Kerner T, Ahlers O, Reschreiter H, Bührer C, Möckel M, Gerlach H
Department of Anesthesiology and Intensive Care Medicine, Charité Medical Center, Virchow Hospital, Humboldt-University, Berlin, Germany.
Crit Care. 2001;5(3):145-50. doi: 10.1186/cc1014. Epub 2001 Apr 6.
Tissue damage after ischemia and reperfusion involves leukocyte endothelial interactions mediated by cell adhesion molecules. This study was designed to determine the time course of soluble adhesion molecules in patients with acute myocardial infarction after attempted reperfusion by thrombolysis with tissue plasminogen activator (tPA) or streptokinase (SK), or percutaneous transluminal coronary angioplasty (PTCA).
In 3 x 10 randomly selected patients with acute myocardial infarction undergoing thrombolysis with tPA or SK, or treated with PTCA, plasma concentrations of soluble L-selectin, P-selectin, E-selectin, intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1) and platelet endothelial cell adhesion molecule-1 (PECAM-1) were measured by enzyme-linked immunosorbent assay, 30 min and 1, 2, 4, 8, 12 and 24 hours after intervention.
After thrombolysis with tPA, soluble L-selectin concentrations were persistently depressed and soluble PECAM-1 concentrations were elevated, compared with controls, SK and PTCA. While soluble VCAM-1 concentrations did not differ within the first hours after interventions between the three groups, soluble VCAM-1 rose by 24 hours after tPA thrombolysis but did not increase after SK and PTCA treatment. Soluble ICAM-1 concentrations were consistently elevated after PTCA compared with controls and thrombolysed patients. Soluble E-selectin was depressed after tPA thrombolysis and PTCA in comparison with controls, while the SK group showed an increase throughout the observation period. Soluble P-selectin was increased after PTCA and SK lysis up to 8 hours after treatment compared with controls, but no significant differences could be found between treatment groups.
Adhesion molecules mediating leukocyte endothelial interactions are altered subsequent to postischemic reperfusion and by treatment with thrombolytic agents and angioplasty. The clinical relevance of these biological changes remains to be determined.
缺血再灌注后的组织损伤涉及由细胞粘附分子介导的白细胞与内皮细胞的相互作用。本研究旨在确定急性心肌梗死患者在尝试通过组织型纤溶酶原激活剂（tPA）或链激酶（SK）溶栓或经皮腔内冠状动脉成形术（PTCA）进行再灌注后可溶性粘附分子的时间进程。
在3×10例随机选择的接受tPA或SK溶栓或PTCA治疗的急性心肌梗死患者中，通过酶联免疫吸附测定法在干预后30分钟以及1、2、4、8、12和24小时测量血浆中可溶性L-选择素、P-选择素、E-选择素、细胞间粘附分子-1（ICAM-1）、血管细胞粘附分子-1（VCAM-1）和血小板内皮细胞粘附分子-1（PECAM-1）的浓度。
与对照组、SK组和PTCA组相比，tPA溶栓后可溶性L-选择素浓度持续降低，可溶性PECAM-1浓度升高。虽然三组在干预后的最初几小时内可溶性VCAM-1浓度无差异，但tPA溶栓后24小时可溶性VCAM-1升高，而SK和PTCA治疗后未升高。与对照组和溶栓患者相比，PTCA后可溶性ICAM-1浓度持续升高。与对照组相比，tPA溶栓和PTCA后可溶性E-选择素降低，而SK组在整个观察期内升高。与对照组相比，PTCA和SK溶栓后治疗后8小时内可溶性P-选择素升高，但各治疗组之间未发现显著差异。
介导白细胞与内皮细胞相互作用的粘附分子在缺血后再灌注以及溶栓剂和血管成形术治疗后会发生改变。这些生物学变化的临床相关性仍有待确定。
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