Effects of acetyl glyceryl ether of phosphorylcholine (platelet activating factor) on ventricular preload, afterload, and contractility in dogs.
Effects of acetyl glyceryl ether of phosphorylcholine (platelet activating factor) on ventricular preload, afterload, and contractility in dogs.
复制标题
磷酸胆碱乙酰甘油醚（血小板激活因子）对狗心室前负荷、后负荷和收缩力的影响。
DOI：
10.1172/jci111528
复制
发表时间：
1984
期刊：
影响因子：
--
通讯作者：
Lange,LG
中科院分区：
文献类型：
--
作者：
Kenzora,JL;Pérez,JE;Bergmann,SR;Lange,LG
磷酸胆碱的乙酰甘油醚（AGEPC），血小板活化因子，是一种强效的膨胀剂，可介导过敏反应期间的血压变化，并可能参与肾源性血压变化。本研究旨在描述这种最近发现的磷脂引起低血压的血流动力学机制。静脉给药AGEPC麻醉开胸犬（n = 5）产生的血液动力学改变，为了分析的目的，分为三个阶段的基础上的平均全身血压的变化。在第I阶段（5-30 s），平均全身血压降低至基线值以下5 - 10%的水平，与心输出量增加和全身血管阻力降低相关。II期（30-90 s）包括全身血压大幅降低至最低点，基线值的50%，同时心输出量降低相似幅度，全身血管阻力升高。第三阶段（90 s-60 min）显示平均全身血压逐渐恢复正常，全身血管阻力增加数倍，心输出量持续较低。在循环右侧，AGEPC的主要作用是I期肺动脉压明显一过性升高，与II期肺阻力升高相关。乙胺嗪几乎阻断了AGEPC引起的所有这些血流动力学变化; FPL 55712基本上阻断了III期全身血管阻力的升高。这些结果表明，白三烯可能介导的AGEPC诱导的至少一些血液动力学效应，但需要进一步的研究时，更具体的白三烯阻断剂变得可用。如在III期期间使用收缩末期压力-尺寸关系评估的，心肌性能本身降低。AGGPC诱导的负性变力作用的发生在离体克雷布斯灌注豚鼠心脏和离体血液灌注兔心脏中得到进一步证实。结果表明，AGEPC控制性降压的机制是复杂的，影响血管张力和心肌的正性肌力状态。
Acetyl glyceryl ether of phosphorylcholine (AGEPC), platelet activating factor, is a potent hypotensive agent that may mediate changes in blood pressure during anaphylaxis and may be involved in blood pressure variations of renal origin. This study was designed to characterize the hemodynamic mechanisms responsible for hypotension induced by this recently identified phospholipid. Intravenous administration of AGEPC to anesthetized open-chest dogs (n = 5) produced hemodynamic alterations which, for the purpose of analysis, were divided into three phases based on changes in the mean systemic blood pressure. During phase I (5-30 s) mean systemic blood pressure decreased to levels 5 to 10% below baseline values in association with a rise in cardiac output and a decrease in systemic vascular resistance. Phase II (30-90 s) consisted of a substantial reduction in systemic blood pressure to its nadir, 50% of baseline values, together with a decrease of similar magnitude in cardiac output and a rise in systemic vascular resistance. Phase III (90 s-60 min) exhibited a gradual recovery of mean systemic blood pressure toward normal with a several-fold rise in systemic vascular resistance and a continued low cardiac output. On the right side of the circulation, the predominant effect of AGEPC was a marked transient increase in pulmonary artery pressure in phase I, associated with an elevation of pulmonary resistance during phase II. Diethylcarbamazine blocked virtually all of these hemodynamic changes induced by AGEPC; FPL 55712 substantially blocked the rise in systemic vascular resistance in phase III. These results suggest that leukotrienes may mediate at least some of the hemodynamic effects induced by AGEPC, but further studies will be required when more specific leukotriene blocking agents become available. As assessed during phase III with the end-systolic pressure-dimension relation, myocardial performance itself was diminished. The occurrence of an AGEPC-induced negative inotropic effect was further confirmed in isolated Krebs-perfused guinea pig hearts and isolated blood-perfused rabbit hearts. The results indicate that the mechanism of AGEPC-induced hypotension is complex, affecting both vascular tone and the inotropic state of the myocardium.Images