Acetyl glyceryl ether phosphorylcholine (AGEPC). A putative mediator of cardiac anaphylaxis in the guinea pig.
Acetyl glyceryl ether phosphorylcholine (AGEPC). A putative mediator of cardiac anaphylaxis in the guinea pig.
复制标题
乙酰甘油醚磷酰胆碱（AGEPC）。
DOI：
10.1161/01.res.54.2.117
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发表时间：
1984
影响因子：
20.1
通讯作者：
Pinckard,RN
中科院分区：
文献类型：
--
作者：
Levi,R;Burke,JA;Guo,ZG;Hattori,Y;Hoppens,CM;McManus,LM;Hanahan,DJ;Pinckard,RN
血小板活化因子是一种新型的磷脂，被认为是急性过敏反应的重要介质。静脉注射乙酰甘油醚磷酸胆碱（一种纯的合成血小板活化因子）可引起家兔心电图变化，与全身过敏反应的特征性表现相似。为了确定血小板活化因子是否有助于过敏性心功能不全，我们测量了血小板活化因子释放从致敏豚鼠心脏在体外挑战特异性抗原，并比较所产生的心功能不全与乙酰甘油醚磷酸胆碱注射到非致敏心脏。这些研究的结果证明，在离体豚鼠心脏的速发过敏反应期间，血小板活化因子释放到冠状动脉流出物中，其具有与乙酰甘油醚磷酸胆碱相似的理化和功能特性。心内给予乙酰甘油醚磷酸胆碱（10（-14）至3 × 10（-9）mol）可诱导剂量相关的左心室收缩力（-5至85%）和冠状动脉流量（-5至85%）降低，以及房室传导受损。乙酰甘油醚磷酸胆碱的负性肌力作用也存在于心脏灌流在恒定流量。尽管在这些心脏中，乙酰甘油醚磷酸胆碱增加了冠状动脉阻力，这可能导致局部分流和缺血，但乙酰甘油醚磷酸胆碱的负性肌力作用不太可能继发于冠状动脉流量的变化，因为乙酰甘油醚磷酸胆碱也在电起搏中引起剂量依赖性负性肌力作用，非冠状动脉灌注的左心房和右心室乳头肌。（250字处删节）
Platelet-activating factor is a novel phospholipid that has been implicated as an important mediator of acute allergic reactions. The intravenous administration of acetyl glyceryl ether phosphorylcholine, a pure, synthetic platelet-activating factor, causes electrocardiographic changes in the rabbit similar to those which are characteristic manifestations of systemic anaphylaxis. To determine whether platelet-activating factor contributes to anaphylactic cardiac dysfunction, we measured platelet-activating factor release from the sensitized guinea pig heart challenged in vitro with specific antigen and compared the resulting cardiac dysfunction with that induced by the injection of acetyl glyceryl ether phosphorylcholine into nonsensitized hearts. The results of these studies document that, during anaphylaxis in the isolated guinea pig heart, a platelet-activating factor is released into the coronary effluent that has physicochemical and functional properties similar to those of acetyl glyceryl ether phosphorylcholine. The intracardiac administration of acetyl glyceryl ether phosphorylcholine (10(-14) to 3 X 10(-9) mol) induced dose-related decreases in left ventricular contractile force (-5 to -85%) and coronary flow (-5 to -85%), as well as impaired atrioventricular conduction. The negative inotropic effect of acetyl glyceryl ether phosphorylcholine also was present in hearts perfused at constant flow. Although, in these hearts, acetyl glyceryl ether phosphorylcholine increased coronary resistance, which may have caused regional shunting and ischemia, it is unlikely that the negative inotropic effect of acetyl glyceryl ether phosphorylcholine was secondary to changes in coronary flow, since acetyl glyceryl ether phosphorylcholine also caused a dose-dependent negative inotropic effect in the electrically paced, noncoronary-perfused left atrium and right ventricular papillary muscle.(ABSTRACT TRUNCATED AT 250 WORDS)