Brain mitochondrial oxidative metabolism during and after cerebral hypoxia-ischemia studied by simultaneous phosphorus magnetic-resonance and broadband near-infrared spectroscopy.
Brain mitochondrial oxidative metabolism during and after cerebral hypoxia-ischemia studied by simultaneous phosphorus magnetic-resonance and broadband near-infrared spectroscopy.
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DOI：
10.1016/j.neuroimage.2013.08.016
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发表时间：
2014-11-15
期刊：
影响因子：
5.7
通讯作者：
Golay X
中科院分区：
文献类型：
--
作者：
Bainbridge A;Tachtsidis I;Faulkner SD;Price D;Zhu T;Baer E;Broad KD;Thomas DL;Cady EB;Robertson NJ;Golay X
结合宽带近红外光谱（NIRS）和磷磁共振波谱（31 P MRS）的多模态测量评估了新生仔猪短暂脑缺氧缺血（HI）期间和之后脑线粒体细胞色素c氧化酶（Δ[oxCCO]）氧化态变化与31 P代谢物峰面积比之间的关联。24只小猪（年龄< 24 h）接受短暂HI（吸入氧分数9%和双侧颈动脉闭塞约20 min）。每分钟采集全脑31 P MRS和NIRS数据。通过31 P MRS测量无机磷酸盐（Pi）/epp、磷酸肌酸（PCr）/epp和总核苷酸三磷酸盐（NTP）/epp，并在HI和恢复期间与Δ[oxCCO]作图（epp =可交换磷酸盐池= Pi + PCr + 2γ-NTP + β-NTP）。在HI Δ[oxCCO]期间，PCr/epp和NTP/epp下降，Pi/epp升高。31 P比值与Δ[oxCCO]之间存在显著相关性;在HI期间，确定了Δ[oxCCO]与NTP/epp和Pi/epp之间关系显著变化的阈值点。48 h的结局与HI后1 h Δ[oxCCO]和31 P比值的恢复有关（存活：1 h NTP/epp 0.22 ± 0.02，Δ[oxCCO] − 0.29 ± 0.50 μM;死亡：1 h NTP/epp 0.10 ± 0.04，Δ[oxCCO] − 2.41 ± 1.48 μM）。HI后1h Δ[oxCCO]和NTP/epp均降低，表明线粒体损伤。在HI后1 h，48 h前死亡的动物的Δ[oxCCO]和31 P比值恢复较慢。短暂性缺氧缺血时和缺氧缺血后31 P MRS与宽带NIRS相关。双线性模型最能描述HI期间NTP/epp与Δ[oxCCO]的关系。双线性模型中的阈值点解释为ATP生产的停止。不良结局与31 P MRS比值和Δ[oxCCO]恢复较弱相关。线粒体功能障碍可能是Δ[oxCCO]降低的原因。
Multimodal measurements combining broadband near-infrared spectroscopy (NIRS) and phosphorus magnetic resonance spectroscopy (31P MRS) assessed associations between changes in the oxidation state of cerebral mitochondrial cytochrome-c-oxidase (Δ[oxCCO]) and 31P metabolite peak-area ratios during and after transient cerebral hypoxia–ischemia (HI) in the newborn piglet. Twenty-four piglets (aged < 24 h) underwent transient HI (inspired oxygen fraction 9% and bilateral carotid artery occlusion for ~ 20 min). Whole-brain 31P MRS and NIRS data were acquired every minute. Inorganic phosphate (Pi)/epp, phosphocreatine (PCr)/epp, and total nucleotide triphosphate (NTP)/epp were measured by 31P MRS and were plotted against Δ[oxCCO] during HI and recovery (epp = exchangeable phosphate pool = Pi + PCr + 2γ-NTP + β-NTP). During HI Δ[oxCCO], PCr/epp and NTP/epp declined and Pi/epp increased. Significant correlations were seen between 31P ratios and Δ[oxCCO]; during HI a threshold point was identified where the relationship between Δ[oxCCO] and both NTP/epp and Pi/epp changed significantly. Outcome at 48 h related to recovery of Δ[oxCCO] and 31P ratios 1 h post-HI (survived: 1-h NTP/epp 0.22 ± 0.02, Δ[oxCCO] − 0.29 ± 0.50 μM; died: 1-h NTP/epp 0.10 ± 0.04, Δ[oxCCO] − 2.41 ± 1.48 μM). Both lowered Δ[oxCCO] and NTP/epp 1 h post-HI indicated mitochondrial impairment. Animals dying before 48 h had slower recovery of both Δ[oxCCO] and 31P ratios by 1 h after HI. 31P MRS correlated with broadband NIRS during and after transient hypoxia–ischemia. A double-linear model best describes NTP/epp vs Δ[oxCCO] during HI. Threshold point in double-linear model interpreted as cessation of ATP manufacture. Poor outcome correlates with weaker recovery of both 31P MRS ratios and Δ[oxCCO]. Mitochondrial dysfunction may be the cause of reduction of Δ[oxCCO].
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影响因子：
2.9
作者：
MATCHER, SJ;ELWELL, CE;DELPY, DT
通讯作者：
DELPY, DT
影响因子：
3.5
作者：
MATCHER, SJ;COOPER, CE
通讯作者：
COOPER, CE
影响因子：
3.4
作者：
Kolyva, Christina;Tachtsidis, Ilias;Elwell, Clare E.
通讯作者：
Elwell, Clare E.
影响因子：
4.7
作者：
Cady, Ernest B.;Iwata, Osuke;Robertson, Nicola J.
通讯作者：
Robertson, Nicola J.
DOI：
10.1098/rstb.1997.0048
发表时间：
1997-06-29
影响因子：
6.3
作者：
Cooper, CE;Springett, R
通讯作者：
Springett, R