|
兩年前，我們課題組曾經報導，呼吸氫氣對新生兒缺血缺氧腦損傷具有保護作用，本研究是採用豬為模型，用停止呼吸來模擬窒息，更符合臨床新生兒窒息的實際，結果發現呼吸氫氣對窒息引起的神經損傷有明確的保護作用，而且對窒息後腦網膜血管二氧化碳反應性有明顯增加效應，提示對血管損傷也有很好的保護作用。從作者單位是匈牙利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.這是自日本、中國和美國之後，另外增加了一個國家參與氫氣生物學效應研究的國家：匈牙利
論文摘要，氫氣能中和毒性活性氧，氧化應激是新生兒窒息後神經損傷的重要機制。本研究讓動物呼吸含2.1%氫氣的空氣，結果發現能有效保護窒息引起的腦血管反應性和腦組織病理改變。動物分成2組，呼吸空氣組和空氣含氫氣組，並分別分成不同的時間組。窒息方法是停止呼吸10分鐘，然後通氣4小時。復蘇後，腦組織進行形態學觀察。腦膜血管直徑通過在體血管反應性檢測，動物呼吸5-10%二氧化碳和10-4M NMDA，採用顱骨開窗，顯微鏡檢測窒息前和窒息後1小時對比血管直徑。病理學檢測結果發現，呼吸氫氣能對所有檢測部位：如大腦皮層、海馬、基底核、小腦和腦幹窒息引起的神經損傷均有明顯的治療作用。而且呼吸氫氣能有效保護窒息引起的腦血管反應性降低（二氧化碳呼吸，但對NMDA誘導效應無作用）。研究結果提示，呼吸氫氣對新生兒窒息後神經損傷具有非常理想的保護作用。
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.
Published Ahead-of-Print
|