缺血-再灌注損傷

1、患者：男，58歲，上午8時(shí)，起床后感到胸悶，30min后突感 心胸前區(qū)劇烈絞痛，9時(shí)入急診病房。體查：血壓75/50mmHg，意識淡漠，心率65次/min，律齊。 心電圖示度房室傳導(dǎo)阻滯。冠狀動脈造影：右冠狀動脈上段85%狹窄，中段78%狹窄。入院治療：立即給予阿托品、多巴胺、低分子右旋糖酐等進(jìn) 行擴(kuò)冠治療。上午10時(shí)靜脈點(diǎn)滴尿激酶。10.30分患者 出現(xiàn)陣發(fā)性心室顫動（室顫），立即給予除顫，到下 午13時(shí)反復(fù)發(fā)生室性心動過速、室顫，共計(jì)6次。到下 午16時(shí)，經(jīng)給予利多卡因、小劑量異丙腎上腺素后心 律轉(zhuǎn)為竇性，血壓平穩(wěn)，意識清楚。 Usually blood reperfusion shoul

2、d reduce the ischemia injury. However, recent clinical observations and animal ex- periments showed that blood reperfusion sometimes indu- ces or aggravates the further reversible even irreversible cell damage, especially for a prolonged ischemia. 內(nèi)皮素的作用 高能磷酸化合物缺乏 The increase free radicals, calcium

3、 overload, neutrophils activation, play the principal roles in ischemia-reperfusion injury.O2 （O Ca2+超載MPO：過氧化物酶 ：磷脂酶A 、LT：白三烯 The ischemia region could not be reperfused sufficiently after relieving the occlusion to recover the blood flow.O2 炎癥介質(zhì)炎癥介質(zhì)The energy metabolism mainly focus on the generat

4、ion and utilization of ATP in myocardium. In normally the ischemic injury should relieve after reperfusion recover. It is revealed that the high-energy phosphates stored in heart do not increase followed by reperfusion, instead of deplete further. That means the generation of ATP is lower because the mitochondria damaged by oxygen free radicals and calcium overload. O2O2 eO2 OH + H2O 3e3H+2eO2 H2O2 2H+4eO2 2H2O4H+2 Reactive oxygen species (ROS) are composed by oxygen-derived free radicals (OFR) and non free radical substances, such as superoxide anion radical ( ), hydroxyl ra