Acute Carbon Research Articles

Assessment of sTWEAK protein, neutrophil-lymphocyte ratio, blood lactate and carboxyhemoglobin as predictors of delayed neurological sequelae after acute carbon

Assessment of sTWEAK protein, neutrophil-lymphocyte ratio, blood lactate and carboxyhemoglobin as predictors of delayed neurological sequelae after acute carbon

Preventive effect of salmon sperm DNA on acute carbon tetrachloride-induced liver injury in mice through Nrf2/ARE and mitochondrial apoptosis pathway.

Liver injury refers to the damage of liver function, which will seriously harm the body's health if it is not prevented and treated in time. Sporadic researches have reported that ingestion of DNA has a hepatoprotective effect, but its effect and mechanism were not clarified. The purpose of this study was to explore the preventive effect and mechanism of salmon sperm DNA on acute liver injury in mice induced by carbon tetrachloride (CCl4). Six-week-old ICR (Institute of Cancer Research) male mice were used to establish a liver injury model by injecting with 4% CCl4, silymarin, and three different concentrations of DNA solutions were given to mice by gavage for 14 days. The histological and pathological changes in the liver were observed. The levels of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) in serum and the levels of oxidative and antioxidant markers such as malondialdehyde (MDA), superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and glutathione (GSH) in liver tissue were determined. The levels of interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) were detected by enzyme-linked immunosorbent assay (ELISA), and hepatic oxidative stress and apoptosis-related markers were determined by western blotting. The results showed that compared with the model group, the DNA test group significantly improved the liver pathological changes and the level of liver function, regulated liver oxidative stress, reduced hepatocyte apoptosis, and decreased the levels of inflammatory factors such as TNF-α and IL-6. Compared with the silymarin group, the high dose of DNA was even more effective in preventing liver injury. In conclusion, salmon sperm DNA has a potential protective effect against acute liver injury induced by CCl4, which is achieved by regulating the Nrf2/ARE (nuclear factor erythroid 2 (NF-E2)-related factor 2/antioxidant responsive element) oxidative stress pathway and mitochondrial apoptosis pathway.

The neuroprotective effect of targeted regulation Nrf2 gene on injured brain caused by acute severe carbon monoxide poisoning in rats

Objective To explore the neuroprotective effect of targeted regulation Nrf2 gene on rats with brain injury caused by acute severe carbon monoxide (CO) poisoning. Methods A total of 180 healthy adult SD rats were divided into 4 groups at random: normal control group(NC group), CO poisoning group(CO group), lentivirus group(LV group) and Nrf2 gene therapy group(Nrf2 group), and 45 rats in each group. An acute CO toxic rat model was established by inhalation in a hyperbaric oxygen tank. The lentivirus group was directly injected with lentivirus dilution (4×106 TU/μl) into striatum with a microsyringe guided by a stereotactic apparatus, and the Nrf2 gene therapy group was administrated the same dose of recombinant Nrf2 gene lentivirus dilution, while rats in the normal control group and the CO poisoning group were received the same amount of normal saline. Five rats were taken and decapitated at day 1, day 7 and week 2 from each group, respectively. The mitochondrial membrane potential (MMP) of neurons in brain tissue was detected by JC-1 method, and the expressions of Nrf2 and GCLC proteins were observed by immunohistochemistry and Western Blot. Results Compared with the NC group (cortex: (75.3±6.8); hippocampus: (76.4±7.1); striatum: (73.8±7.3)) at the same time point, the MMPs of neurons in CO group (cortex: (34.5±6.7); hippocampus: (30.3±5.6); striatum: (41.5±6.1) and LV group (cortex: (36.8±6.2); hippocampus: (30.8±6.0); striatum: (42.7±6.3)) were significantly decreased, and the difference was significant(P 0.05). A small amount of Nrf2 protein (0.22±0.05) and GCLC protein (0.24±0.04) were expressed in the brain tissue of normal control rats. The expressions of Nrf2 protein (0.31±0.06, 0.31±0.05) and GCLC protein (0.30±0.04, 0.31±0.07) in CO group and LV group were slightly increased (P 0.05). The MMPs value of nerve cells in the Nrf2 group (cortex: (53.3±5.3); hippocampus: (56.9±6.1); striatum: (60.6±6.0)) also decreased, but it was significantly higher than that in the CO group and the LV group at the same time point (P 0.05). Conclusion CO poisoning could induce oxidative stress and damage mitochondrial function of nerve cells. The active state of targeted regulation Nrf2 could significantly enhance the antioxidant capacity of rats and positively protect rats against brain injury induced by acute severe CO poisoning. Key words: Carbon monoxide poisoning; Brain injury; Mitochondrial membrane potential; Nuclear factor E2 related factor 2

