Montalescot G, Huerta J M, Braquet P, Zapol W M
Department of Anesthesia, Massachusetts General Hospital, Boston 02114.
J Appl Physiol (1985). 1992 Dec;73(6):2604-7. doi: 10.1152/jappl.1992.73.6.2604.
Platelet-activating factor (PAF) infusion into sheep, as well as protamine reversal of heparin anticoagulation, causes thromboxane release into plasma, pulmonary hypertension, hypoxemia, and leukopenia. We investigated the possible role of PAF in the heparin-protamine reaction. Intravenous protamine was administered to neutralize heparin anticoagulation in five awake sheep and caused an increase of mean pulmonary arterial pressure from 16.6 +/- 1 (SE) mmHg at base-line to 47 +/- 9 mmHg at 1 min after protamine injection (P < 0.01) because of a 4.5-fold increase of pulmonary vascular resistance. This neutralization reaction induced a 25% reduction of circulating leukocyte count and arterial PO2. Undetectable blood levels of PAF were measured by bioassay and high-performance liquid chromatography during these heparin-protamine reactions. Infusion of BN 52021 (20 mg/kg), a PAF receptor antagonist, before rechallenging the same sheep with heparin and then protamine did not reduce the level of peak pulmonary hypertension or the degree of hypoxemia and leukopenia. We conclude that the leukopenia and thromboxane-mediated pulmonary vasoconstriction occurring after rapid intravascular formation of heparin-protamine complexes in sheep are not due to the release of PAF.
给绵羊输注血小板活化因子（PAF）以及用鱼精蛋白逆转肝素抗凝作用，会导致血栓素释放到血浆中，引起肺动脉高压、低氧血症和白细胞减少。我们研究了PAF在肝素-鱼精蛋白反应中可能起的作用。对5只清醒的绵羊静脉注射鱼精蛋白以中和肝素抗凝作用，注射后1分钟平均肺动脉压从基线时的16.6±1（标准误）mmHg升高至47±9 mmHg（P<0.01），这是由于肺血管阻力增加了4.5倍。这种中和反应导致循环白细胞计数和动脉血氧分压降低了25%。在这些肝素-鱼精蛋白反应过程中，通过生物测定和高效液相色谱法检测到血液中PAF水平无法测出。在用肝素然后鱼精蛋白再次刺激同一只绵羊之前，输注PAF受体拮抗剂BN 52021（20 mg/kg），并未降低肺动脉高压峰值水平或低氧血症和白细胞减少的程度。我们得出结论，绵羊体内肝素-鱼精蛋白复合物在血管内快速形成后发生的白细胞减少和血栓素介导的肺血管收缩并非由PAF释放所致。
