Blood COHb Research Articles

Effects of acute carbon monoxide poisoning on liver damage and comparisons of related oxygen therapies in a rat model

Acute carbon monoxide (CO) poisoning may cause liver damage and liver dysfunction. Therefore, in this study, we aimed to compare the efficiency of normobaric oxygen (NBO) and high-flow nasal cannula oxygen (HFNCO) treatments on liver injury. For that purpose, 28 male Wistar albino rats were divided into four groups (Control, CO, CO + NBO, and CO + HFNCO). The control group was allowed to breath room air for 30 min. Acute CO poisoning in CO, CO + NBO, CO + HFNCO was induced by CO exposure for 30 min. Thereafter, NBO group received 100% NBO with reservoir mask for 30 min. HFNCO group received high-flow oxygen through nasal cannula for 30 min. At the end of the experiment, all animals were sacrificed by cardiac puncture under anesthesia. Serum liver function tests were measured. Liver tissue total antioxidant status (TAS), total oxidant status (TOS), and oxidative stress index (OSI) levels, tissue histomorphology and immunoexpression levels of Bax, Caspase 3, TNF-α, IL-1β, and NF-κB were also examined. Our observations indicated that acute CO poisoning caused significant increases in blood COHb, serum aminotransferase (AST), alanine aminotransferase (ALT0, alkaline phosphatase (ALP), total protein, albumin, and globulin levels but a decrease in albumin to globulin ratio (all, p < 0.05). Furthermore, acute CO poisoning significantly increased the OSI value, and the immunoexpresssion of Bax, Caspase 3, TNF-α, IL-1β, and NF-κB in liver tissue (all, p < 0.05). These pathological changes in serum and liver tissue were alleviated through both of the treatment methods. In conclusion, both the NBO and HFNCO treatments were beneficial to alleviate the acute CO poisoning associated with liver injury and dysfunction.

Imaging of glutamate in acute carbon monoxide poisoning using chemical exchange saturation transfer.

This study adopted the Glutamate Chemical Exchange Saturation Transfer (GluCEST) imaging technique to quantitatively analyze cranial glutamate and discussed the effectiveness of GluCEST values in identifying the pathogenesis of encephalopathy after CO poisoning. The routine MRI and functional MRI scans of two cohorts of subjects (CO group, n = 29; Control group, n = 21) were performed. Between-group comparisons were conducted for GluCEST% in regions of interest (ROI), including the basal ganglia, the thalamus, the frontal lobe, the occipital lobe, the genu of corpus callosum, the cingulate gyrus, and the cuneus. Moreover, an age-stratified subgroup analysis was devised, and a correlational analysis was performed for GluCEST% in each ROI, including the time in coma, Simple Mini-Mental State Examination Scale (MMSE) score, Hamilton Anxiety Scale score, and blood COHb%. As compared to the healthy control, the CO group led to significantly increasing GluCEST% in the basal ganglia, the occipital lobe, the genu of the corpus callosum, the cingulate gyrus, and the cuneus (p < 0.05). In the subgroup analysis for age, adult patients had higher GluCEST% in the basal ganglia, the thalamus, the occipital lobe, the cingulate gyrus, and the cuneus compared to healthy adults (p < 0.05). In addition, the correlational analysis of CO-poisoned patients revealed a statistical association between the GluCEST% and the MMSE in the thalamus and the genu of the corpus callosum. The GluCEST technique is superior to routine MRI in that it can identify the cerebral biochemical changes sooner after acute CO poisoning, which is significant for our understanding of the role of neurotransmitters in the pathological basis of this disease. Brain injury caused by CO poisoning may be different in adults and children.

Data validation of non- invasive carboxyhemoglobin measurement in recipient blood using numerical modeling data: a case of Himalayan regions' households of Nepal.

