Montalescot G
Service de cardiologie, hôpital de la Salpétrière, Paris, France.
Arch Mal Coeur Vaiss. 1990 Apr;83(4):555-60.
The neutralisation of heparin by protamine can cause life-threatening pulmonary hypertension. We studied this reaction in animal experimental models (sheep and rat) to determine the cellular mechanisms of the pulmonary vasoconstriction. The heparin-protamine reaction (H-P) with pulmonary hypertension (peak of mean pulmonary artery pressure = 57.3 +/- 2.2 mmHg), decreased cardiac output (-20%), leukopenia (-30%) and plasma release of high concentrations of thromboxane B2 (6.03 +/- 0.03 ng/ml) was constantly observed in sheep. The reaction was identical in sheep with induced thrombocytopenia by administration of antiplatelet antibodies. On the other hand, the neutralisation of heparin by protamine in rats did not cause thromboxane release or pulmonary vasoconstriction although the leukopenia was identical to that observed in sheep. Therefore, the platelets and white blood cells did not seem to cause the pulmonary vasoconstriction induced by the H-P complexes. The inter-species difference observed suggests that pulmonary intravascular macrophages may be responsible for the liberation of eicosanoids and acute pulmonary vasoconstriction occurring during the neutralisation of heparin by protamine.
鱼精蛋白中和肝素可导致危及生命的肺动脉高压。我们在动物实验模型（绵羊和大鼠）中研究了这种反应，以确定肺血管收缩的细胞机制。在绵羊中持续观察到肝素-鱼精蛋白反应（H-P）伴有肺动脉高压（平均肺动脉压峰值 = 57.3 ± 2.2 mmHg）、心输出量降低（-20%）、白细胞减少（-30%）以及血浆中高浓度血栓素B2释放（6.03 ± 0.03 ng/ml）。在通过给予抗血小板抗体诱导血小板减少的绵羊中，该反应相同。另一方面，尽管大鼠中白细胞减少情况与绵羊中观察到的相同，但鱼精蛋白中和肝素并未导致血栓素释放或肺血管收缩。因此，血小板和白细胞似乎并未引起H-P复合物诱导的肺血管收缩。观察到的种间差异表明，肺血管内巨噬细胞可能是鱼精蛋白中和肝素过程中类花生酸释放和急性肺血管收缩的原因。
