Abstract
Lactoferrin is recently under intense investigation because of its proposed several pharmacologically positive effects. Based on its iron-binding properties and its physiological presence in the human body, it may have a significant impact on pathological conditions associated with iron-catalysed reactive oxygen species (ROS). Its effect on a catecholamine model of myocardial injury, which shares several pathophysiological features with acute myocardial infarction (AMI) in humans, was examined. Male Wistar rats were randomly divided into four groups according to the received medication: control (saline), isoprenaline (ISO, 100 mg kg(-1) s.c.), bovine lactoferrin (La, 50 mg kg(-1) i.v.) or a combination of La + ISO in the above-mentioned doses. After 24 h, haemodynamic functional parameters were measured, a sample of blood was withdrawn and the heart was removed for analysis of various parameters. Lactoferrin premedication reduced some impairment caused by ISO (e.g. a stroke volume decrease, an increase in peripheral resistance and calcium overload). These positive effects were likely to have been mediated by the positive inotropic effect of lactoferrin and by inhibition of ROS formation due to chelation of free iron. The failure of lactoferrin to provide higher protection seems to be associated with the complexity of catecholamine cardiotoxicity and with its hydrophilic character.
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