In:
American Journal of Physiology-Heart and Circulatory Physiology, American Physiological Society, Vol. 280, No. 6 ( 2001-06-01), p. H2572-H2580
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 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.
Type of Medium:
Online Resource
ISSN:
0363-6135
,
1522-1539
DOI:
10.1152/ajpheart.2001.280.6.H2572
Language:
English
Publisher:
American Physiological Society
Publication Date:
2001
detail.hit.zdb_id:
1477308-9
SSG:
12
