Rinder C S, Gaal D, Student L A, Smith B R
Department of Anesthesiology, Yale University School of Medicine, New Haven, Conn. 06510.
J Thorac Cardiovasc Surg. 1994 Jan;107(1):280-8.
Cardiopulmonary bypass has been shown in adults to activate platelets and leukocytes, lead to the formation of circulating platelet-leukocyte conjugates, and alter adhesive receptors on both cell types. Pediatric patients with congenital heart disease undergoing cardiopulmonary bypass, however, have not been extensively studied and may represent a group at particular clinical risk for bleeding and pulmonary dysfunction. We studied 13 patients with congenital heart disease undergoing operations necessitating bypass, 7 with cyanotic and 6 with noncyanotic congenital heart disease. We determined that (1) the surface density of platelet glycoprotein Ib was significantly lower at baseline and throughout bypass in patients with cyanotic heart disease than in noncyanotic patients; (2) platelet glycoprotein Ib in both cyanotic and noncyanotic congenital heart disease decreased significantly during bypass, with a nadir of 75% of baseline values; (3) platelets were activated to a high degree, comparable with that seen in adults; (4) mean circulating monocyte-platelet conjugates rose significantly during bypass, increasing from 36% to 66% by the end of bypass, whereas neutrophil-platelet conjugates and lymphocyte-platelet conjugates declined; and (5) both monocytes and neutrophils were activated by cardiopulmonary bypass, as assessed by increased surface expression of CD11b and, in the case of monocytes, CD11b expression continued to increase even after termination of bypass. Patients with cyanotic and noncyanotic heart disease did not differ with respect to platelet or leukocyte activation or the formation of platelet-leukocyte conjugates. We conclude that in children with congenital heart disease cardiopulmonary bypass causes loss of platelet adhesion receptors, activation of platelets, formation of platelet-leukocyte conjugates, and leukocyte activation. Cyanotic and noncyanotic patients are qualitatively similarly affected; however, cyanotic patients demonstrate a baseline deficit in the platelet adhesion receptor glycoprotein Ib. These cellular changes may contribute to both the hemostatic and inflammatory complications associated with cardiopulmonary bypass.
体外循环已被证明在成人中会激活血小板和白细胞，导致循环中的血小板 - 白细胞结合物形成，并改变两种细胞类型上的黏附受体。然而，接受体外循环的先天性心脏病儿科患者尚未得到广泛研究，他们可能是出血和肺功能障碍临床风险特别高的群体。我们研究了13例因手术需要进行体外循环的先天性心脏病患者，其中7例为青紫型先天性心脏病，6例为非青紫型先天性心脏病。我们确定：（1）青紫型心脏病患者在基线时以及整个体外循环过程中，血小板糖蛋白Ib的表面密度显著低于非青紫型患者；（2）青紫型和非青紫型先天性心脏病患者的血小板糖蛋白Ib在体外循环期间均显著降低，最低点为基线值的75%；（3）血小板被高度激活，与成人中观察到的情况相当；（4）平均循环单核细胞 - 血小板结合物在体外循环期间显著增加，到体外循环结束时从36%增加到66%，而中性粒细胞 - 血小板结合物和淋巴细胞 - 血小板结合物减少；（5）通过CD11b表面表达增加评估，体外循环激活了单核细胞和中性粒细胞，对于单核细胞而言，即使在体外循环结束后CD11b表达仍持续增加。青紫型和非青紫型心脏病患者在血小板或白细胞激活以及血小板 - 白细胞结合物形成方面没有差异。我们得出结论，在先天性心脏病儿童中，体外循环会导致血小板黏附受体丧失、血小板激活、血小板 - 白细胞结合物形成以及白细胞激活。青紫型和非青紫型患者在性质上受到类似影响；然而，青紫型患者在血小板黏附受体糖蛋白Ib方面表现出基线缺陷。这些细胞变化可能导致与体外循环相关的止血和炎症并发症。
