尼可地尔是硝酸盐和atp敏感的钾离子通道打开剂的混合物,在经皮冠状动脉腔内成形术中对人心脏缺血起预先作用。

T. Yasuda, K. Hashimura, Y. Matsu-ura, Y. Kato, T. Ueda, I. Mori, Y. Kijima
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引用次数: 33

摘要

在经皮腔内冠状动脉成形术(PTCA)中反复球囊膨胀后,人类心脏对缺血的耐受性逐渐增强。本研究调查了硝酸和atp敏感的钾通道打开剂之间的杂交种尼可地尔是否影响这种缺血预处理。对16例由左前降支病变引起的稳定型心绞痛患者行2次球囊充气术,持续时间2 min,再灌注时间3 min。其中7例患者作为对照组,其余9例患者在PTCA过程中静脉注射尼可地尔(6 mg/h)(尼可地尔组)。在每次缺血后30s测定两组乳酸提取比(LERpost-1和LERpost-2)。对照组LERpost-1阳性比LERpost-2阴性(-185.7+/-74.2 vs -98.0+/-37.3%, p<0.01)。对照组第二次充气时(sumST-2, 0.94+/-0.66 mV)与第一次充气时(sumST-1, 1.43+/-1.17 mV)心前导联ST抬高之和之比为0.72+/-0.16,低于尼可地尔组(1.06+/-0.13,p<0.01)。尼可地尔消除了两种缺血性事件之间的差异(LERpost-1, -45.1+/-41.6 vs LERpost-2, -43.5+/-51.1%;sumST-1, 1.38 + / - -0.80 vs sumST-2, 1.46 + / - -0.90 mV)。尼可地尔组的LER阴性程度低于对照组(LERpost-1, -45.1+/-41.6 vs -185.7+/-74.2%, p<0.01;LERpost-2 -43.5 + / - -51.1 vs -98.0 + / - -37.3%, p < 0.05)。因此,尼可地尔改善PTCA期间的乳酸代谢,但不显著影响st段抬高。总之,静脉预给药尼可地尔似乎在PTCA期间对人类心脏有前置作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Nicorandil, a hybrid between nitrate and ATP-sensitive potassium channel opener, preconditions human heart to ischemia during percutaneous transluminal coronary angioplasty.
The human heart progressively becomes more tolerant to ischemia after repeated balloon inflations during percutaneous transluminal coronary angioplasty (PTCA). The present study investigated whether nicorandil, a hybrid between nitrate and an ATP-sensitive potassium channel opener, affects this ischemic preconditioning. Sixteen patients with stable angina pectoris caused by left anterior descending artery lesions were subjected to 2 balloon inflations of 2-min duration with a 3-min reperfusion period. Seven of these patients served as the control group and in the remaining 9 patients, nicorandil was administered intravenously (6 mg/h) throughout the PTCA procedure (nicorandil group). The lactate extraction ratio (LER) was obtained at 30 s after each ischemic event (LERpost-1 and LERpost-2) in both groups. In the control group, LERpost-1 was more negative than LERpost-2 (-185.7+/-74.2 vs -98.0+/-37.3%, p<0.01). The ratio of the sum of the ST elevation in the precordial leads during the second inflation (sumST-2, 0.94+/-0.66 mV) to that during the first inflation (sumST-1, 1.43+/-1.17 mV) was 0.72+/-0.16 in the control group, which was less than the ratio in the nicorandil group (1.06+/-0.13, p<0.01). Nicorandil abolished the difference between the 2 ischemic events (LERpost-1, -45.1+/-41.6 vs LERpost-2, -43.5+/-51.1%; sumST-1, 1.38+/-0.80 vs sumST-2, 1.46+/-0.90 mV). LER was less negative in the nicorandil group than that in the control group (LERpost-1, -45.1+/-41.6 vs -185.7+/-74.2%, p<0.01; LERpost-2, -43.5+/-51.1 vs -98.0+/-37.3%, p<0.05). Thus, nicorandil improved lactate metabolism during PTCA without significantly influencing ST-elevation. In conclusion, intravenous pre-administration of nicorandil appears to precondition the human heart during PTCA.
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