Carbon monoxide decreases the oxygen carrying capacity of blood. As a result, it reduces the supply of oxygen into body cells and tissues including vital organs. It is poisonous during pregnancy as it leads to high risk for the mother and foetus. It causes the developmental disorders, cerebral anoxic lesions and even death of foetus. The major aim of this study is to validate the non- invasive % COHb monitored data with modelled data. IAQ instruments are administered to monitor CO concentraction and % COHb level in recipient's blood. Thus, the level of % COHb in blood is approximated using numerical modeling to validate the monitored data with modeled data. Twenty four hours average CO concentration with TCS house is found 8.65 ± 7.77ppm, 7.39 ± 5.62ppm, 6.69 ± 7.16ppm, 4.76 ± 7.19ppm, 4.48 ± 6.10ppm in the order of case II > case I > case V > case III > case IV, respectively. Twenty four hours average CO concentration with ICS house is found 3.54 ± 4.41ppm, 2.41 ± 3.93ppm, 2.30 ± 2.24ppm, 1.70 ± 2.93ppm and 1.51 ± 1.24ppm in the order of case I > case V > case II > case IV > case III respectively. The average CO concentration in breath by cook is found 3.75 (3.75 ± 2.35)ppm in ICS using house and 5.36 (5.36 ± 4.54)ppm in TCS using house with minimum 0.60ppm and maximum 31.34ppm. The CO exposure is found more than 13h a day for TCS using house and 9h a day for ICS using house. The average cook_CO exposure is found 5.36 (5.36 ± 4.54)ppm and 3.75 (3.75 ± 2.35)ppm in sampled house using TCS and ICS respectively. The average percentage COHb in sampled house using TCS and ICS is found 4.31 (4.3 ± 5.35) % and 3.72 (3.72 ± 2.67) % respectively. The correlation between numerical modelling of COHb with non- invasive COHb measurement is found significant i.e. P value <0.00001 establishing r2 value 0.95 and 0.97 for ICS and TCS using house respectively.

Study of Effectiveness of CO and Smoke Alarm in Smoldering Fire

Introduction One of the main causes of home fires in Japan is smoking in bed, and carbon monoxide poisoning and suffocation account for a high proportion of cause of death in bedding fires [1]. In this study, using a full-scale building model, a smoldering fire initiated with a lighted cigarette placed still on cotton bedding was reproduced. The COHb concentration (blood COHb concentration) inhaled into a human body and the density and concentration behavior of smoke and CO alarms were compared by monitoring the change in the CO concentrations while smoldering fire. Early detection of fires and effects on a human body were discussed based on the data and the effectiveness of a smoke and CO alarm placed on an indoor wall was examined. Experimental In this study, single function CO gas sensor modules and smoke and CO alarms equipped with photoelectric smoke detectors and electrochemical CO sensors were arranged in a full-scale building model, as shown in Figure 1. Smoldering fire was caused in cotton bedding using a cigarette as a source of fire, and the COHb concentration of an expiratory position and the smoke densities and the CO concentrations of smoke and CO alarms placed on walls were examined. The laboratory was W2.12 ×D2.58 × H2.42 m and a set of cotton bedding was arranged. The source of the fire was set almost at the center of the laboratory and the CO sensor modules were arranged at the pillow, in the bedding, and on the upper part of the bedding (L1-300～L5-400), and on the lower part of the ceiling (L1-2120～L5-2120). Also, smoke and CO alarms (A1～A4) were placed 300 mm off the ceiling on the four walls of the laboratory. The CO concentration outputs and smoke density outputs at each measuring point were collected per 5 seconds using data loggers. After the lighted cigarette (MEVIUS SUPER LIGHTS) was placed still, each measured data was being continuously monitored. Also, based on the CO concentration data from the CO sensor modules surrounding the bedding, the COHb concentration accumulated in a human body was calculated. Result and Conclusions Each CO concentration data from the CO sensor modules placed 400 mm above the lower part of the mattress, in the bedding, and at the expiratory position were extracted as representative data (Fig.2). The CO concentration right above the fire point started rising 50 seconds after the cigarette was placed still, sharply surged to a high concentration level over 1000 ppm at 440 seconds. The CO concentration under the coverlet also suddenly surged a bid later than the one right above the source of the fire, exceeding 1000 ppm at 350 seconds. For the CO concentration at position near the pillow as expiratory position, the rise of CO concentration was confirmed 380 seconds after the cigarette was placed still and the concentration exceeded 1000 ppm at 1240 seconds. Figure 3 shows it is sufficiently possible to detect CO on the wall’s position since it was found in the comparison of the data of the CO sensor module near the ceiling and the smoke and CO alarms on the laboratory walls that the trends of CO concentration were similar in terms of the ways of rising and the concentration values. In this experiment, assuming a respiratory position of a sleeping person, the COHb concentration accumulated through breathing based on the CO concentrations of the upper part of the bedding (L2-300～L5-400) and the CO concentrations and smoke densities of the alarms placed on the walls were compared. Here, the smoke and CO alarms were set to at 10%/m for smoke and 100ppm for CO. Figure 4 shows the relationship between the CO concentration and smoke density values of A2 which responded last among the alarms placed on the walls and the COHb concentrations of the pillow position was related to these data. It was found that the CO alarm detected 280 seconds faster than the smoke alarm. The COHb concentration at the pillow position in the case of this extremely dangerous situation was calculated and it was found that the concentration was 15.1% when the smoke alarm went off. From the results above, it has been confirmed that the CO detection function of a CO and smoke alarm placed on a wall enables people to evacuate well in advance and the alarm is effective in early detection of fire.

