Delayed encephalopathy after acute carbon monoxide poisoning: a case study.

Delayed encephalopathy after acute carbon monoxide poisoning (DEACMP) is a relatively rare inflammatory-associated neurometabolic complication. In this article, we present a case report of a 50-year-old male patient with a history of carbon monoxide poisoning. This acute poisoning, although successfully controlled during a stay in the intensive care unit of a local hospital, later led to persistent neurological symptoms. The patient was then treated in the inpatient unit of the rehabilitation clinic, where cognitive deterioration began to develop 20 days after admission. Subsequent examination using EEG and magnetic resonance imaging confirmed severe encephalopathy later complicated by SARS-CoV-2 infection with fatal consequences due to bronchopneumonia. Because currently there are no approved guidelines for the management of DEACMP, we briefly discuss the existing challenges for future studies, especially the application of rational immunosuppressive therapy already in the acute treatment phase of CO poisoning, which could prevent the development of a severe form of DEACMP.

The Role of Bismuth in Suppressing the CO Poisoning in Alkaline Methanol Electrooxidation: Switching the Reaction from the CO to Formate Pathway.

While tuning the electronic structure of Pt can thermodynamically alleviate CO poisoning in direct methanol fuel cells, the impact of interactions between intermediates on the reaction pathway is seldom studied. Herein, we contrive a PtBi model catalyst and realize a complete inhibition of the CO pathway and concurrent enhancement of the formate pathway in the alkaline methanol electrooxidation. The key role of Bi is enriching OH adsorbates (OHad) on the catalyst surface. The competitive adsorption of CO adsorbates (COad) and OHad at Pt sites, complementing the thermodynamic contribution from alloying Bi with Pt, switches the intermediate from COad to formate that circumvents CO poisoning. Hence, 8% Bi brings an approximately 6-fold increase in activity compared to pure Pt nanoparticles. This notion can be generalized to modify commercially available Pt/C catalysts by a microwave-assisted method, offering opportunities for the design and practical production of CO-tolerance electrocatalysts in an industrial setting.

Phase Engineering of Intermetallic PtBi2 Nanoplates for Formic Acid Electrochemical Oxidation.

Phase engineering of Pt-based intermetallic catalysts has been demonstrated as a promising strategy to optimize catalytic properties for a direct formic acid fuel cell. Pt-Bi intermetallic catalysts are attracting increasing interest due to their high catalytic activity, especially for inhibiting CO poisoning. However, the phase transformation and synthesis of intermetallic compounds usually occurring at high temperatures leads to a lack of control of the size and composition. Here, we report the synthesis of intermetallic ß-PtBi2 and γ-PtBi2 two-dimensional nanoplates with controlled sizes and compositions under mild conditions. The different phases of intermetallic PtBi2 can significantly affect the catalytic performance of the formic acid oxidation reaction (FAOR). The obtained ß-PtBi2 nanoplates exhibit an excellent mass activity of 1.1 ± 0.01 A mgPt-1 for the FAOR, which is 30-fold higher than that of commercial Pt/C catalysts. Moreover, intermetallic PtBi2 demonstrates high tolerance to CO poisoning, as confirmed by in situ infrared absorption spectroscopy.

Graphitic Armor: A Natural Molecular Sieve for Robust Hydrogen Electroxidation.

Carbon coating layers have been found to improve the catalytic performance of transition metals, which is usually explained as an outcome of electronic synergistic effect. Herein we reveal that the defective graphitic carbon, with a unique interlayer gap of 0.342 nm, can be a highly selective natural molecular sieve. It allows efficient diffusion of hydrogen molecules or radicals both along the in-plane and out-of-plane direction, but sterically hinders the diffusion of molecules with larger kinetic diameter (e.g., CO and O2) along the in-plane direction. As a result, poisonous species lager than 0.342 nm are sieved out, even when their adsorption on the metal is thermodynamically strong; at the same time, the interaction between H2 and the metal is not affected. This natural molecular sieve provides a very chance for constructing robust metal catalysts for hydrogen-relevant processes, which are more tolerant to chemical or electrochemical oxidation or CO-relevant poisoning.

