The role of the lectin pathway of complement activation in cardiac ischemia-reperfusion injury

心脏病发作造成的伤害程度是预后和存活率的主要决定因素。被堵塞的动脉的大小以及在心脏病发作后再次开放的速度是确定损伤程度的重要因素。然而，现在很明显，另一种形式的伤害也发生了，矛盾的是，在血液供应恢复的时候。这就是所谓的缺血-再灌注损伤。这种类型的损伤的确切原因尚不清楚，尽管有证据表明，血液中一种称为补体系统的系统通过一种称为凝集素途径的途径激活起到了作用。我们开发了一种独特的模型来研究这一通路在缺血-再灌注损伤中的作用。这项拟议的研究将提供明确的信息，说明这一途径在导致缺血再灌注损伤中的重要性，以及抑制这一系统是否将是心脏病发作后保护心脏的有价值的方式。

The amount of injury caused by heart attacks is the main determinant of outcome and survival. The size of the artery that is blocked and how quickly it is opened again after the onset of the heart attack is an important factor in determining the amount of injury. However, it is now clear that another form of injury also occurs, paradoxically at the time when the blood supply is restored. This is called ischaemia-reperfusion injury. The precise cause of this type of injury is not known although there is evidence that activation of a system in the blood called the complement system by a pathway called the lectin pathway plays a role. We have developed a unique model to investigate the role of this pathway in ischaemia-reperfusion injury. The proposed studies will provide definitive information on the importance of this pathway in causing ischaemia-reperfusion injury and whether inhibiting this system would be valuable way of protecting the heart after heart attacks.