Mitochondrial Injury in Human Acute Carbon Monoxide Poisoning: The Effect of Oxygen Treatment

被引:34
作者
Garrabou, G. [1 ,2 ]
Inoriza, J. M. [3 ]
Moren, C. [1 ,2 ]
Oliu, G. [3 ]
Miro, O. [1 ,2 ]
Marti, M. J. [3 ]
Cardellach, F. [1 ,2 ]
机构
[1] IDIBAPS Univ Barcelona, Hosp Clin Barcelona, Mitochondrial Res Lab, Muscle Res Unit,Internal Med Dept, Barcelona 08036, Catalunya, Spain
[2] CIBERER, Valencia, Spain
[3] Hosp Palamos, Hyperbar Med Unit, Serv Salut Integrats Baix Emporda, Girona, Spain
关键词
Mitochondrial toxicity; carbon monoxide (CO); hyperbaric oxygen treatment (HBO); normobaric oxygen treatment (NBO); cytochrome c oxidase (COX) or mitochondrial complex IV (mtCIV); oxidative stress (lipid peroxidation); late neurological syndrome (LNS); CYTOCHROME-C-OXIDASE; RESPIRATORY-CHAIN FUNCTION; HYPERBARIC-OXYGEN; RAT-BRAIN; EMERGENCY-DEPARTMENT; LIPID-PEROXIDATION; OXIDATIVE STRESS; ANTIOXIDANT; SMOKING; INHIBITION;
D O I
10.1080/10590501.2011.551316
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
The best oxygen therapy for acute carbon monoxide poisoning (ACOP) remains unestablished. Reported mitochondrial complex IV (mtCIV) inhibition, together with carboxyhaemoglobin (COHb)-induced hypoxia, may influence acute clinical symptoms and outcome. To omitochondriallyo evaluate treatment efficacy, we correlated intoxication severity and symptoms with mitochondrial function (mtCIV activity) and oxidative stress (lipid peroxidation) in 60 poisoned patients and determined ACOP recovery depending on either normobaric or hyperbaric oxygen therapy along a 3-month follow-up. In the present article we positively evaluate mtCIV as a good marker of ACOP recovery, treatment effectiveness, and late neurological syndrome development, which advocates for hyperbaric oxygen therapy as the treatment of choice. However, we discourage its usefulness as a severity marker because of its excessive sensitivity. We additionally evaluate oxidative stress role and prognostic factors for neurological sequelae development.
引用
收藏
页码:32 / 51
页数:20
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