Dilute RuCo Alloy Synergizing Single Ru and Co Atoms as Efficient and CO-Resistant Anode Catalyst for Anion Exchange Membrane Fuel Cells.

Ruthenium (Ru) is considered a promising candidate catalyst for alkaline hydroxide oxidation reaction (HOR) due to its hydrogen binding energy (HBE) like that of platinum (Pt) and its much higher oxygenophilicity than that of Pt. However, Ru still suffers from insufficient intrinsic activity and CO resistance, which hinders its widespread use in anion exchange membrane fuel cells (AEMFCs). Here, we report a hybrid catalyst (RuCo)NC+SAs/N-CNT consisting of dilute RuCo alloy nanoparticles and atomically single Ru and Co atoms on N-doped carbon nanotubes The catalyst exhibits a state-of-the-art activity with a high mass activity of 7.35 A mgRu -1. More importantly, when (RuCo)NC+SAs/N-CNT is used as an anode catalyst for AEMFCs, its peak power density reaches 1.98 W cm-2, which is one of the best AEMFCs properties of noble metal-based catalysts at present. Moreover, (RuCo)NC+SAs/N-CNT has superior long-time stability and CO resistance. The experimental and density functional theory (DFT) results demonstrate that the dilute alloying and monodecentralization of the exotic element Co greatly modulates the electronic structure of the host element Ru, thus optimizing the adsorption of H and OH and promoting the oxidation of CO on the catalyst surface, and then stimulates alkaline HOR activity and CO tolerance of the catalyst.

Self-Accelerating Effect in a Covalent-Organic Framework with Imidazole Groups Boosts Electroreduction of CO2 to CO.

Solvent effect plays an important role in catalytic reaction, but there is little research and attention on it in electrochemical CO2 reduction reaction (eCO2 RR). Herein, we report a stable covalent-organic framework (denoted as PcNi-im) with imidazole groups as a new electrocatalyst for eCO2 RR to CO. Interestingly, compared with neutral conditions, PcNi-im not only showed high Faraday efficiency of CO product (≈100 %) under acidic conditions (pH ≈ 1), but also the partial current density was increased from 258 to 320 mA cm-2 . No obvious degradation was observed over 10 hours of continuous operation at the current density of 250 mA cm-2 . The mechanism study shows that the imidazole group on the framework can be protonated to form an imidazole cation in acidic media, hence reducing the surface work function and charge density of the active metal center. As a result, CO poisoning effect is weakened and the key intermediate *COOH is also stabilized, thus accelerating the catalytic reaction rate.

Early predictors of brain injury in patients with acute carbon monoxide poisoning and the neuroprotection of mild hypothermia.

INTRODUCTION: Carbon monoxide (CO) poisoning can cause serious neurological sequelae. However, there is neither effective treatment strategy nor reliable indicators to determine the prognosis of patients with CO poisoning. The present study aimed to observe the changes of neurological function score, disease severity score, cerebral oxygen utilization (O2UCc), bispectral (BIS) index and neuron-specific enolase (NSE) concentration, and to elucidate the clinical significance of these potential indicators and the neuroprotective effect of mild hypothermia on brain injury in patients with severe acute CO poisoning. MATERIALS AND METHODS: A total of 277 patients with acute severe CO poisoning from 2013 to 2018 were enrolled in our hospital. Patients were divided into three groups according to their body temperature on the day of admission and their willingness to treat: a fever group (n = 78), a normal temperature group (NT group, n = 113), and a mild hypothermia group (MH group, n = 86). All patients were given hyperbaric oxygen therapy, while those in the MH group received additional mild hypothermia treatment. The severity of the disease, the neurobehavioral status, the incidence of delayed encephalopathy after acute carbon monoxide poisoning (DEACMP), and other indicators including BIS, O2UCc, NSE were further evaluated in all patients at given time-points. RESULTS: Mild hypothermia therapy improved the prognosis of patients with CO poisoning, significantly decreased the value of O2UCc and NSE, and up-regulated BIS. The incidence of DEACMP at 6 months was 27% in the fever group, 23% in the NT group, and 8% in the MH group. The values of Glasgow-Pittsburgh coma scale (G-P score), BIS index and NSE were closely related to the occurrence of DEACMP, the cutoff values were 12.41, 52.17 and 35.20 ng/mL, and the sensitivity and specificity were 79.3%, 77.6%, 79.3% and 67.6%, 89.5%, 88.6% in the receiver operating characteristic curve (ROC), respectively. CONCLUSIONS: Early mild hypothermia treatment could significantly reduce the severity of brain injury after CO poisoning, and might be further popularized in clinic. G-P scores, NSE and BIS index can be regarded as the prediction indicators in the occurrence and development of DEACMP. CLINICAL TRIAL REGISTRATION: The study protocol was granted from Qingdao University Research Ethics Committee (Clinical trial registry and ethical approval number: QD81571283).

