Effects of exogenous hydrogen sulfide on brain metabolism and early neurological function in rabbits after cardiac arrest
Effects of exogenous hydrogen sulfide on brain metabolism and early neurological function in rabbits after cardiac arrest
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外源性硫化氢对心脏骤停后家兔脑代谢及早期神经功能的影响
DOI：
10.1007/s00134-012-2714-x
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发表时间：
2012-09
影响因子：
38.9
通讯作者：
Bing Zhang
中科院分区：
文献类型：
--
作者：
Wei Xia;Duan Le;Bai Liqun;Tian Miaomiao;Li Wenzhi;Bing Zhang
目的硫化氢（H2S）的神经保护作用部分归因于全身低代谢和体温过低。然而，心脏骤停（CA）后全身代谢可能比脑代谢变化更显著。作者研究了吸入外源性硫化氢对家兔CA和复苏后脑代谢和神经功能的影响。方法麻醉家兔随机分为sham组、sham/H2S组、CA组和CA/H2S组。Sham/H2S组和CA/H2S组给予外源性80 ppm H2S，CA/H2S组通过窒息和复苏遭受未经处理的CA 3 min。观察CA对脑代谢（脑氧摄取率（CEO2）、动-颈静脉葡萄糖差值[AJVD（glu）]和乳酸清除率）、S100 B、存活神经元计数、神经功能障碍评分和存活率的影响。吸入80 ppm H2S显著增加CEO2（25.04 ± 7.11 vs. 16.72 ± 6.12%）和AJVD（血糖）降低（0.77 ± 0.29 vs 1.18 ± 0.38 mmol/L）和乳酸复苏后30min，CA组血浆NO浓度为（5.11 ± 0.43）mmol/L，对照组为（6.01 ± 0.64）mmol/L，两组比较差异均有统计学意义（P <0.05）。此外，神经功能缺损评分，活神经元计数，和生存率显着更好，而S100 B减少后H2S inhalation.ConclusionsThe本研究表明，吸入80 ppm H2S减少神经组织病理学损伤，并提高早期神经功能CA和复苏后，在兔。CEO 2增加、AJVD（glu）降低和乳酸清除率增加可能与其保护作用有关。
PurposeSome of the neuroprotective effects of hydrogen sulfide (H2S) have been attributed to systemic hypometabolism and hypothermia. However, systemic metabolism may vary more dramatically than brain metabolism after cardiac arrest (CA). The authors investigated the effects of inhaled exogenous hydrogen sulfide on brain metabolism and neurological function in rabbits after CA and resuscitation.MethodsAnesthetized rabbits were randomized into a sham group, a sham/H2S group, a CA group, and a CA/H2S group. Exogenous 80 ppm H2S was administered to the sham/H2S group and the CA/H2S group which suffered 3 min of untreated CA by asphyxia and resuscitation. Effects on brain metabolism (cerebral extraction of oxygen (CEO2), arterio-jugular venous difference of glucose [AJVD(glu)] and lactate clearance), S100B, viable neuron counts, neurological dysfunction score, and survival rate were evaluated.ResultsCEO2, AJVD(glu), and lactate increased significantly after CA. Inhalation of 80 ppm H2S significantly increased CEO2(25.04 ± 7.11 vs. 16.72 ± 6.12 %) and decreased AJVD(glu) (0.77 ± 0.29 vs. 1.18 ± 0.38 mmol/L) and lactate (5.11 ± 0.43 vs. 6.01 ± 0.64 mmol/L) at 30 min after resuscitation when compared with the CA group (allP< 0.05). In addition, neurologic deficit scores, viable neuron counts, and survival rate were significantly better whereas S100B was decreased after H2S inhalation.ConclusionsThe present study reveals that inhalation of 80 ppm H2S reduced neurohistopathological damage and improves early neurological function after CA and resuscitation in rabbits. The increased CEO2and decreased AJVD(glu) and enhanced lactate clearance may be involved in the protective effects.
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影响因子：
3.6
作者：
Chen, Meng-Hua;Xie, Lu;Mo, Shu-Rong
通讯作者：
Mo, Shu-Rong
影响因子：
4.4
作者：
M. Müllner;F. Sterz;H. Domanovits;A. Zeiner;A. Laggner
通讯作者：
M. Müllner;F. Sterz;H. Domanovits;A. Zeiner;A. Laggner
DOI：
10.1523/jneurosci.22-09-03386.2002
发表时间：
2002-05
期刊：
The Journal of Neuroscience
影响因子：
--
作者：
K. Eto;Miki Ogasawara;K. Umemura;Y. Nagai;H. Kimura
通讯作者：
K. Eto;Miki Ogasawara;K. Umemura;Y. Nagai;H. Kimura
影响因子：
8.3
作者：
BAKER, AJ;ZORNOW, MH;LARSON, AA
通讯作者：
LARSON, AA
影响因子：
3.3
作者：
A. Stein;Zhengkuan Mao;J. Morrison;M. Fanucchi;E. Postlethwait;R. Patel;D. Kraus;J. Doeller;S. Bailey
通讯作者：
A. Stein;Zhengkuan Mao;J. Morrison;M. Fanucchi;E. Postlethwait;R. Patel;D. Kraus;J. Doeller;S. Bailey