Montalescot G, Kreil E, Lynch K, Greene E M, Torres A, Carvalho A, Fitzgibbon C, Robinson D R, Lowenstein E, Zapol W M
Department of Anesthesia, Massachusetts General Hospital, Boston 02114.
J Appl Physiol (1985). 1989 May;66(5):2344-50. doi: 10.1152/jappl.1989.66.5.2344.
In six awake sheep the control heparin-protamine reaction was associated with a 150-fold rise in arterial plasma thromboxane B2 (TxB2) levels, a 4.5-fold increase in pulmonary vascular resistance, a 20% decrease in cardiac output, a 30% decrease in arterial PO2, and a 30% reduction in arterial white blood cell concentrations. Depletion of 99% of circulating platelets by antibodies did not prevent either acute and severe pulmonary hypertension or increased plasma TxB2 levels induced by heparin-protamine administration. We produced sheep platelet aggregation in vitro with bovine thrombin and measured marked TxB2 release (36.3 +/- 16.3 ng/10(9) platelets). In contrast, neither heparin, protamine, nor heparin-protamine complexes over a 10,000-fold range of concentrations induced platelet aggregation and release of thromboxane in vitro. Therefore sheep platelets are not the source of thromboxane production associated with acute pulmonary hypertension during the heparin-protamine reaction, and other cells must produce the thromboxane.
在六只清醒的绵羊中，对照性肝素-鱼精蛋白反应与动脉血浆血栓素B2（TxB2）水平升高150倍、肺血管阻力增加4.5倍、心输出量减少20%、动脉血氧分压降低30%以及动脉白细胞浓度降低30%相关。用抗体使99%的循环血小板耗竭并不能预防肝素-鱼精蛋白给药所诱导的急性重度肺动脉高压或血浆TxB2水平升高。我们在体外使用牛凝血酶诱导绵羊血小板聚集，并检测到显著的TxB2释放（36.3±16.3 ng/10⁹血小板）。相比之下，在浓度范围超过10000倍的情况下，肝素、鱼精蛋白以及肝素-鱼精蛋白复合物在体外均未诱导血小板聚集和血栓素释放。因此，绵羊血小板不是肝素-鱼精蛋白反应期间与急性肺动脉高压相关的血栓素产生的来源，其他细胞必定产生了血栓素。
