Effect of Therapy with Oxygen under High Pressure on Regional Cerebral Blood Flow in the Interval Form of Carbon Monoxide Poisoning: Observation from Subtraction of Technetium-99m HMPAO SPECT Brain Imaging

Maeda, Yuta; Kawasaki, Yukiko; Jibiki, Itsuki; Yamaguchi, Nobuo; Matsuda, Hiroshi; Hisada, Kinichi

doi:10.1159/000116698

Cited by 23 publications

(13 citation statements)

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“…Except for 1 H-MRS and diffusion-weighted imaging (DWI) used in this study, conventional MRI, EEG, and single-photon emission computed tomography were proposed previously [8,9,10]. However, there were several problems encountered when these techniques were used in our 2 patients.…”

Section: Discussionmentioning

confidence: 99%

Serial Assessments of Delayed Encephalopathy after Carbon Monoxide Poisoning Using Magnetic Resonance Spectroscopy and Diffusion Tensor Imaging on 3.0T System

Terajima¹,

Igarashi²,

Hirose

et al. 2007

Eur Neurol

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To elucidate the still unclear mechanism of delayed encephalopathy after carbon monoxide (CO) poisoning, we serially performed single-voxel proton magnetic resonance spectroscopy (¹H-MRS) and diffusion tensor imaging (DTI) on a 3.0T system and intelligence tests in 2 patients, while they were undergoing hyperbaric oxygenation therapy. The chronological changes in ¹H-MRS- and DTI-derived parameters indicated the following: (1) White matter demyelination, aerobic metabolism inhibition, and cytotoxic edema persisted for at least 3 months even after starting the hyperbaric oxygenation therapy; (2) the axonal function and structural integrity of the white matter were initially severely impaired and then gradually and partially improved for 5 months, showing changes similar to those in the scores of the intelligence tests. The results demonstrated that brain damage after CO poisoning may persist longer than expected, and that the ¹H-MRS- and DTI-derived parameters are good indicators of the clinical progress of a patient. The combination of ¹H-MRS and DTI on a 3.0T system is useful for monitoring the changes in brain damage and the clinical symptoms of patients with delayed encephalopathy after CO poisoning.

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Section: Discussionmentioning

confidence: 99%

Serial Assessments of Delayed Encephalopathy after Carbon Monoxide Poisoning Using Magnetic Resonance Spectroscopy and Diffusion Tensor Imaging on 3.0T System

Terajima¹,

Igarashi²,

Hirose

et al. 2007

Eur Neurol

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“…The goal of the current investigation was to evaluate the mechanism for cell death and manifestations of oxidative stress in cultured endothelial cells exposed to CO. Studies in humans have suggested that CO exposures will cause vascular and perivascular abnormalities (22)(23)(24)(25); these suggestions increase interest regarding the effects of CO on endothelial cells. Our previous work with experimental animals has shown that CO has a number of effects on the vasculature.…”

mentioning

confidence: 99%

Adaptive responses and apoptosis in endothelial cells exposed to carbon monoxide

Thom

Fisher

et al. 2000

Proc. Natl. Acad. Sci. U.S.A.