Molecular-Level Insights into the Notorious CO Poisoning of Platinum Catalyst.

Carbon monoxide (CO) is notorious for its strong adsorption to poison platinum group metal catalysts in the chemical industry. Here, we conceptually distinguish and quantify the effects of the occupancy and energy of d electrons, emerging as the two vital factors in d-band theory, for CO poisoning of Pt nanocatalysts. The stepwise defunctionalization of carbon support is adopted to fine-tune the 5d electronic structure of supported Pt nanoparticles. Excluding other promotional mechanisms, the increase of Pt 5d band energy strengthens the competitive adsorption of hydrogen against CO for the preferential oxidation of CO, affording the scaling relationship between Pt 5d band energy and CO/H2 adsorption energy difference. The decrease of Pt 5d band occupancy lowers CO site coverage to promote its association with oxygen for the total oxidation of CO, giving the scaling relationship between Pt 5d occupancy and activation energy. The above insights outline a molecular-level understanding of CO poisoning.

A neuroglobin-based high-affinity ligand trap reverses carbon monoxide-induced mitochondrial poisoning.

Carbon monoxide (CO) remains the most common cause of human poisoning. The consequences of CO poisoning include cardiac dysfunction, brain injury, and death. CO causes toxicity by binding to hemoglobin and by inhibiting mitochondrial cytochrome c oxidase (CcO), thereby decreasing oxygen delivery and inhibiting oxidative phosphorylation. We have recently developed a CO antidote based on human neuroglobin (Ngb-H64Q-CCC). This molecule enhances clearance of CO from red blood cells in vitro and in vivo Herein, we tested whether Ngb-H64Q-CCC can also scavenge CO from CcO and attenuate CO-induced inhibition of mitochondrial respiration. Heart tissue from mice exposed to 3% CO exhibited a 42 ± 19% reduction in tissue respiration rate and a 33 ± 38% reduction in CcO activity compared with unexposed mice. Intravenous infusion of Ngb-H64Q-CCC restored respiration rates to that of control mice correlating with higher electron transport chain CcO activity in Ngb-H64Q-CCC-treated compared with PBS-treated, CO-poisoned mice. Further, using a Clark-type oxygen electrode, we measured isolated rat liver mitochondrial respiration in the presence and absence of saturating solutions of CO (160 µm) and nitric oxide (100 µm). Both CO and NO inhibited respiration, and treatment with Ngb-H64Q-CCC (100 and 50 µm, respectively) significantly reversed this inhibition. These results suggest that Ngb-H64Q-CCC mitigates CO toxicity by scavenging CO from carboxyhemoglobin, improving systemic oxygen delivery and reversing the inhibitory effects of CO on mitochondria. We conclude that Ngb-H64Q-CCC or other CO scavengers demonstrate potential as antidotes that reverse the clinical and molecular effects of CO poisoning.

Doping Platinum with Germanium: An Effective Way to Mitigate the CO Poisoning.