Serum N-terminal proBNP, not troponin I, at presentation predicts long-term neurologic outcome in acute charcoal-burning carbon monoxide intoxication

Objective: This study aimed to investigate whether the serum N-terminal pro-brain natriuretic peptide (NT-proBNP) and troponin I levels at emergency department (ED) presentation predict long-term neurologic outcomes after acute charcoal-burning carbon monoxide (CO) poisoning.Methods: This retrospective study included 220 patients suffering from charcoal-burning CO poisoning. The demographics, serum NT-proBNP and troponin I levels at ED presentation, treatment, clinical course during hospitalization, and long-term neurologic outcomes were collected.Results: The median serum NT-proBNP level at presentation was 48.8 (16.5–259) pg/mL, and 78 patients (35.5%) had elevated troponin I (>0.04 ng/mL) after acute charcoal-burning CO poisoning. The upper NT-proBNP and elevated troponin I groups had higher prevalences of respiratory failure, hypotension, and myocardial injury during hospitalization and altered mentality (GCS ≤14) at discharge than the lower NT-proBNP and normal troponin I groups. The incidence of persistent severe neurologic sequelae at 25 months after acute CO poisoning was 10.9%. The upper NT-proBNP and elevated troponin I groups had a higher incidence of poor long-term neurologic outcome than the counterpart groups. Log-transformed NT-proBNP and elevated troponin I were associated with poor long-term neurologic outcome in the univariate analysis, but only the adjusted log-transformed NT-proBNP remained an independent factor in the multivariate analysis. Compared with a predictive model including previously proposed predictors, the addition of log NT-proBNP improved the diagnostic accuracy for predicting poor long-term neurologic outcome. The serum NT-proBNP values for predicting poor long-term neurologic outcome were 74.6 and 32.7 pg/mL at fixed sensitivities of 95 and 99%, respectively.Conclusions: Elevated serum NT-proBNP at ED presentation is correlated with a risk of poor long-term neurologic outcome after discharge in cases of acute charcoal-burning CO poisoning. NT-proBNP could significantly improve the risk stratification of patients who will experience poor long-term neurologic outcome after CO poisoning. This potentially valuable marker should be further validated.

Initial diffusion-weighted MRI and long-term neurologic outcomes in charcoal-burning carbon monoxide poisoning

Context: This study assessed the results of diffusion-weighted imaging (DWI) at presentation for acute charcoal-burning carbon monoxide (CO) poisoning and investigated whether the initial DWI results can predict long-term neurologic outcomes.Methods: The study included 128 patients who suffered from CO poisoning after burning charcoal and underwent DWI. These patients were divided into two groups based on imaging results: a normal DWI group and an abnormal DWI group. Data regarding clinical courses and long-term neurologic outcomes (persistent severe neurologic sequelae) were collected and compared.Results: The rate of abnormal DWI findings at presentation was 23.4%, and the most common site of abnormalities was the globus pallidus. All lesions in abnormal DWI had decreased apparent diffusion coefficient (ADC) values. The long-term neurologic state was assessed at a median follow-up of 19.5 months, and the frequency of poor long-term neurologic outcome was significantly higher in the abnormal DWI group (40.0% in the abnormal DWI group vs. 1.0% in the normal DWI group; p < .001). Abnormal DWI (odds ratio [OR]): 31.3, 95% confidence interval [CI]: 2.5–397) and old age (OR 1.1, 95% CI: 1.001–1.13) were independent factors for poor long-term neurologic outcomes, whereas the Glasgow Coma Scale score at presentation (OR: 0.7, 95% CI: 0.6–0.9) was negatively associated with the risk of poor long-term neurologic outcome.Conclusions: In cases involving CO poisoning due to charcoal burning, DWI at presentation may help predict the long-term neurological outcome after discharge.

