Kupinski A M, Feustel P J, Shah D M, Karmody A M, Leather R P
Department of Surgery, Albany Medical College, NY 12208.
J Vasc Surg. 1988 Apr;7(4):549-53.
We hypothesized that chronic ischemia of peripheral vascular disease would lead to increased thromboxane A2 (TxA2) and decreased prostacyclin (PGI2) production and surgical correction of the ischemia would stabilize TxA2 and PGI2 at normal levels. TxA2 and PGI2 concentrations were determined in 22 patients before, during, and after arterial reconstruction for limb salvage and in 10 control subjects. Control samples and preoperative patient samples had no detectable TxA2 or PGI2 (less than 26 pg/ml). Five minutes after reperfusion TxA2 increased (TxA2 = 76.27 +/- 48.9 pg/ml, mean +/- SEM) and persisted at 1 day (TxA2 = 190.1 +/- 80.1 pg/ml), 2 days (TxA2 = 224.7 +/- 131.7 pg/ml), 5 days (TxA2 = 334.8 +/- 272.8 pg/ml), and 7 days postoperatively (TxA2 = 256.6 +/- 149.0 pg/ml). Elevated TxA2 production was not associated with chronic ischemia of peripheral vascular disease. Reperfusion of the severely ischemic limb caused significant TxA2 release.
我们推测，外周血管疾病的慢性缺血会导致血栓素A2（TxA2）生成增加，前列环素（PGI2）生成减少，而对缺血进行手术矫正会使TxA2和PGI2稳定在正常水平。我们测定了22例因肢体挽救而接受动脉重建手术的患者在手术前、手术中和手术后的TxA2和PGI2浓度，并与10名对照受试者进行了比较。对照样本和患者术前样本中未检测到TxA2或PGI2（低于26 pg/ml）。再灌注5分钟后，TxA2升高（TxA2 = 76.27 +/- 48.9 pg/ml，平均值 +/- 标准误），并在术后1天（TxA2 = 190.1 +/- 80.1 pg/ml）、2天（TxA2 = 224.7 +/- 131.7 pg/ml）、5天（TxA2 = 334.8 +/- 272.8 pg/ml）和7天（TxA2 = 256.6 +/- 149.0 pg/ml）持续升高。TxA2生成增加与外周血管疾病的慢性缺血无关。严重缺血肢体的再灌注导致TxA2大量释放。