The vulnerability towards CO poisoning is a major drawback affecting the efficiency and long-term performance of platinum catalysts in fuel cells. In the present work, by a combination of density functional theory calculations and mass spectrometry experiments, we test and explain the promotional effect of Ge on Pt catalysts with higher resistance to deactivation via CO poisoning. A thorough exploration of the configurational space of gas-phase Ptn + and GePtn-1 + (n=5-9) clusters using global minima search techniques and the subsequent electronic structure analysis reveals that germanium doping reduces the binding strength between Pt and CO by hindering the 2π-back-donation. Importantly, the clusters remain catalytically active towards H2 dissociation. The ability of Ge to weaken the Pt-CO interaction was confirmed by mass spectrometry experiments. Ge can be a promising alloying agent to tune the selectivity and improve the durability of Pt particles, thus opening the way to novel catalytic alternatives for fuel cells.

Neuroprotective effect of targeted regulatory Nrf2 gene on rats with acute brain injury induced by carbon monoxide poisoning.

Oxidative stress has been considered as an important cause of neurocyte damage induced by carbon monoxide (CO) poisoning; however, the precise mechanisms are not fully understood. The study aimed to elucidate the molecular mechanism and the neuroprotective effect of targeted regulatory nuclear factor erythroid2-related factor 2 (Nrf2) gene on acute brain injury in CO poisoning rats. An acute CO poisoning rat model was established by CO inhalation in hyperbaric oxygen chamber and followed by the administration of Nrf2 gene-loaded lentivirus. Mitochondrial membrane potential (ΔΨM), the levels of Nrf2, glutamate-cysteine ligase catalytic subunit (GCLC), catalase (CAT) and glutathione peroxidase (GSH-Px), and cell apoptosis were determined in brain tissue in rats. We found that CO poisoning could decrease ΔΨm of cells, slightly increase the expressions of Nrf2 and GCLC at mRNA and protein levels, reduce CAT and GSH-Px, and thus initiate apoptosis process. The Nrf2 gene treatment could obviously enhance the expressions of Nrf2 at mRNA and protein levels, and increase the concentrations of CAT and GSH-Px, maintain the ΔΨm of cells in brain tissue, significantly inhibit cell apoptosis as compared with the CO poisoning group (p < .05). These findings suggest that CO poisoning could induce oxidative stress and impair mitochondrial function of cells in brain tissue. The administration of Nrf2 gene could notably strengthen the antioxidant capacity of cells through regulating the downstream genes of Nrf2/antioxidant responsive element signal pathway, and positively protect cells against brain injury induced by acute severe CO poisoning.

Association Between Carbon Monoxide Intoxication and Incidence of Ischemic Stroke: A Retrospective Nested Case-Control Study in South Korea.

OBJECTIVES: Severe neurological sequelae occur in patients with carbon monoxide (CO) intoxication; however, whether the latter increases the long-term risk of developing ischemic stroke is unclear. We investigated the association between CO intoxication and ischemic stroke using data from the Korean National Health Information Database. MATERIALS AND METHODS: We performed a retrospective, nested case-control study of 27,984 individuals treated for CO intoxication and 27,984 sex- and age-matched controls. Initially, we calculated the overall incidence and hazard ratio (HR) of ischemic stroke using conditional logistic regression. Thereafter, we calculated the incidences and HRs according to covariates and follow-up periods. RESULTS: The CO intoxication group had a significantly higher risk of developing ischemic stroke than the control group (adjusted HR 2.31, 95% CI [confidence interval] = 2.01-2.65). Male sex (adjusted HR 2.73, 95% CI = 2.23-3.34), age <40 (adjusted HR 3.53, 95% CI = 2.15-5.82), low income (adjusted HR 2.55, 95% CI = 1.56-4.15), comorbidities (adjusted HR 2.59, 95% CI = 1.48-4.52), and current smokers (adjusted HR 3.55, 95% CI = 1.67-7.60) had a higher risk of ischemic stroke. The risk of ischemic stroke was highest within 2 years after CO intoxication (adjusted HR 7.47, 95% CI = 2.76-20.26), and even >6 years after, the risk remained significantly higher than in the control group (adjusted HR 1.84, 95% CI = 1.53-2.20). CONCLUSIONS: CO intoxication and the long-term risk of ischemic stroke are associated.

