Gaspardone A, Crea F, Tomai F, Versaci F, Pellegrino A, Chiariello L, Gioffré P A
Divisione di Cardiochirurgia, Università di Roma Tor Vergata, Rome, Italy.
J Am Coll Cardiol. 1999 Jul;34(1):216-22. doi: 10.1016/s0735-1097(99)00147-3.
This study assessed the algesic activity of bradykinin (BK) in humans and the effects of acetylsalicylate on muscular and cardiac BK-induced pain.
Bradykinin is released by the ischemic myocardium and may be involved in the genesis of ischemic pain.
Increasing doses of BK (from 30 to 960 ng/min) were randomly infused, for periods of 2 min each, into the iliac artery of 10 patients. The same protocol was repeated 30 min after the IV administration of 1 g of acetylsalicylate. In eight other patients with coronary artery disease, the same increasing doses of BK, for periods of 2 min each, were infused into the left coronary artery. The same protocol was repeated 30 min after the IV administration of 1 g of acetylsalicylate. Time to pain onset and maximal pain severity were obtained.
Before acetylsalicylate administration, all patients experienced pain during intra-iliac infusion of BK. After acetylsalicylate, eight patients did not experience any pain during BK infusion (p = 0.0014), and in the two remaining patients, time to pain onset and maximal pain severity were similar to those recorded before acetylsalicylate. Before acetylsalicylate administration, all patients experienced pain similar to their habitual angina during intracoronary BK infusion. After acetylsalicylate, six patients did not experience any pain during BK infusion (p = 0.0098), whereas in the two remaining patients time to pain onset and maximal pain severity were similar to those recorded before acetylsalicylate.
Intra-iliac infusion of BK causes muscular pain, and its intracoronary infusion in patients with coronary artery disease causes cardiac pain, which is similar to their habitual angina. The BK-induced pain is abolished or reduced by acetylsalicylate, thus suggesting that acetylsalicylate-sensitive mediators, such as prostaglandins, are involved in its pathogenesis.
本研究评估缓激肽(BK)在人体中的致痛活性以及乙酰水杨酸对肌肉和心脏BK诱导疼痛的影响。
缺血心肌会释放缓激肽,其可能参与缺血性疼痛的发生。
将递增剂量的BK(从30至960 ng/分钟)以每次2分钟的时长随机输注到10名患者的髂动脉中。在静脉注射1 g乙酰水杨酸30分钟后重复相同方案。在另外8名冠心病患者中,将相同递增剂量的BK以每次2分钟的时长输注到左冠状动脉中。在静脉注射1 g乙酰水杨酸30分钟后重复相同方案。记录疼痛发作时间和最大疼痛严重程度。
在给予乙酰水杨酸之前,所有患者在髂内输注BK期间均经历疼痛。给予乙酰水杨酸后,8名患者在BK输注期间未经历任何疼痛(p = 0.0014),其余2名患者的疼痛发作时间和最大疼痛严重程度与给予乙酰水杨酸之前记录的相似。在给予乙酰水杨酸之前,所有患者在冠状动脉内输注BK期间经历的疼痛与其习惯性心绞痛相似。给予乙酰水杨酸后,6名患者在BK输注期间未经历任何疼痛(p = 0.0098),而其余2名患者的疼痛发作时间和最大疼痛严重程度与给予乙酰水杨酸之前记录的相似。
髂内输注BK会引起肌肉疼痛,在冠心病患者中冠状动脉内输注BK会引起心脏疼痛,这与其习惯性心绞痛相似。乙酰水杨酸可消除或减轻BK诱导的疼痛,因此表明对乙酰水杨酸敏感的介质,如前列腺素,参与了其发病机制。