Lee Tsung-Ming, Lin Mei-Shu, Tsai Chang-Her, Chang Nen-Chung
Cardiology Section, Department of Medicine, Chi-Mei Medical Centre, Taipei Medical University, Tainan, Taiwan.
Clin Sci (Lond). 2005 Sep;109(3):267-76. doi: 10.1042/CS20050046.
Systemic markers of inflammation may be increased in patients after percutaneous coronary intervention. In the present study, we evaluated whether IP (ischaemic preconditioning) attenuated inflammation by activating KATP (ATP-sensitive potassium) channels in patients undergoing coronary angioplasty. Patients (n=36) undergoing angioplasty of a major left coronary artery were allocated randomly to one of four groups: a control group, a group receiving nicorandil (an agonist of KATP channels), an IP group or an IP group pretreated with glibenclamide (an antagonist of KATP channels). To measure the release of sCD40L, P-selectin and myeloperoxidase from the ischaemic region, blood samples were drawn simultaneously from the ascending aorta and the great cardiac vein before and 15 min after coronary angioplasty. At 15 min after angioplasty, a significant increase in sCD40L and P-selectin levels in the great cardiac vein in the control group was observed. IP- and nicorandil-treated patients did not show a significant change in sCD40L and P-selectin levels in response to angioplasty. However, the IP-induced attenuation of sCD40L and P-selectin release was abolished by administering glibenclamide. The change in myeloperoxidase levels mirrored those of sCD40L and P-selectin. The levels of inflammatory markers in the aorta remained stable throughout the study. Patients undergoing angioplasty had increased sCD40L and P-selectin levels in the ischaemic region. In conclusion, IP abolished angioplasty-induced myeloperoxidase release by preventing activated platelet-induced P-selectin release via a KATP-channel-initiated pathway. Therefore, in addition to its primary effect on cardioprotection, IP may also provide beneficial anti-inflammatory effects on the interaction between platelets and neutrophils.
经皮冠状动脉介入治疗后的患者体内炎症的全身标志物可能会升高。在本研究中，我们评估了缺血预处理（IP）是否通过激活接受冠状动脉血管成形术患者的ATP敏感性钾通道（KATP）来减轻炎症。接受左冠状动脉主要血管成形术的患者（n = 36）被随机分为四组之一：对照组、接受尼可地尔（一种KATP通道激动剂）的组、IP组或用格列本脲（一种KATP通道拮抗剂）预处理的IP组。为了测量缺血区域sCD40L、P选择素和髓过氧化物酶的释放，在冠状动脉血管成形术前和术后15分钟同时从升主动脉和心大静脉采集血样。血管成形术后15分钟，观察到对照组心大静脉中sCD40L和P选择素水平显著升高。接受IP和尼可地尔治疗的患者在血管成形术后sCD40L和P选择素水平没有显著变化。然而，给予格列本脲可消除IP诱导的sCD40L和P选择素释放的减弱。髓过氧化物酶水平的变化与sCD40L和P选择素的变化一致。在整个研究过程中，主动脉中炎症标志物的水平保持稳定。接受血管成形术的患者缺血区域的sCD40L和P选择素水平升高。总之，IP通过KATP通道启动的途径阻止活化血小板诱导的P选择素释放，从而消除血管成形术诱导的髓过氧化物酶释放。因此，除了其对心脏保护的主要作用外，IP还可能对血小板与中性粒细胞之间的相互作用提供有益的抗炎作用。