Knowledge about carbon monoxide poisoning among medical and non-medical students living in Kraków - questionnaire study.

O b j e c t i v e s: Accidental exposure to non-fire related carbon monoxide (CO) in young people is largely unquantified. Our aim was to estimate the possibility of exposure to CO and the awareness of intoxication in the population of students living in Kraków, one of the largest academic cities in Poland. M e t h o d s: Anonymous questionnaires about CO poisoning were distributed among medical and non-medical students living in Kraków. R e s u l t s: 1081 questionnaires were collected - 16% of study participants knew a person who had been poisoned with carbon monoxide, 51.2% of students using a bathroom water heater believed that they had no risk of CO poisoning. Medical students gained significantly higher scores in the CO-poisoning knowledge test than non-medical ones. C o n c l u s i o n s: There is still unsatisfactory awareness of CO poisoning among non-medical students in Kraków.

Argyrophilic nucleolar organizer regions as a promising biomarker for the detection of brain hypoxia levels caused by different doses of carbon monoxide poisoning.

OBJECTIVES: The purpose of the study is to investigate whether there is any relationship between mean argyrophilic nucleolar organizing regions (AgNOR) number and total AgNOR area/total nuclear area (TAA/TNA) ratio and the levels of brain hypoxia after exposure to different acute doses of carbon monoxide (CO) gas. METHODS: Each experimental group was exposed to CO gas (concentrations of 1,000, 3,000 and 5,000 ppm). Then, the rats were anesthetized, and blood samples were taken from the right jugular vein for carboxyhemoglobin levels detection. The rats were sacrificed on seventh day. AgNOR staining was applied to brain tissues. TAA/TNA and mean AgNOR number were detected for each nucleus. RESULTS: Significant differences were detected among all groups for TAA/TNA ratio, mean AgNOR number and carboxyhemoglobin level. According to a double comparison of groups, the differences between control and 1,000 ppm, control and 3,000 ppm, control and 5,000 ppm, and between 1,000 and 5,000 ppm were significant for TAA/TNA ratio. When mean AgNOR number was considered, significant differences were detected between control and 1,000 ppm, control and 3,000 ppm, control and 5,000 ppm, and between 1,000 and 3,000 ppm. CONCLUSION: AgNOR proteins may be used for early detection of the duration, intensity, and damage of brain injury caused by CO poisoning. Thus, effective treatment strategies can be developed for the prevention of hypoxic conditions.

OBJETIVOS: El objetivo del estudio es investigar si existe alguna relación entre el número medio de regiones organizadoras nucleolares argirófilas (AgNOR) y la proporción de área total de AgNOR/área nuclear total (TAA/TNA) y los niveles de ­hipoxia cerebral en la exposición a diferentes dosis agudas de gas monóxido de carbono (CO). MÉTODOS: Cada grupo experimental fue expuesto a gas CO (concentraciones de 1,000, 3,000 y 5,000 ppm). Luego las ratas fueron anestesiadas, se tomaron muestras de sangre de la vena yugular derecha para la detección de los niveles de carboxihemoglobina. Las ratas se sacrificaron el séptimo día. Se aplicó tinción con AgNOR en los tejidos cerebrales. Se detectaron el TAA/TNA y el número medio de AgNOR para cada núcleo. RESULTADOS: Se detectaron diferencias significativas entre todos los grupos para la relación TAA/TNA, el número medio de AgNOR y el nivel de carboxihemoglobina. Según la doble comparación de grupos, las diferencias entre control y 1,000 ppm, control y 3,000 ppm, control y 5,000 ppm y 1,000 y 5,000 ppm fueron significativas para la relación TAA/TNA. Cuando se consideró el número de AgNOR medio, se detectaron diferencias significativas entre control y 1,000ppm, control y 3,000ppm, control y 5,000 ppm y 1,000 y 3,000 ppm. CONCLUSIÓN: Las proteínas AgNOR pueden usarse para la detección temprana de la duración, intensidad y daño de la lesión cerebral causada por la intoxicación por CO. Por lo tanto, se pueden desarrollar estrategias de tratamiento efectivas para la prevención de condiciones hipóxicas.