Maternal age ? 35 years, Nulliparity, High Blood COHb Levels, and Low Serum Nitric Oxide Levels Increased Risk of Preeclampsia

Objective: To find out the risk factors for preeclampsia. Materials and Methods: a case-control study was between March 2018 and December 2018. Pregnant women who with gestational age of at least 22 weeks live in residential areas, exposed to smoke from combustion of tile or brick were divided into two groups. Cases were those diagnosed with preeclampsia. Controls were normotensive pregnant women who had a history of preeclampsia in previous pregnancy. CO (carbon monoxide) exposure in pregnant women was determined by examining COHb levels in the blood. Serum Nitric Oxide levels were measured using the ELISA (Enzyme-Linked Immunosorbent Assay) method. Data were analyzed by Chi-square test or Fisher’s exact test, Independent T-Test and regression analysis. Adjusted odds ratio (ORs) with 95% confidence interval (CI) was calculated. Results: The results of Blood COHb levels were significantly higher in preeclampsia (4.58±1.2) than the case of control group (2.85±0.4). Serum nitric oxide levels in preeclampsia were significantly lower in preeclampsia (18.28±4.1) than the case of control group (35.15±7.2). Maternal age ? 35 years, nulliparity, high blood COHb levels &gt; 3.5%, and low serum Nitric Oxide levels &lt; 25 ?mol/L were significantly associated with increased risk of preeclampsia. Conclusion: Low serum Nitric Oxide levels (&lt; 25 ?mol/L) due to exposure to CO from the smoke of combustion of tiles or brick carried an increased risk of developing preeclampsia (ORs 25.5;95% CI 4.3- 29.7). These results can help health workers in pregnancy care counseling and prevention of preeclampsia in pregnant women located in areas exposed to carbon monoxide from the smoke of combustion of tiles or brick

Study of Effectiveness of CO and Smoke Alarm in Smoldering Fire

Study of Effectiveness of CO and Smoke Alarm in Smoldering Fire

Effects on the respiration and nervous system of rat exposed to the thermobaric bomb simulated gas

Objective: To investigate the effects of simulated-thermobaric explosive gas on the respiration and nervous system in rats. Methods: 70 of SPF SD rats were randomly divided into four thermobaric explosive gas groups, two restoration observation groups and control group from April to August in 2018. The exposure time of in four thermobaric explosive gas groups were 3.75, 7.5, 15.0 and 30 min, respectively. The restoration observation groups were designed to observe for 30 and 120 min after exposure thermobaric explosive gas 30 min. The bloods were collected and analyzed at the end of exposure and recovery observation. The endogenous carbon monoxide (CO) , nitric oxide (NO) , glutamic acid (GLU) , acetylcholinesterase (AchE) and dopamine (DA) were detected in brain tissues, respectively. Results: The blood gas index (pH, PCO(2), PO(2), COHb, O(2)Hb, MeHbt) and blood electrolytes (Na(+), K(+), Ca(2+) and Cl(-)) in exposure groups have significant differences with these in control (P<0.05) . The pH value decreased with the exposure time longer. However, it basically returned to normal level when terminating exposure for 120 min. The concentration of PCO(2), MeHb and CoHb increased first and then decreased with the exposure time extension. Conversely, The PO(2) and O(2)Hb decreased first and then increased with the exposure time longer. The concentration of endogenous CO, GLU, and AchE decreased and NO increased in exposure group 4 and the restoration observation group 1 compared with those in control (P<0.01) . In addition, there were pathological changes in lung and brain tissue of exposure group, such as inflammatory cell infiltration and edema. Conclusion: The blood gas index, electrolytes, neurotransmitter, histopathology of lung and brain were changed to various degrees by thermobaric bomb gas exposure. These findings would provide some beneficial support for evaluating the damage effect of thermobaric bomb gas on organisms.

