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首页> 外文期刊>Resuscitation. >Inhibition of peroxynitrite precursors, NO and O2, at the onset of reperfusion improves myocardial recovery.
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Inhibition of peroxynitrite precursors, NO and O2, at the onset of reperfusion improves myocardial recovery.

机译：在再灌注开始时抑制过氧亚硝酸盐前体NO和O2可改善心肌的恢复。

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AIM OF STUDY: Previous reports note an increase in both reactive oxygen species (ROS) and nitric oxide (*NO) at the onset of myocardial reperfusion. We tested the hypothesis that inhibition of *NO or ROS production at the time of reperfusion improves recovery of post-ischemic myocardial function. METHODS AND MATERIALS: Isolated rat hearts were perfused with temperature controlled (37.4 degrees C) modified Krebs Henseleit buffer solution at 85 mm Hg. Following 20 min of global ischemia, hearts were reperfused for the first 10 min with: (1) standard buffer (control), (2) buffer with a NOS inhibitor, N-nitro-L-arginine methyl ester (L-NAME), (3) buffer with superoxide dismutase (SOD) or (4) buffer with N-morpholinosydnonimine hydrochloride (SIN-1), a peroxynitrite generator. Tissue O(2) and *NO were continuously measured with thin electrochemical probes embedded in the wall of the LV. ROS was measured with the spin trap 5,5-dimethyl-1-pyrroline N-oxide (DMPO) (40 mM). LV contractile function was continuously monitored. RESULTS: Recovery of LV contractile function was significantly improved in hearts initially reperfused with L-NAME and SOD and significantly depressed in hearts reperfused with SIN-1 compared with control (p<0.01, n=5-8 per group). DMPO-adduct during reperfusion (measure of ROS) was significantly decreased with SOD (p<0.001 versus L-NAME and Control, n=4 per group) and unchanged with L-NAME and SIN-1 compared with Control. With L-NAME, tissue *NO and PO(2) were significantly decreased, independent of coronary flow, during reperfusion compared with control and SIN-1. CONCLUSIONS: Inhibition of O(2)*(-) or *NO at the time of reperfusion improves early reperfusion LV function and alters tissue oxygen tension. In contrast to pre-ischemic treatments, intervention to reduce peroxynitrite generation at the onset of reperfusion can effectively improve post-ischemic myocardial recovery.
机译：研究目的：先前的报告指出，心肌再灌注开始时活性氧（ROS）和一氧化氮（* NO）均增加。我们测试了以下假设：在再灌注时抑制* NO或ROS产生可改善缺血后心肌功能的恢复。方法和材料：在85 mm Hg的温度下（37.4摄氏度）改良的Krebs Henseleit缓冲溶液灌注离体大鼠心脏。全球缺血20分钟后，在最初的10分钟内，将心脏再灌注：（1）标准缓冲液（对照），（2）含NOS抑制剂的缓冲液，N-硝基-L-精氨酸甲酯（L-NAME）， （3）具有超氧化物歧化酶（SOD）的缓冲液或（4）具有过氧化亚硝酸盐生成剂的N-吗啉代亚砜盐酸盐（SIN-1）的缓冲液。组织O（2）和* NO是用嵌入LV壁的薄电化学探针连续测量的。用自旋阱5,5-二甲基-1-吡咯啉N-氧化物（DMPO）（40 mM）测量ROS。持续监测左室收缩功能。结果：与对照组相比，最初用L-NAME和SOD再灌注的心脏的LV收缩功能恢复显着提高，而用SIN-1再灌注的心脏的LV收缩功能显着降低（每组p <0.01，n = 5-8）。与对照相比，SOD显着降低了再灌注期间的DMPO加合物（ROS的测量值）（与L-NAME和对照组相比，p <0.001，每组n = 4），与对照组相比，L-NAME和SIN-1则没有变化。与对照组和SIN-1相比，使用L-NAME可使组织* NO和PO（2）显着降低，而与冠状动脉血流无关。结论：再灌注时抑制O（2）*（-）或* NO可改善早期再灌注左室功能并改变组织氧张力。与缺血前的治疗相反，减少再灌注时过氧亚硝酸盐生成的干预措施可以有效改善缺血后的心肌恢复。

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