全身性血小板活化因子（PAF）对兔脊髓微循环的影响。

Effect of systemic platelet-activating factor (PAF) on the rabbit spinal cord microcirculation.

作者信息

Lindsberg P J, Jacobs T P, Paakkari I A, Hallenbeck J M, Feuerstein G

机构信息

Department of Neurology, F. Edward Hebért School of Medicine, Uniformed Services University of the Health Sciences, Bethesda, MD 20814-4799.

出版信息

J Lipid Mediat. 1990 Jan-Feb;2(1):41-58.

PMID:2133267

Abstract

Platelet-activating factor (PAF) is an endogenous phospholipid mediator with pro-inflammatory and vasoactive properties. Since PAF has been implicated in ischemic neuroinjury, we determined its effects on rabbit spinal cord microcirculation (SCM). Using laser-Doppler flow measurements, we monitored mean arterial pressure and SCM continuously on-line during and after i.v. infusion (1 min) of 0.5 nmol/kg of PAF (n = 20) and measured thromboxane B2 (TXB2) and 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha) in arterial blood 1.5 min after the infusion. Responses were compared to those after indometacin pretreatment (4 mg/kg, n = 11). During the infusion, spinal cord blood flow (SCBF) decreased by 14 +/- 5% (P less than 0.05) paralleling the systemic hypotensive changes (17 +/- 5%, P less than 0.01) with no changes in vascular resistance (SCVR). However, immediately after termination of PAF infusion, SCVR decreased by 17 +/- 5% (P less than 0.01) while SCBF rapidly recovered. Plasma levels of both TXB2 and 6-keto-PGF1 alpha were significantly elevated. TXB2 release was correlated with the degree of hypotension during the PAF infusion (r greater than 0.72; P less than 0.05) while 6-keto-PGF1 alpha release correlated well with the decrease in SCVR during the infusion period (r greater than 0.64; P less than 0.05). Indomethacin blocked both the hemodynamic events and the eicosanoid release induced by PAF. Our data suggest that PAF modulates SCM through eicosanoid-mediated mechanism.

摘要

血小板活化因子（PAF）是一种具有促炎和血管活性特性的内源性磷脂介质。由于PAF与缺血性神经损伤有关，我们研究了其对兔脊髓微循环（SCM）的影响。通过激光多普勒血流测量，我们在静脉输注（1分钟）0.5 nmol/kg的PAF（n = 20）期间及之后连续在线监测平均动脉压和SCM，并在输注后1.5分钟测量动脉血中的血栓素B2（TXB2）和6-酮-前列腺素F1α（6-酮-PGF1α）。将这些反应与吲哚美辛预处理后（4 mg/kg，n = 11）的反应进行比较。在输注期间，脊髓血流量（SCBF）下降了14±5%（P<0.05），与全身低血压变化（17±5%，P<0.01）平行，而血管阻力（SCVR）无变化。然而，PAF输注终止后立即，SCVR下降了17±5%（P<0.01），而SCBF迅速恢复。TXB2和6-酮-PGF1α的血浆水平均显著升高。TXB2的释放与PAF输注期间的低血压程度相关（r>0.72；P<0.05），而6-酮-PGF1α的释放在输注期间与SCVR的下降密切相关（r>0.64；P<0.05）。吲哚美辛阻断了PAF诱导的血流动力学事件和类花生酸释放。我们的数据表明，PAF通过类花生酸介导的机制调节SCM。