactic Acid; D000255:Adenosine Triphosphate; D010741:Phospholipases A; D054501:Group II Phospholipases A2; D054467:Phospholipases A2