A carbon monoxide poisoning case due to lung diffusion test.

Carbon monoxide (CO) poisoning occurs due to CO gas which is produced by the incomplete combustion of hydrocarbons. Several causes of CO poisoning have been defined in the literature. The most frequent causes are defective heaters, fires and exposure to exhaust gas in closed areas. The lung diffusion test is a method used to detect alveolar membrane diffusion capacity. The standart gas used in the diffusion test is CO. The case is here presented of a patient who was poisoned by CO during a DLCO test. To the best of our knowledge, this is the first case report defining CO poisoning during a DLCO test and treated at the Emergency Department.

Atomic Carbon Layers Supported Pt Nanoparticles for Minimized CO Poisoning and Maximized Methanol Oxidation.

Maximizing activity of Pt catalysts toward methanol oxidation reaction (MOR) together with minimized poisoning of adsorbed CO during MOR still remains a big challenge. In the present work, uniform and well-distributed Pt nanoparticles (NPs) grown on an atomic carbon layer, that is in situ formed by means of dry-etching of silicon carbide nanoparticles (SiC NPs) with CCl4 gas, are explored as potential catalysts for MOR. Significantly, as-synthesized catalysts exhibit remarkably higher MOR catalytic activity (e.g., 647.63 mA mg-1 at a peak potential of 0.85 V vs RHE) and much improved anti-CO poisoning ability than the commercial Pt/C catalysts, Pt/carbon nanotubes, and Pt/graphene catalysts. Moreover, the amount of expensive Pt is a few times lower than that of the commercial and reported catalyst systems. As confirmed from density functional theory (DFT) calculations and X-ray absorption fine structure (XAFS) measurements, such high performance is due to reduced adsorption energy of CO on the Pt NPs and an increased amount of adsorbed energy OH species that remove adsorbed CO fast and efficiently. Therefore, these catalysts can be utilized for the development of large-scale and industry-orientated direct methanol fuel cells.

CO Gas Induced Phase Separation in PtPb@Pt Catalyst and Formation of Ultrathin Pb Nanosheets Probed by In Situ Transmission Electron Microscopy.

PtPb@Pt catalysts are very useful and widely applied in various industrial reactions. Here, the phase stability of such catalysts is compared in both CO gas and vacuum conditions at elevated temperatures using aberration-corrected in situ transmission electron microscopy (TEM). A Pt aggregation process takes place affected by CO gas, which results in direct exposure of the PtPb core to CO. A phase separation process, in which Pb atoms are stripped off the original PtPb@Pt nanoparticles, is unambiguously identified in CO gas. At initial stages, the as nucleated Pb islands are amorphous. Once the ultrathin Pb islands reach ≈3.5 nm or higher, they suddenly became crystalline. The interaction between Pb and CO gas stabilizes the ultrathin Pb nanosheets, resulting in the formation of a large quantity of Pb nanosheets and Pb-depleted PtPb0.08 nanoparticles. In sharp contrast, when heated up in a vacuum, the PtPb@Pt catalyst remains intact. The results of this study shine light on the "toxic" effect of CO that results in failures of many Pt-based catalysts and discloses formation mechanism of ultrathin Pb nanosheets.

Garage carbon monoxide levels from sources commonly used in intentional poisoning.

