Preservation of mitochondrial function with cardiopulmonary resuscitation in prolonged cardiac arrest in rats.
Preservation of mitochondrial function with cardiopulmonary resuscitation in prolonged cardiac arrest in rats.
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DOI：
10.1016/j.yjmcc.2009.09.003
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发表时间：
2009-12
影响因子：
5
通讯作者：
Angelos, Mark G.
中科院分区：
文献类型：
--
作者：
Yeh, Steve T.;Lee, Hsin-Ling;Aune, Sverre E.;Chen, Chwen-Lih;Chen, Yeong-Renn;Angelos, Mark G.
关键词：
在心脏骤停 (CA) 期间，心肌灌注完全依赖于心肺复苏 (CPR)，尽管胸外按压仅提供正常心肌灌注的约 10-20%。该研究在整个动物心肺复苏模型中进行，以确定心肺复苏产生的氧气输送是否会保留或恶化线粒体功能。雄性Sprague-Dawley大鼠（400-450克）被随机分为四组：1）BL（仅使用仪器，无心脏骤停），2）CA15（15分钟心脏骤停，无需CPR），3）CA25（25分钟心脏骤停，无需CPR）和4）CPR（15分钟心脏骤停，然后进行10分钟CPR）。通过透射电子显微镜（TEM）测量线粒体呼吸、电子传递链（ETC）复合物活性和线粒体超微结构来评估组间差异。 CA25 组线粒体呼吸和 ETC 复合物活性受损最严重 (I-III)。相比之下，CPR 组在线粒体功能的所有测量方面与 CA15 组没有不同。复合物 I 比其他复合物更容易受到缺血性损伤，并且是线粒体功能障碍的主要决定因素。 TEM 对线粒体超微结构的观察与生化结果一致。研究结果表明，尽管血流量和氧气输送量较低，心肺复苏仍能够在持续的全身缺血期间保持心脏线粒体功能和活力。临床研究表明，心脏骤停期间复合物 I 活性和线粒体功能的保留可能是 CPR 有益作用的重要机制。
During cardiac arrest (CA), myocardial perfusion is solely dependent on cardiopulmonary resuscitation (CPR) although closed-chest compressions only provide about 10–20% of normal myocardial perfusion. The study was conducted in a whole animal CPR model to determine whether CPR-generated oxygen delivery preserves or worsens mitochondrial function. Male Sprague-Dawley rats (400–450 g) were randomly divided into four groups: 1) BL (instrumentation only, no cardiac arrest), 2) CA15 (15 min cardiac arrest without CPR), 3) CA25 (25 min cardiac arrest without CPR) and 4) CPR (15 min cardiac arrest, followed by 10 min CPR). The differences between groups were evaluated by measuring mitochondrial respiration, electron transport chain (ETC) complex activities and mitochondrial ultrastructure by transmission electron microscopy (TEM). The CA25 group had the greatest impairment of mitochondrial respiration and ETC complex activities (I–III). In contrast, the CPR group was not different from the CA15 group regarding all measures of mitochondrial function. Complex I was more susceptible to ischemic injury than the other complexes and was the major determinant of mitochondrial dysfunction. Observations of mitochondrial ultrastructure by TEM were compatible with the biochemical results. The findings suggest that, despite low blood flow and oxygen delivery, CPR is able to preserve heart mitochondrial function and viability during ongoing global ischemia. Preservation of complex I activity and mitochondrial function during cardiac arrest may be an important mechanism underlying the beneficial effects of CPR which have been shown in clinical studies.
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影响因子：
3
作者：
CHEN, S;GUILLORY, RJ
通讯作者：
GUILLORY, RJ
影响因子：
8.8
作者：
Klawitter, PF;Murray, HN;Angelos, MG
通讯作者：
Angelos, MG
影响因子：
5
作者：
FLAMENG, W;ANDRES, J;VANBELLE, H
通讯作者：
VANBELLE, H
影响因子：
5
作者：
ROUSLIN, W;RANGANATHAN, S
通讯作者：
RANGANATHAN, S
影响因子：
3.9
作者：
WILLIAMS, JN
通讯作者：
WILLIAMS, JN