Five-Day Changes in Biomarkers of Exposure Among Adult Smokers After Completely Switching From Combustible Cigarettes to a Nicotine-Salt Pod System.

IntroductionThis study examined changes in biomarkers of exposure (BoE) after 5 days of nicotine-salt pod system (NSPS) use, compared with continuation of usual-cigarette smoking and cigarette abstinence, among adult combustible cigarette smokers.Aims and MethodsA randomized, open-label, parallel-cohort, confinement study of healthy adult smokers, naive to NSPS use, was conducted. Participants (N = 90) were randomized to six cohorts (n = 15 each): exclusive ad libitum use of NSPS (four flavors: Virginia Tobacco, Mint, Mango, Creme), continuation of usual-brand cigarette smoking, or cigarette abstinence. Total nicotine equivalents and BoE (NNN, NNAL, 3-HPMA, MHBMA, S-PMA, HMPMA, CEMA, 1-OHP, and COHb) were measured.ResultsEight non-nicotine BoEs, measured in urine, were reduced by an aggregate of 85.0% in the pooled NSPS cohort; increased by 14.4% in the cigarette cohort (p < .001 for pooled NSPS vs. cigarette); and reduced by 85.3% in the abstinence cohort (p > .05; 99.6% relative reduction between pooled NSPS vs. abstinence). Similar changes in individual BoEs were also observed (p < .001 for each BoE between pooled NSPS vs. cigarettes; and abstinence vs. pooled NSPS; p > .05 for each BoE between pooled NSPS vs. abstinence). Blood COHb decreased by 71.8% in the pooled NSPS cohort and 69.1% in the abstinence cohort (p > .05) and increased by 13.3% in the cigarette cohort (p < .001). Mean total urine nicotine equivalents increased in the pooled NSPS and cigarette cohorts by 9% and 26%, respectively, and did not significantly differ (p > .05).ConclusionComplete switching from cigarettes to NSPS produced significant reductions in key non-nicotine BoEs associated with cigarette smoking.ImplicationsThe results of this study concorded with evidence that complete switching from combustible cigarettes to tobacco and nontobacco-flavored vapor products may reduce exposure to key carcinogens and other toxicants known to be associated with tobacco-related diseases. Future research is needed to assess the long-term health effects of NSPS use. These results should not be interpreted to mean that the use of NSPS is without any risk, particularly for nonusers of tobacco products.

Oxidative gastric mucosal damage induced by ischemia/reperfusion and the mechanisms of its prevention by carbon monoxide-releasing tricarbonyldichlororuthenium (II) dimer

