Transient ischemia reduces norepinephrine release during sustained ischemia. Neural preconditioning in isolated rat heart.
Transient ischemia reduces norepinephrine release during sustained ischemia. Neural preconditioning in isolated rat heart.
复制标题
短暂性缺血会减少持续缺血期间去甲肾上腺素的释放。
作者：
M. Seyfarth;G. Richardt;Anna Mizsnyak;T. Kurz;A. Schömig
内源性儿茶酚胺的释放可能作为心肌预适应过程中的触发因子或靶点在缺血预适应中发挥作用。因此，我们研究了短暂缺血（TI）对离体大鼠心脏持续缺血时去甲肾上腺素释放的影响。与缺血预处理方案相比，通过多次全脑缺血再灌注诱导TI，每次持续5分钟。TI后，去甲肾上腺素的释放引起持续的全球缺血，缺氧，氰化物中毒，酪胺，或电刺激。在TI期间，未观察到去甲肾上腺素洗脱，去甲肾上腺素的组织浓度未发生变化。然而，在持续缺血20分钟后，TI将去甲肾上腺素溢出从239 +/- 26 pmol/g（对照）减少到79+/-8 pmol/g（减少67%，P <0.01）。当心脏在无葡萄糖的情况下经历短暂缺氧时，观察到缺血诱导的去甲肾上腺素释放从192 +/- 22 pmol/g（对照）到90 +/- 15 pmol/g的类似减少（P <0.05）。再灌注5 ~ 90 min时，TI对去甲肾上腺素释放的抑制作用逐渐消失。对TI的敏感性是持续缺血诱导的去甲肾上腺素释放的独特特征，因为缺氧、氰化物中毒、酪胺或电刺激诱发的去甲肾上腺素释放不受TI影响。我们提出了TI对神经组织的保护作用，这可能会减少去甲肾上腺素引起的损伤，在长期的心肌缺血。
Endogenous catecholamine release may play a role in ischemic preconditioning either as a trigger or as a target within the process of myocardial preconditioning. Therefore, we investigated the effect of transient ischemia (TI) on norepinephrine release during sustained ischemia in isolated rat hearts. TI was induced by multiple cycles of global ischemia followed by reperfusion with a duration of 5 minutes each, comparable to ischemic preconditioning protocols. After TI, norepinephrine release was evoked by either sustained global ischemia, anoxia, cyanide intoxication, tyramine, or electrical stimulation. During TI, no washout of norepinephrine was observed, and tissue concentrations of norepinephrine were not changed. TI, however, reduced norepinephrine overflow after 20 minutes of sustained ischemia from 239 +/- 26 pmol/g (control) to 79+/-8 pmol/g (67% reduction, P <.01 ). A similar reduction of ischemia-induced norepinephrine release from 192 +/- 22 pmol/g (control) to 90 +/- 15 pmol/g was observed when hearts underwent transient anoxia without glucose (P < .05). When reperfusion between TI and sustained ischemia was prolonged from 5 to 90 minutes, the inhibitory effect of TI on norepinephrine release was gradually lost. Susceptibility to TI was a unique feature of norepinephrine release induced by sustained ischemia, since release of norepinephrine evoked by anoxia, cyanide intoxication, tyramine, or electrical stimulation remained unaffected by TI. We propose a protective effect of TI on neural tissue, which may reduce norepinephrine-induced damage during prolonged myocardial ischemia.
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影响因子：
20.1
作者：
A. Tsuchida;Yongge Liu;G. S. Liu;Michael V. Cohen;J. M. Downey
通讯作者：
A. Tsuchida;Yongge Liu;G. S. Liu;Michael V. Cohen;J. M. Downey
影响因子：
20.1
作者：
HAGAR, JM;HALE, SL;KLONER, RA
通讯作者：
KLONER, RA
影响因子：
10.8
作者：
Y. Shizukuda;R. Mallet;Shang-Chiun Lee;Downey Hf
通讯作者：
Y. Shizukuda;R. Mallet;Shang-Chiun Lee;Downey Hf
儿茶酚胺可以诱导腺苷受体介导的心肌保护，但不参与兔子的缺血预适应。
影响因子：
20.1
作者：
Thornton,JD;Daly,JF;Cohen,MV;Yang,XM;Downey,JM
通讯作者：
Downey,JM
影响因子：
20.1
作者：
DEALBUQUERQUE, CP;GERSTENBLITH, G;WEISS, RG
通讯作者：
WEISS, RG