Endogenous hydrogen sulfide mediates the cardioprotection induced by ischemic postconditioning in the early reperfusion phase.
Endogenous hydrogen sulfide mediates the cardioprotection induced by ischemic postconditioning in the early reperfusion phase.
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内源性硫化氢介导再灌注早期缺血后处理诱导的心脏保护作用
DOI：
10.3892/etm.2012.733
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发表时间：
2012-12
影响因子：
2.7
通讯作者：
Jiang ZS
中科院分区：
文献类型：
--
作者：
Huang YE;Tang ZH;Xie W;Shen XT;Liu MH;Peng XP;Zhao ZZ;Nie DB;Liu LS;Jiang ZS
硫化氢 (H2S) 由心血管系统中的胱硫醚-γ-裂解酶 (CSE) 产生，被认为是除一氧化氮 (NO) 和一氧化碳 (CO) 之外的第三种气体递质。本研究旨在探讨 H2S 在再灌注早期缺血后处理 (IPO) 中的作用。当再灌注开始时，进行 IPO，先进行 6 次 10 秒再灌注，然后再进行 6 次 10 秒缺血（IPO 2'）。在再灌注1、2、3、4、5、10、20、30、60、90和120分钟时测量心脏动力学和H2S浓度。在再灌注结束时测定乳酸脱氢酶（LDH）水平和梗塞面积。对照组的H2S浓度在整个实验过程中保持稳定，而缺血再灌注（IR）组的H2S浓度在再灌注第一分钟达到峰值。与 IR 组相比，IPO 2' 组再灌注第一分钟的 H2S 浓度较高，这与心脏保护作用相关，包括改善心脏收缩功能、减少梗塞面积和 LDH 水平。然而，在全脑缺血前用 DL-炔丙基甘氨酸进行预处理 20 分钟，阻断内源性 H2S 的产生，从而减弱了 IPO 2' 的上述作用。此外，我们发现其他形式的IPO，即再灌注后1分钟开始的IPO（延迟IPO）或仅持续1分钟（IPO 1’），未能增加H2S浓度并保护心肌。我们得出结论，再灌注早期内源性 H2S 的峰值是 IPO 诱导心脏保护的关键。
Hydrogen sulfide (H2S), produced by cystanthionine-γ-lysase (CSE) in the cardiovascular system, has been suggested to be the third gasotransmitter in addition to nitric oxide (NO) and carbon monoxide (CO). The present study aimed to investigate the role of H2S in ischemic postconditioning (IPO) during the early period of reperfusion. IPO with 6 episodes of 10 sec reperfusion followed by 6 episodes of 10 sec ischemia (IPO 2’) was administered when reperfusion was initiated. Cardiodynamics and the concentration of H2S were measured at 1, 2, 3, 4, 5, 10, 20, 30, 60, 90 and 120 min of reperfusion. Lactate dehydrogenase (LDH) levels and infarct size were determined at the end of the reperfusion. The concentration of H2S was stable during the whole experiment in the control group, whereas it reached a peak at the first minute of reperfusion in the ischemia-reperfusion (IR) group. The concentration of H2S at the first minute of reperfusion in the IPO 2’ group was higher compared to that of the IR group, which correlated with cardioprotection including improved heart contractile function and reduced infarct size and LDH levels. However, the above effects of IPO 2’ were attenuated by pre-treatment with blockade of endogenous H2S production with DL-propargylglycine for 20 min prior to global ischemia. Furthermore, we found that other forms of IPO, IPO commencing at 1 min after reperfusion (delayed IPO) or lasting only for 1 min (IPO 1’), failed to increase the concentration of H2S and protect the myocardium. We conclude that the peak of endogenous H2S in the early reperfusion phase is the key to cardioprotection induced by IPO.
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DOI：
10.1124/jpet.105.092023
发表时间：
2006-02-01
影响因子：
3.5
作者：
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影响因子：
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10.1152/ajpregu.00419.2003
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2004-04-01
影响因子：
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通讯作者：
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