Endogenous gaseous mediators, such as nitric oxide, hydrogen sulfide or carbon monoxide (CO) are known to exert anti-inflammatory and anti-oxidative activity due to modulation of various molecular pahtways.Therefore, we aimed to investigate if CO released from tricarbonyldichlororuthenium (II) dimer (CORM-2) prevents gastric mucosa against ischemia/reperfusion (I/R)-induced injury in male Wistar rats. Animals were pretreated i.g. With vehicle (DMSO and saline, 1:10), CORM-2 (1, 5 or 10 mg/kg) or zinc protoporphyrin IX (ZnPP, 10 mg/kg i.p.), the HMOXs inhibitor. In separate series, rats were pretreated with CORM-2 (5 mg/kg) applied in combination with glibenclamide (10 mg/kg i.g.), NG-nitro-l-arginine (L-NNA, 20 mg/kg i.p.), 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ, 10 mg/kg i.p.) or indomethacin (5 mg/kg i.p.). I/R-injuries were induced by clamping celiac artery for 30 min (I) followed by removal of the clamp to obtain R for 3 h. The macroscopic and microscopic area of gastric damage, mucus production and protein expression for HMOX-1/Nrf-2 was determined by planimetry, histology and immunohistochemistry, respectively. Gastric mucosal HMOX-1, HMOX-2, COX-1, COX-2, Kir6.1, Sur2, sGC-α1, sGC-α2, iNOS and eNOS mRNA expression was assessed by real-time PCR. COHb in blood and gastric mucosal CO concentration was analyzed by gas chromatography. Serum content of TGF-β1, TGF-β2, TGF-β3, IL-1α, IL-1β, IL-2, IL-4, IL-5, IL-6, IL-10, IL-12, TNF-α, IFN-γ, GM-CSF was evaluated using Luminex platform. PGE2 concentration and 8-hydroxyguanozine (8-OHG) concentration in gastric mucosa was determined by ELISA.Exposure to I/R induced extensive hemorrhagic erosions in gastric mucosa pretreated with vehicle as compared with intact rats and the area of this gastric damage was reduced by pretreatment with CORM-2 (5 mg/kg i.g.). This effect of CO donor was accompanied by the increased PGE2 content and a significant decrease in 8-OHG and expression of pro- and anti-inflammatory markers mRNA and proteins. Concurrent treatment of CORM-2 with glibenclamide, L-NNA, ODQ but not with indomethacin significantly increased the area of I/R-induced injury and significantly decreased GBF as compared with the group treated with CORM-2 alone.We conclude that CO releasing CORM-2 prevents gastric mucosal oxidative damage induced by I/R improving GBF, decreasing DNA oxidation and inflammatory response on systemic level. This CO-gastroprotection is mediated by the activity of sGC, NOS and K-ATP channels. CO delivered from its donor maintained physiological gastric mucosal PGE2 concentration but the involvement of endogenous COX in beneficial activity of this gaseous mediator at least in this model is questionable.

Correlation study of Carbon Monoxide (CO) air exposure level with blood COHb level of Basement Officer in Surabaya Mall

Gas CO is formed as a result of incomplete combustion. The material containing carbon monoxide is gas emission from motorcycle vehicle which is toxic to humans. This study aims to analyze the correlation between CO gas that also known as Carbon monoxide gas in the air with COHb level of blood parking basement officers in Surabaya "x" mall. This study was analytical observational with cross sectional design and the data was analyzed by Chi-Square test. The number of samples used was 15 parking basement officers and a control group of 15 people as a comparison. The results of measurement of CO gas levels in 3 parking points were more than standards recommendation. While the other 3 points in the control area were below the quality standard. All of samples in the parking basement officers had COHb levels &gt;5% and for control areas there were 11 persons who had COHb levels of &lt;5% and 4 people who had COHb levels of &gt;5%. The results suggested that there was a significant correlation between the characteristics of individuals with COHb levels, such as duration of work (p = 0.040), nutritional status (p = 0.047) and smoking habits (p = 0.046). While variable of age (p = 0.070) and personal protective equipment (PPE) use (p = 0.128) showed no significant correlation. In addition, there was a significant correlation between exposure of CO gas and blood COHb levels in basement car park officers in Surabaya “X” Mall (p = 0.000), and there was a distinction between COHb level of blood basement car park officers in the "x" mall building and the control group with a value of p = 0.000. Based on the results, it is suggested for car park officers to cease smoking, go to places with more oxygen, maintain diet and do exercise regularly. It is also suggested and recommended for agencies is to put more attention regarding exhaust fans’ maintenance and sufficiency.

