Alterations in cerebral and cardiac mitochondrial function in a porcine model of acute carbon monoxide poisoning.
Alterations in cerebral and cardiac mitochondrial function in a porcine model of acute carbon monoxide poisoning.
复制标题
急性一氧化碳中毒猪模型中脑和心脏线粒体功能的改变。
DOI：
10.1080/15563650.2020.1870691
复制
发表时间：
2021-09
期刊：
影响因子：
--
通讯作者：
Kilbaugh TJ
中科院分区：
文献类型：
--
作者：
Jang DH;Piel S;Greenwood JC;Kelly M;Mazandi VM;Ranganathan A;Lin Y;Starr J;Hallowell T;Shofer FS;Baker WB;Lafontant A;Andersen K;Ehinger JK;Kilbaugh TJ
本研究的目的是建立一氧化碳(CO)中毒的猪模型，以研究脑和心脏线粒体功能的变化。两组大动物CO中毒模型。实验室。将10头猪随机分为两组：对照组(n=4)和对照组(n=6)。CO组给予200ppm的小剂量CO超过90分钟，然后在室内空气中复氧30分钟。对照组吸室内空气120min。采用无创光学监护仪测量脑血流量和氧合情况。进行脑微透析以获得半实时脑代谢状态的测量。暴露结束后，立即采集新鲜脑组织(皮质和海马区组织)和心脏(心尖组织)，测量线粒体呼吸和活性氧(ROS)生成，并采集血液以评估血浆细胞因子浓度。CO组大鼠海马区和心尖区线粒体呼吸显着降低，皮质组织未见明显变化。在所有测量的组织类型中，线粒体ROS的生成也显著增加。CO组大鼠脑组织乳酸/丙酮酸比值显著升高。CO组血浆IL-8和肿瘤坏死因子α水平均显著高于对照组。虽然不显着，但在CO组中，光学测量的脑血流量和血红蛋白浓度有增加的趋势。小剂量一氧化碳中毒与早期线粒体的破坏有关，在可观察到的表型之前，突出了线粒体功能在一氧化碳中毒的病理中的重要作用。这可能代表了一条重要的可干预的治疗和干预途径。
The purpose of this study is the development of a porcine model of carbon monoxide (CO) poisoning to investigate alterations in brain and heart mitochondrial function. Two group large animal model of CO poisoning. Laboratory. Ten swine were divided into two groups: Control (n = 4) and CO (n = 6). Administration of a low dose of CO at 200 ppm to the CO group over 90 min followed by 30 min of re-oxygenation at room air. The Control group received room air for 120 min. Non-invasive optical monitoring was used to measure cerebral blood flow and oxygenation. Cerebral microdialysis was performed to obtain semi real time measurements of cerebral metabolic status. At the end of the exposure, both fresh brain (cortical and hippocampal tissue) and heart (apical tissue) were immediately harvested to measure mitochondrial respiration and reactive oxygen species (ROS) generation and blood was collected to assess plasma cytokine concentrations. Animals in the CO group showed significantly decreased Complex IV-linked mitochondrial respiration in hippocampal and apical heart tissue but not cortical tissue. There also was a significant increase in mitochondrial ROS generation across all measured tissue types. The CO group showed a significantly higher cerebral lactate-to-pyruvate ratio. Both IL-8 and TNFα were significantly increased in the CO group compared with the Control group obtained from plasma. While not significant there was a trend to an increase in optically measured cerebral blood flow and hemoglobin concentration in the CO group. Low-dose CO poisoning is associated with early mitochondrial disruption prior to an observable phenotype highlighting the important role of mitochondrial function in the pathology of CO poisoning. This may represent an important intervenable pathway for therapy and intervention.
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影响因子：
4.7
作者：
Doll DN;Rellick SL;Barr TL;Ren X;Simpkins JW
通讯作者：
Simpkins JW
影响因子：
6.1
作者：
Huang YQ;Peng ZR;Huang FL;Yang AL
通讯作者：
Yang AL
影响因子：
7.4
作者：
Cadenas, E;Davies, KJA
通讯作者：
Davies, KJA
DOI：
10.1016/j.ajem.2017.08.048
发表时间：
2018-03
期刊：
The American journal of emergency medicine
影响因子：
--
作者：
Ran T;Nurmagambetov T;Sircar K
通讯作者：
Sircar K
DOI：
10.1093/ejcts/ezx467
发表时间：
2018-07-01
期刊：
European journal of cardio-thoracic surgery : official journal of the European Association for Cardio-thoracic Surgery
影响因子：
--
作者：
Mavroudis CD;Karlsson M;Ko T;Hefti M;Gentile JI;Morgan RW;Plyler R;Mensah-Brown KG;Boorady TW;Melchior RW;Rosenthal TM;Shade BC;Schiavo KL;Nicolson SC;Spray TL;Sutton RM;Berg RA;Licht DJ;Gaynor JW;Kilbaugh TJ
通讯作者：
Kilbaugh TJ