BACKGROUND: The incidence of intentional carbon monoxide (CO) poisoning is believed to have declined due to strict federal CO emissions standards for motor vehicles and the uniform application of catalytic converters (CC). We sought to compare ambient CO levels produced by automobiles with and without catalytic converters in a residential garage, as well as from other CO sources commonly used for intentional poisoning. METHODS: CO levels were measured inside a freestanding 73 m3 one-car garage. CO sources included a 1971 automobile without CC, 2003 automobile with CC, charcoal grill, electrical generator, lawn mower and leaf blower. RESULTS: After 20 minutes of operation, the CO level in the garage was 253 PPM for the car without a catalytic converter and 30 PPM for the car equipped withone. CO levels after operating or burning the other sources were: charcoal 200 PPM; generator >999 PPM; lawn mower 198 PPM; and leaf blower 580 PPM. CONCLUSIONS: While emissions controls on automobiles have reduced intentional CO poisonings, alternate sources may produce CO at levels of the same magnitude as vehicles manufactured prior to the use of catalytic converters. Those involved in the care of potentially suicidal individuals should be aware of this.

Effects of hyperbaric oxygen on hippocampal neuronal apoptosis in rats with acute carbon monoxide poisoning.

INTRODUCTION: Acute carbon monoxide (CO) poisoning causes serious health problems such as neuropsychological sequelae. This study aimed to investigate neuronal apoptosis and the effects of hyperbaric oxygen (HBO2) on different regions of the rat hippocampus after CO poisoning. METHODS: 90 mature male Sprague Dawley rats were randomly divided into three groups: the normal control group (NC group), the acute carbon monoxide-poisoned group (CO group) and the hyperbaric oxygen treatment group (HBO2 group). CO exposure included 0, 1, 3, 7, 14 and 21 treatment days, one exposure on the first day, and sacrifice on each of the following days. HBO2 exposure included treatment for 0, 1, 3, 7, 14 and 21 days, daily treatment after CO exposure, and sacrifice after the last HBO2 treatment on each of those days. Hematoxylin-eosin staining, immunohistochemical staining, immunofluorescence staining, and western blot analysis were performed to detect apoptosis in brain tissue samples. RESULTS: MMP-9 and caspase-3 were prominently increased by CO exposure and inhibited by HBO2 in the CA3 region in the hippocampus at one, three and seven days (immunohistochemical staining [IHC]: P ⟨ 0.05). Neu N and the ratio of Bcl-2/ BAX were prominently decreased by CO exposure and rescued by HBO2 in the CA3 region after seven days of treatment (IHC: P ⟨ 0.05). CONCLUSION: These findings indicated that neuronal apoptosis in the rat hippocampus could be induced by acute CO exposure, especially in the CA3 region. HBO2 could effectively inhibit neuronal apoptosis, especially in the CA3 region after seven days of treatment. The application of HBO2 to inhibit MMP-9 and apoptosis may contribute to brain recovery after acute CO poisoning.

Brain temperature measured by 1H-magnetic resonance spectroscopy in acute and subacute carbon monoxide poisoning.

INTRODUCTION: Brain temperature (BT) is associated with the balance between cerebral blood flow and metabolism according to the "heat-removal" theory. The present study investigated whether BT is abnormally altered in acute and subacute CO-poisoned patients by using (1)H-magnetic resonance spectroscopy (MRS). METHODS: Eight adult CO-poisoned patients underwent 3-T magnetic resonance imaging in the acute and subacute phases after CO exposure. MRS was performed on deep cerebral white matter in the centrum semiovale, and MRS-based BT was estimated by the chemical shift difference between water and the N-acetyl aspartate signal. We defined the mean BT + 1.96 standard deviations of the BT in 15 healthy controls as the cutoff value for abnormal BT increases (p < 0.05) in CO-poisoned patients. RESULTS: BT of CO-poisoned patients in both the acute and subacute phases was significantly higher than that of the healthy control group. However, BT in the subacute phase was significantly lower than in the acute phase. On the other hand, no significant difference in body temperature was observed between acute and subacute CO-poisoned patients. BT weakly correlated with body temperature, but this correlation was not statistically significant (rho = 0.304, p = 0.2909). CONCLUSIONS: The present results suggest that BT in CO-poisoned patients is abnormally high in the acute phase and remains abnormal in the subacute phase. BT alteration in these patients may be associated with brain perfusion and metabolism rather than other factors such as systemic inflammation and body temperature.