The Description of CO Levels, COHb Levels, And Blood Pressure of Basement Workers X Shopping Centre, Malang

CO is one of air pollutants that harmful to humans. CO that inhaled by humans will react with hemoglobin and forming COHb in the blood. The purpose of this research is describe the CO levels of basement, COHb levels, and blood pressure basement workers of X shopping center Malang. This research was observational research that was included in a cross sectional study. This research done by the interview with respondents that all of the 14 workers, related to the characteristics of the respondents, measured of the CO levels, examinated of COHb levels and measured of blood pressure. The average of CO levels at the basement work area was 23,93 ppm, less than the standard. 13 workers had high levels of COHb &gt;5%. 9 of the 13 workers with high blood COHb levels had high blood pressure. Workers who had about 47-55 years old, working in the basement of &gt; 6 years, and had a smoking habit tends to had high levels of COHb and high blood pressure. Preferably basement workers who every day exposed by the CO to stop smoking so as not to get exposure CO gas from smoking.

Neuroprotection with Polynitroxylated PEGylated Hemoglobin as a Macromolecular Superoxide Dismutase/Catalase Mimetic Drug for Resuscitation after Traumatic Brain Injury Combined with Hemorrhage Shock

In polynitroxylated PEGylated hemoglobin (PNPH aka SanFlow), polynitroxylation of hemoglobin confers superoxide dismutase/catalase (SOD/CAT) mimetic activities that may directly protect the brain from oxidative stress in addition to facilitating O2 transport. PEGylation of cell‐free hemoglobin also limits extravasation and renal clearance and increases its oncotic pressure, thereby allowing it to be used as a small volume resuscitation fluid in the field. Furthermore, stabilization of PNPH with bound CO prevents metHb formation during storage and permits it to serve as a CO donor that is converted to an oxygen carrier after infusion. We determined whether transfusion of a 4% solution PNPH with bound CO is neuroprotective after traumatic brain injury (TBI) + hemorrhagic shock (HS) as a model of polytrauma. Guinea pigs were used because, like humans, they do not synthesize their own ascorbic acid, which is important in reducing metHb. TBI was produced by a 5‐mm diameter cortical impactor that briefly displaced the dura 3 mm. TBI was followed by 20 mL/kg hemorrhage to a mean arterial pressure (MAP) of 40 mmHg. At 90 min after HS, the guinea pigs were resuscitated with 20 mL/kg lactated Ringer's solution (LR) or 10 mL/kg PNPH over a 90‐min period. Additional doses were infused one and two days later. Compared with animals that received LR, resuscitation with PNPH significantly augmented the early recovery of MAP after HS by 10–18 mmHg (n=12; P &lt;0.001). After infusion of PNPH, total blood metHb and COHb increased by 2% as CO from PNPH equilibrated with the larger erythrocyte hemoglobin pool. At 9 days of recovery, there was no statistical difference in lesion volume or the total volume of the underlying hippocampus among the sham and the two TBI+HS groups. However, accompanying the loss of cerebral cortex, ventricular enlargement as much as three‐fold occurred. In those receiving PNPH, ventricular enlargement was attenuated by 23% (n=12; P &lt;0.05). Most importantly, unbiased stereology analysis revealed that PNPH infusion increased the number of viable neurons in the hippocampus CA1+2 region (Naïve+sham groups = 271,000 ± 39,000; TBI+HS+LR = 159,000 ± 28,000; TBI+HS+PNPH = 235,000 ± 49,000 viable neurons; n=12/group; P &lt;0.05 LR vs PNPH and LR vs Naïve/sham; 6 naïve and 6 sham‐operated guinea pigs did not differ and were combined). In conclusion, resuscitation with PNPH after TBI+HS in guinea pigs provides significant neuroprotection in hippocampus and attenuation of hydrocephalus. These effects may be attributed, in part, to its ability to augment MAP as a hyperoncotic, small volume resuscitation fluid, by its SOD/CAT mimetic activities, and by serving as a CO donor, which at low CO concentrations exerts anti‐apoptotic and anti‐inflammatory effects. PNPH may serve as a multi‐potential resuscitation fluid for polytrauma involving TBI and HS.Support or Funding InformationSupported by the US Army Medical Research and Materiel Command under Contract No. W81XWH‐17‐C‐0223 to CJCH.This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

Association Between Near Infrared Spectroskopy (NIRS) and Normobaric and Hyperbaric Oxygen Treatment in Acute Carbon Monoxide Poisoning