Hepatoprotective and Nephroprotective Effects of Methanolic Extract of Different Parts of Tamarindus Indica Linn in Rats Following Acute and Chronic Carbon Tetrachloride Intoxication

Hepatoprotective and Nephroprotective Effects of Methanolic Extract of Different Parts of Tamarindus Indica Linn in Rats Following Acute and Chronic Carbon Tetrachloride Intoxication

Su1592 The Role of Macrophage Migration Inhibitory Factor (MIF) in Acute and Chronic Carbon Tetrachloride Induced Liver Injury: MIF Inhibits Chronic CCl4-Induced Liver Fibrosis

Su1592 The Role of Macrophage Migration Inhibitory Factor (MIF) in Acute and Chronic Carbon Tetrachloride Induced Liver Injury: MIF Inhibits Chronic CCl4-Induced Liver Fibrosis

Respiratory Burns: A Clinical Review

Respiratory injury in burns occurs as a result of thermal, chemical or systemic inflammatory effects. Inhalation injury occurs in up to 40% of patients admitted to hospital following burns. Three stages in the evolution of inhalation injury are described. The early phase (first 48 hours) is associated with pulmonary edema, acute respiratory distress syndrome, airway obstruction, and carbon monoxide and cyanide toxicity. During the middle phase (days to weeks), pneumonia and venous thromboembolism may develop. Late sequelae (months to years post burn injury), while uncommon, include reactive airways dysfunction syndrome, bronchiolitis obliterans and tracheal stenosis. Specific interventions early in the management of inhalation injury are necessary to prevent worsening the injury and minimizing late sequelae.

Age-related changes in cardiac and respiratory adaptation to acute ozone and carbon black exposures: Interstrain variation in mice

Context: Epidemiological studies show positive associations between increased ambient air pollutant levels and adverse cardiopulmonary effects. These studies suggest that the elderly and those with certain genetic polymorphisms are susceptible to adverse air pollution-associated health events.Hypothesis/objective: We hypothesize that physiological responses to air pollutants vary with age and are genetically influenced.Materials and methods: To test this hypothesis, we exposed mice from three inbred strains (C57BL/6J, B6; C3H/HeJ, HeJ; C3H/HeOuJ, OuJ) to ozone (O3) and carbon black (CB) at two ages, (5 months, 12 months), for 3 consecutive days, to either filtered air (FA), CB particles, or O3 and CB sequentially (O3CB) (CB, 550 µg/m3; O3, 600 ppb). Heart rate (HR), HR variability (HRV), breathing, and core temperature (Tco) responses were analyzed.Results: We observed time-dependent physiological changes in response to O3CB exposure in each strain, relative to FA exposure for both age groups. Each mouse strain showed distinct adaptation profiles to repeated acute exposures to O3. In younger mice, several time-dependent effects (decreased HR and increased HRV) were prominent in HeJ and OuJ mice but not B6 mice. We also observed variability in adaptation in older mice. However, responses in older mice were generally attenuated when compared to the younger mice. In addition, cardiac–respiratory interactions were affected with CB and O3CB exposures albeit with patterns differing by age or exposure.Discussion/conclusion: Our results suggest that age considerably attenuates physiological responses to O3 and O3CB exposures. Age-related physiological changes such as increased oxidative stress in mouse tissue may be involved in this attenuation.

Mouse model for thoracic congenital scoliosis.

This study sought to produce a dose-response curve for acute and chronic maternal carbon monoxide (CO) exposure versus vertebral anomalies in mouse offspring and to determine the critical day of exposure. In Part I, pregnant CD-1 mice were exposed to an acute dose of CO at 9 days of gestation. A positive dose-response relationship of acute maternal CO exposure and vertebral anomalies in the offspring was produced. In Part II, pregnant females were exposed to chronic CO for the first 11 days of gestation. Chronic exposure to CO did not produce significant vertebral anomalies. In Part III, pregnant females were exposed to an acute dose of 600 ppm of CO at gestation day 8, 9, or 10. Day 9 in this mouse breed is the critical day for maternal exposure to CO. The detected anomalies were predominately in the thoracic spine.

Effect of carbon monoxide intoxication on skin perfusion in anaesthetized rats.

Carbon monoxide intoxication decreases systemic blood pressure and peripheral resistance. In order to assess the role of the skin in this process, we measured the perfusion of hind limb shaven skin in anaesthetized rats during acute moderate carbon monoxide intoxication. At a steady blood level of 25% carboxyhaemoglobin, the red blood cell flux was measured as an index of tissue perfusion, using laser Doppler fluxmetry. The mean blood pressure decreased by 30% during carbon monoxide exposure, but there was no change in mean red blood cell flux of the hind limb skin microvessel bed. Thus, rat hind limb skin perfusion was not affected by acute moderate steady state carbon monoxide intoxication.

Blood Transfusion in Treatment of Acute Severe Carbon Monoxid Poisoning.

Blood Transfusion in Treatment of Acute Severe Carbon Monoxid Poisoning.