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可逆性心肌缺血期间血小板激活因子释放缺乏。

Lack of platelet-activating factor release during reversible myocardial ischaemia.

作者信息

Montalescot G, Maclouf J, Drobinski G, Mencia-Huerta J M, Ankri A, Grosgogeat Y, Thomas D

机构信息

Department of Cardiology, Hôpital Pitie-Salpétrière, Paris, France.

出版信息

Eur Heart J. 1992 Dec;13(12):1641-4. doi: 10.1093/oxfordjournals.eurheartj.a060118.

Abstract

Platelet-activating factor (PAF) is involved in experimental models of myocardial ischaemia, and PAF infusion can cause thromboxane release. Thromboxane is produced during brief episodes of reversible myocardial ischaemia in patients with coronary heart disease. To learn whether PAF synthesis is associated with thromboxane production in mild myocardial ischaemia, we performed rapid atrial pacing in four patients with angina pectoris which caused chest pain, ST segment depression (delta ST = -1.8 +/- 0.2 mm) and lactate excretion in the coronary sinus (percent lactate extraction decreased from 20 +/- 6% to -15 +/- 9%). Thromboxane B2 was produced causing a positive transmyocardial gradient (from 88 +/- 154 pg.ml-1 baseline to 1770 +/- 1407 pg.ml-1 at the peak) but there was no PAF release into coronary sinus blood. In four other patients we determined whether more pronounced ischaemia could be associated with PAF synthesis. Coronary sinus blood was sampled before and during balloon occlusion of a major coronary artery: PAF was not detected in coronary sinus, whereas percent lactate extraction decreased from 24 +/- 6% to -63 +/- 22% (n = 4). We conclude that PAF plays a minor role in short episodes of reversible ischaemia and does not participate in thromboxane production.

摘要

血小板活化因子(PAF)参与心肌缺血的实验模型,输注PAF可导致血栓素释放。血栓素在冠心病患者短暂的可逆性心肌缺血发作期间产生。为了解在轻度心肌缺血中PAF合成是否与血栓素产生有关,我们对4例心绞痛患者进行了快速心房起搏,这导致了胸痛、ST段压低(δST = -1.8±0.2 mm)以及冠状窦乳酸排泄(乳酸摄取百分比从20±6%降至-15±9%)。血栓素B2产生,导致跨心肌梯度为正(从基线时的88±154 pg.ml-1升至峰值时的1770±1407 pg.ml-1),但没有PAF释放到冠状窦血液中。在另外4例患者中,我们确定更明显的缺血是否可能与PAF合成有关。在主要冠状动脉球囊闭塞前和闭塞期间采集冠状窦血样:冠状窦中未检测到PAF,而乳酸摄取百分比从24±6%降至-63±22%(n = 4)。我们得出结论,PAF在短暂的可逆性缺血发作中起次要作用,且不参与血栓素的产生。

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