Abstract
In myocardial ischemia the contractile function of the heart is quickly disturbed. This is due to several factors, including injury to membranes of the sarcoplasmic reticulum (SR) [13]. Among the basic mechanisms of membrane damage an essential role is ascribed to activation of lipid peroxidation (LPO) and of phospholipolysis. Experiments in vitro have shown that phospholipase A2 [I0] and the xanthine--xanthine oxidase oxygen radical generation system [12] inhibit Calcium uptake by SR. Some investigators consider that the dominant role in damage to the Ca++-transport function of SR in ischemia is played by activation of LPO [4]. Activation of LPO in the liver microsomes during ischemia was observed much earlier than accumulation of lysophospholipids [2]. The determinant role of phospholipases in ischemic damage to the liver mitochondria [3] and an increase in the content of lysophospholipids even in the initial period of cardiac ischemia [8] have been demonstrated.
Published Version
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