Effect of platelet depletion on lung vasoconstriction in heparin-protamine reactions.
Effect of platelet depletion on lung vasoconstriction in heparin-protamine reactions.
复制标题
肝素-鱼精蛋白反应中血小板耗竭对肺血管收缩的影响。
DOI：
10.1152/jappl.1989.66.5.2344
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发表时间：
1989
期刊：
影响因子：
--
通讯作者：
Zapol,WM
中科院分区：
文献类型：
--
作者：
Montalescot,G;Kreil,E;Lynch,K;Greene,EM;Torres,A;Carvalho,A;Fitzgibbon,C;Robinson,DR;Lowenstein,E;Zapol,WM
在6只清醒绵羊中，对照肝素-鱼精蛋白反应与动脉血浆血栓素B2（TxB 2）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PO 2减少30%和动脉白色血细胞浓度减少30%相关。通过抗体消耗99%的循环血小板并不能预防由肝素-鱼精蛋白给药诱导的急性和重度肺动脉高压或血浆TxB 2水平升高。我们在体外用牛凝血酶诱导绵羊血小板聚集，并测量了明显的TxB 2释放（36.3 +/- 16.3 ng/10（9）血小板）。相比之下，无论是肝素，鱼精蛋白，也没有肝素鱼精蛋白复合物超过10,000倍的浓度范围诱导血小板聚集和释放血栓素在体外。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，其他细胞必须产生血栓素。
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.