两年前，我们课题组曾经报道，呼吸氢气对新生儿缺血缺氧脑损伤具有保护作用，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。从作者名字看似乎是法国或德国，查找作者单位可能是Department
of Physiology and Pharmacology, Wake Forest University School of Medicine,
Winston Salem, North Carolina 27157 1010, USA(等待证实)
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
Domoki, Ferenc; Oláh, Orsolya; Zimmermann, Aliz; Németh, István;
Tóth-Szuki, Valéria; Hugyecz, Marietta; Temesvári, Péter; Bari, Ferenc
Department of Physiology and Pharmacology, Wake Forest University School of
Medicine, Winston Salem, North Carolina 27157 1010, USA
Published Ahead-of-Print
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
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