氢分子医学分享 http://blog.sciencenet.cn/u/孙学军 对氢气生物学效应感兴趣者。可合作研究:sunxjk@hotmail.com 微信 hydrogen_thinker

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氢气对新生儿窒息后脑损伤有保护作用

已有 5953 次阅读 2010-7-27 11:05 |个人分类:呼吸氢气|系统分类:科研笔记|关键词:学者| 氢气

两年前,我们课题组曾经报道,呼吸氢气缺血缺氧损伤具有保护作用,本研究是采用猪为模型,用停止呼吸来模拟窒息,更符合临床新生儿窒息的实际,结果发现呼吸氢气对窒息引起的神经损伤有明确的保护作用,而且对窒息后脑网膜血管二氧化碳反应性有明显增加效应,提示对血管损伤也有很好的保护作用。从作者单位是匈牙利Department of Physiology [F.D., O.O., A.Z., V.T., M.H.], Department of Dermatology and Allergology [I.N.], Department of Medical Informatics [F.B.] University of Szeged School of Medicine, Szeged, H-6720, Hungary; Department of Pediatrics [P.T.], University Teaching Hospital Orosháza, Orosháza, H-5900, Hungary.这是自日本、中国和美国之后,另外增加了一个国家参与氢气生物学效应研究的国家:匈牙利

论文摘要,氢气能中和毒性活性氧,氧化应激是新生儿窒息后神经损伤的重要机制。本研究让动物呼吸含2.1%氢气的空气,结果发现能有效保护窒息引起的脑血管反应性和脑组织病理改变。动物分成2组,呼吸空气组和空气含氢气组,并分别分成不同的时间组。窒息方法是停止呼吸10分钟,然后通气4小时。复苏后,脑组织进行形态学观察。脑膜血管直径通过在体血管反应性检测,动物呼吸5-10%二氧化碳和10-4M NMDA,采用颅骨开窗,显微镜检测窒息前和窒息后1小时对比血管直径。病理学检测结果发现,呼吸氢气能对所有检测部位:如大脑皮层、海马、基底核、小脑和脑干窒息引起的神经损伤均有明显的治疗作用。而且呼吸氢气能有效保护窒息引起的脑血管反应性降低(二氧化碳呼吸,但对NMDA诱导效应无作用)。研究结果提示,呼吸氢气对新生儿窒息后神经损伤具有非常理想的保护作用。

 

Hydrogen is neuroprotective and preserves cerebrovascular reactivity in asphyxiated newborn pigs全文

Domoki, Ferenc; Oláh, Orsolya; Zimmermann, Aliz; Németh, István; Tóth-Szuki, Valéria; Hugyecz, Marietta; Temesvári, Péter; Bari, Ferenc

Department of Physiology [F.D., O.O., A.Z., V.T., M.H.], Department of Dermatology and Allergology [I.N.], Department of Medical Informatics [F.B.] University of Szeged School of Medicine, Szeged, H-6720, Hungary; Department of Pediatrics [P.T.], University Teaching Hospital Orosháza, Orosháza, H-5900, Hungary.

 

Abstract

Hydrogen (H2) has been reported to neutralize toxic reactive oxygen species (ROS). Oxidative stress is an important mechanism of neuronal damage after perinatal asphyxia. We examined if 2.1% H2-supplemented room air (H2-RA) ventilation would preserve cerebrovascular reactivity (CR) and brain morphology after asphyxia/reventilation (A/R) in newborn pigs. Anesthetized, ventilated piglets were assigned to one of the following groups: A/R with RA or H2-RA ventilation (A/R-RA and A/R-H2-RA; n=8,7), and respective time control groups (n=9,7). Asphyxia was induced by suspending ventilation for 10 min, followed by reventilation with the respective gases for 4 hours. After euthanasia, the brains were processed for neuropathological examination. Pial arteriolar diameter changes to graded hypercapnia [5-10%CO2 inhalation] and NMDA, [10-4M]) were determined using the closed cranial window/intravital microscopy before and 1h after asphyxia. Neuropathology revealed that H2-RA ventilation significantly reduced neuronal injury induced by A/R in virtually all examined brain regions including the cerebral cortex, the hippocampus, basal ganglia, cerebellum, and the brainstem. Furthermore, H2-RA ventilation significantly increased CR to hypercapnia after A/R (% vasodilation was 23+/-4% versus 41+/-9%*, *p<0.05). H2-RA ventilation did not affect ROS-dependent CR to NMDA. In summary, H2-RA could be a promising approach to reduce the neurological deficits after perinatal asphyxia.

(C) International Pediatrics Research Foundation, Inc. 2010. All Rights Reserved.

 

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