176

100

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Prior studies have shown that exposure to carbon monoxide (CO) will elevate the steady-state concentration of nitric oxide ( ⅐ NO) in several cell types and body organs and that some toxic effects of CO are directed toward endothelial cells. Studies reported in this paper were conducted with bovine pulmonary artery endothelial cells exposed to 10 to 100 ppm CO to achieve concentrations between 11 and 110 nM in air-saturated buffer. Exposure to 11 nM CO increased synthesis of manganous superoxide dismutase and conferred resistance against the lethal effects of 110 nM CO. At concentrations of 88 nM CO or more, exposures for 1 h or longer caused cell death that became apparent 18 h after the exposure ceased. Caspase-1 was activated in response to CO, and cell death was inhibited by a caspase-1 inhibitor. Alteration of proteolytic pathways by CO was indicated by the presence of ubiquitincontaining intracellular inclusion bodies. Morphological changes and caspase activation indicated that cell death was an apoptotic process. Cells exposed to 110 nM CO had higher concentrations of manganous superoxide dismutase and heme oxygenase-1 but no changes in glutathione peroxidase, glucose-6-phosphate dehydrogenase, thiols, or catalase. Elevated levels of antioxidant enzymes and apoptosis were inhibited by the nitric oxide synthase inhibitor, S-isopropylisothiourea, and the peroxynitrite scavenger, selenomethionine. These results show that biochemical effects of CO occur at environmentally relevant concentrations, that apoptotic cell death follows exposure to relatively high concentrations of CO, and that these actions of CO are mediated by nitric oxide. C arbon monoxide (CO) is a ubiquitous environmental pollutant. The National Ambient Air Quality Standards in the United States for CO have been set at 35 ppm for a 1-h average exposure, and 9 ppm for an 8-h average exposure. Concentrations of CO found in urban environments have been correlated with hospital admissions, mortality, and morbidity caused by cardiovascular and pulmonary diseases (1-8). Average CO concentrations have been found to be 1-9 ppm, but there are many occupational settings where exposures exceed these levels (9-17). The carboxyhemoglobin values associated with levels of CO typically found in the environment are so low that a direct hypoxic stress is doubtful and compensatory responses are sufficient to maintain tissue oxygenation (18-21). Therefore, the pathophysiological basis for toxic effects of low concentrations of CO is not clear.The goal of the current investigation was to evaluate the mechanism for cell death and manifestations of oxidative stress in cultured endothelial cells exposed to CO. Studies in humans have suggested that CO exposures will cause vascular and perivascular abnormalities (22-25); these suggestions increase interest regarding the effects of CO on endothelial cells. Our previous work with experimental animals has shown that CO has a number of effects on the vasculature. Nitrotyrosine is a major product when peroxynitrite reacts w...

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“…But they failed to get SPECT imaging of acute C O poisoning. Maeda et al [12] also described that changes in SPECT images with 99mTc HM -PAO before and after therapy with oxygen under high pressure were measured in a patient with the interval form of C O poisoning. In the case reported herein, the 2nd SPECT performed after onset of delayed sequelae showed diffuse hypoperfusion throughout the cerebral cortex, and the 3rd SPECT per formed when the patient had recovered completely re vealed markedly increased perfusion to normal.…”

Section: Methodsmentioning

confidence: 99%

Early Hypoperfusion of Technetium-99m Hexamethylprophylene Amine Oxime Brain Single Photon Emission Computed Tomography in a Patient with Carbon Monoxide Poisoning

Choi

Lee

1993

Eur Neurol

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Single photon emission computed tomography (SPECT) with technetium-99m (^99mTc) hexamethylprophylene amine oxime (HM-PAO) were repeatedly performed in a 55-year-old woman with carbon monoxide (CO) poisoning. The initial brain SPECT 10 days after anoxic insult showed focal hypoperfusion which appeared 20 days prior to the onset of delayed neurologic sequelae, and the findings of follow-up SPECTs correlated with the clinical course of CO poisoning. The possibilities of early hypoperfusion on SPECT of acute CO poisoning were discussed.

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Effect of Therapy with Oxygen under High Pressure on Regional Cerebral Blood Flow in the Interval Form of Carbon Monoxide Poisoning: Observation from Subtraction of Technetium-99m HMPAO SPECT Brain Imaging

Cited by 23 publications

References 0 publications

Serial Assessments of Delayed Encephalopathy after Carbon Monoxide Poisoning Using Magnetic Resonance Spectroscopy and Diffusion Tensor Imaging on 3.0T System

Serial Assessments of Delayed Encephalopathy after Carbon Monoxide Poisoning Using Magnetic Resonance Spectroscopy and Diffusion Tensor Imaging on 3.0T System

Adaptive responses and apoptosis in endothelial cells exposed to carbon monoxide

Early Hypoperfusion of Technetium-99m Hexamethylprophylene Amine Oxime Brain Single Photon Emission Computed Tomography in a Patient with Carbon Monoxide Poisoning

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