Zalewski Jaroslaw, Claus Piet, Bogaert Jan, Driessche Nina Vanden, Driesen Ronald B, Galan Diogo T, Sipido Karin R, Buszman Piotr, Milewski Krzysztof, Van de Werf Frans
Cardiology, Department of Cardiovascular Sciences, KU Leuven, Herestraat 49, 3000, Leuven, Belgium,
Basic Res Cardiol. 2015 Mar;110(2):18. doi: 10.1007/s00395-015-0475-8. Epub 2015 Feb 27.
Postconditioning and cyclosporine A prevent mitochondrial permeability transition pore opening providing cardioprotection during ischemia/reperfusion. Whether microvascular obstruction is affected by these interventions is largely unknown. Pigs subjected to coronary occlusion for 1 h followed by 3 h of reperfusion were assigned to control (n = 8), postconditioning (n = 9) or cyclosporine A intravenous infusion 10-15 min before the end of ischemia (n = 8). Postconditioning was induced by 8 cycles of repeated 30-s balloon inflation and deflation. After 3 h of reperfusion magnetic resonance imaging, triphenyltetrazolium chloride/Evans blue staining and histopathology were performed. Microvascular obstruction (MVO, percentage of gadolinium-hyperenhanced area) was measured early (3 min) and late (12 min) after contrast injection. Infarct size with double staining was smaller in cyclosporine (46.2 ± 3.1%, P = 0.016) and postconditioning pigs (47.6 ± 3.9%, P = 0.008) versus controls (53.8 ± 4.1%). Late MVO was significantly reduced by cyclosporine (13.9 ± 9.6%, P = 0.047) but not postconditioning (23.6 ± 11.7%, P = 0.66) when compared with controls (32.0 ± 16.9%). Myocardial blood flow in the late MVO was improved with cyclosporine versus controls (0.30 ± 0.06 vs 0.21 ± 0.03 ml/g/min, P = 0.002) and was inversely correlated with late-MVO extent (R(2) = 0.93, P < 0.0001). Deterioration of left ventricular ejection fraction (LVEF) between baseline and 3 h of reperfusion was smaller with cyclosporine (-7.9 ± 2.4%, P = 0.008) but not postconditioning (-12.0 ± 5.5%, P = 0.22) when compared with controls (-16.4 ± 5.5%). In the three groups, infarct size (β = -0.69, P < 0.001) and late MVO (β = -0.33, P = 0.02) were independent predictors of LVEF deterioration following ischemia/reperfusion (R(2) = 0.73, P < 0.001). Despite both cyclosporine A and postconditioning reduce infarct size, only cyclosporine A infusion had a beneficial effect on microvascular damage and was associated with better preserved LV function when compared with controls.
后适应和环孢素A可防止线粒体通透性转换孔开放,在缺血/再灌注期间提供心脏保护作用。这些干预措施是否会影响微血管阻塞在很大程度上尚不清楚。将经历1小时冠状动脉闭塞随后3小时再灌注的猪分为对照组(n = 8)、后适应组(n = 9)或在缺血结束前10 - 15分钟静脉输注环孢素A组(n = 8)。后适应通过8个周期的30秒重复球囊充气和放气诱导。再灌注3小时后进行磁共振成像、氯化三苯基四氮唑/伊文思蓝染色和组织病理学检查。在注射造影剂后早期(3分钟)和晚期(12分钟)测量微血管阻塞(MVO,钆增强区域的百分比)。与对照组(53.8 ± 4.1%)相比,环孢素组(46.2 ± 3.1%,P = 0.016)和后适应组猪(47.6 ± 3.9%,P = 0.008)的双染梗死面积较小。与对照组(32.0 ± 16.9%)相比,环孢素显著降低了晚期MVO(13.9 ± 9.6%,P = 0.047),而后适应组未降低(23.6 ± 11.7%,P = 0.66)。与对照组相比,环孢素改善了晚期MVO区域的心肌血流(0.30 ± 0.06 vs 0.21 ± 0.03 ml/g/min,P = 0.002),且与晚期MVO程度呈负相关(R(2) = 0.93,P < 0.0001)。与对照组(-16.4 ± 5.5%)相比,环孢素组在基线和再灌注3小时之间左心室射血分数(LVEF)的恶化较小(-7.9 ± 2.4%,P = 0.008),而后适应组未改善(-12.0 ± 5.5%,P = 0.22)。在三组中,梗死面积(β = -0.69,P < 0.001)和晚期MVO(β = -0.33,P = 0.02)是缺血/再灌注后LVEF恶化的独立预测因素(R(2) = 0.73,P < 0.001)。尽管环孢素A和后适应均减小了梗死面积,但与对照组相比,仅环孢素A输注对微血管损伤有有益作用,并与更好地保留左心室功能相关。