Viossat I, Chapelat M, Chabrier P E, Braquet P
I.H.B. Research Labs, Les Ulis, France.
Prostaglandins Leukot Essent Fatty Acids. 1989 Dec;38(3):189-94. doi: 10.1016/0952-3278(89)90071-9.
The cardiac effects of PAF and its antagonist BN 52021 have been investigated on the isolated perfused guinea-pig heart maintained at a constant hydrostatic perfusion pressure of 80 cm water. In this model, PAF (1 x 10(-11) to 1 x 10(-7) moles) induced a dose-dependent coronary vasoconstriction, a decrease in heart rate and a fall in contractile force. BN 52021 (1 x 10(-6) to 2 x 10(-4) M) dose-dependently inhibited the vasospasm induced by PAF (1 x 10(-10) moles). BN 52021 also antagonized the decrease in coronary flow and heart rate, but not that of contractile force induced by a high dose of PAF (1 x 10(-7) moles). This dose of PAF also significantly (p less than 0.001) provoked a marked release of TxB2 but did not alter the generation of 6 Keto PGF1 alpha, PGE2 or LTC4. The PAF-induced increase in TxB2 release was completely abolished by BN 52021.
在保持80厘米水柱恒定静水压灌注的离体豚鼠心脏上，研究了血小板活化因子（PAF）及其拮抗剂BN 52021的心脏效应。在该模型中，PAF（1×10⁻¹¹至1×10⁻⁷摩尔）引起剂量依赖性冠状动脉收缩、心率降低和收缩力下降。BN 52021（1×10⁻⁶至2×10⁻⁴摩尔）剂量依赖性地抑制PAF（1×10⁻¹⁰摩尔）诱导的血管痉挛。BN 52021还拮抗冠状动脉血流量和心率的降低，但不拮抗高剂量PAF（1×10⁻⁷摩尔）诱导的收缩力降低。该剂量的PAF还显著（p＜0.001）引起血栓素B2（TxB2）的大量释放，但不改变6-酮-前列腺素F1α、前列腺素E2或白三烯C4（LTC4）的生成。BN 52021完全消除了PAF诱导的TxB2释放增加。
