Winnerkvist A, Wiman B, Valen G, Vaage J
Department of Thoracic Surgery, Karolinska Hospital, Stockholm, Sweden.
Thromb Res. 1996 Jun 15;82(6):533-42. doi: 10.1016/0049-3848(96)00103-x.
Tissue plasminogen activator (t-PA) is a potential marker of endothelial cell activation or injury. The relationship between duration of ischaemia and release of t-PA during reperfusion was investigated in isolated rat hearts exposed to either 5, 10, 20, 30, 40, or 60 min of global, normothermic ischaemia followed by 30 min of reperfusion (n = 8 in each group). t-PA activity was measured (chromogenic peptide substrate assay) in the effluent before ischaemia, and after 2.5, 5, 7.5, 10, 20, and 30 min of reperfusion. Release of lactate dehydrogenase (LD), a marker of myocyte injury, was measured before ischaemia and after 5 min reperfusion. Left ventricular pressures were measured by a balloon in the left ventricle. Ischaemia for 20 min or less had only minor effects on cardiac function. Thirty min or more of ischaemia induced ventricular fibrillation during reperfusion in most hearts. After ischaemia t-PA outflow increased, but without any significant difference between groups. Peak release occurred after either 2.5 or 5 min of reperfusion. After 10 min reperfusion the release was not different from the basal value. In contrast, postischaemic release of LD correlated to the length of ischaemia. To conclude, t-PA release from the ischaemic-reperfused rat heart is independent of the length of ischaemia. Thus the potential of t-PA to quantify endothelial injury appears to be limited.
组织型纤溶酶原激活剂(t-PA)是内皮细胞激活或损伤的一个潜在标志物。在暴露于5、10、20、30、40或60分钟全心、常温缺血然后再灌注30分钟的离体大鼠心脏中(每组n = 8),研究了缺血持续时间与再灌注期间t-PA释放之间的关系。在缺血前以及再灌注2.5、5、7.5、10、20和30分钟后,测量流出液中的t-PA活性(发色肽底物测定法)。在缺血前和再灌注5分钟后,测量乳酸脱氢酶(LD)的释放,LD是心肌细胞损伤的一个标志物。通过左心室内的球囊测量左心室压力。缺血20分钟或更短时间对心脏功能仅有轻微影响。30分钟或更长时间的缺血在大多数心脏的再灌注期间诱发心室颤动。缺血后t-PA流出增加,但各组之间无任何显著差异。在再灌注2.5或5分钟后出现峰值释放。再灌注10分钟后,释放与基础值无差异。相比之下,缺血后LD的释放与缺血时间长度相关。总之,缺血再灌注大鼠心脏中t-PA的释放与缺血时间长度无关。因此,t-PA量化内皮损伤的潜力似乎有限。