Objective: Carbon monoxide (CO) is the main cause of death and morbidity associated with poisoning in developed countries. The most important mortality and morbidity cause of CO poisoning is cerebral hypoxia. Near-infrared spectroscopy (NIRS) is a useful method for assessing brain oxygenation. In this study, we aimed to evaluate the brain oxygenation of CO poisoning patients with NIRS and to investigate its benefits in patients follow up and treatment. Materials and Methods: The study was conducted as a single-center, prospective clinical trial with 33 patients who were diagnosed by measuring blood CO-Hb level or referred from other hospitals diagnosed with CO poisoning. Patients were divided into two groups as normobaric oxygen therapy (NBOT) group and hyperbaric oxygen therapy (HBOT) group according to the treatment method applied. Results: Although average cerebral saturation (ScO2) levels after treatment were higher in the NBOT group than before treatment, no statistically significant difference was found except the left frontal ScO2 values. In HBOT group, there was no difference between ScO2 values before and after treatment sessions. Conclusion: Our study concluded that NIRS may be useful in assessing brain oxygenation in CO poisoned patients, but not in determining the HBOT start-up, and not in monitoring the effectiveness of HBOT.

Identification of CO Exposure, Habits, COHb Blood and Worker’s Health Complaints on Basement Waterplace Apartment, Surabaya

Carbon monoxide (CO) is a silent killer because it is tasteless, colorless, odorless, and causes of death. In the basement, pollution level from vehicle engines combustion is higher than in the ambient air. Workers in the basement potentially expose to CO that trapped while they were working. CO inhaled will form COHb on the blood. This study aims to identify CO exposure, worker habits, COHb blood, and health complaints during their working time in the basement of apartment Waterplace Surabaya. This research was a descriptive with cross-sectional design and used purposive sampling technique with 20 respondents. Data which were collected through observation and interviews. The result showed that CO measurement was below 25 ppm standard. Most characteristics of workers were male (80.0%), 21–29 years old (55.0%), working time for ≤ 12 months (55.0%) and working hours for 12 hours (55.0%). The worker’s habits mostly were smoking (80.0%), regularly consume fruit (55.0%) and vegetables (60.0%). The majority (90.0%) COHb level was above the 3.5% standard. Health worker complaints were dizziness (80.0%), impaired concentration (60.0%) and tired (55.0%) while their working time. Workers that smoking, eating fruits, and vegetables were having a blood COHb levels higher. It was concluded that the levels of CO gas below the standards while blood COHb above the standards. It was suggested to reduce smoking, to start a healthier lifestyle, and to use masker while their working time.

Pathology of carbon monoxide poisoning in two cats

BackgroundCarbon monoxide (CO), a common cause of poisoning in human beings has also been implicated in the death of animals. Though there are multiple studies on CO poisoning and relevant lethal blood COHb concentrations in humans, there are no reliable reports of diagnostic lethal carboxyhemoglobin percentage of saturation (COHb%) in cats. Additionally, due to shared housing environments, exposures to companion animals can be a surrogate for lethal exposures in human beings and provide valuable information in concurrent forensic investigations.Case presentationTwo adult Singapura brown ticked cats were submitted to the California Animal Health and Food Safety Laboratory (CAHFS) for necropsy and diagnostic work-up. These animals were found dead along with their two deceased owners. Similar lesions were observed in both cats. At necropsy, gross lesions consisted of multifocal, large, irregular, bright red spots on the skin of the abdomen and the inner surface of ear pinnae, bright red muscles and blood. The carcasses, and tissues fixed in formalin retained the bright red discoloration for up to two weeks. Microscopic lesions included diffuse pulmonary congestion and edema, and multifocal intense basophilia of cardiomyocytes mostly affecting whole fibers or occasionally a portion of the fiber. Based on the clinical history,gross and microscopic changes, cyanide or carbon monoxide poisoning was suspected. Blood samples analyzed for carbon monoxide showed 57 and 41% carboxyhemoglobin COHb%. Muscle samples were negative for cyanide.ConclusionThere are no established reference values for lethal COHb concentration in cats. The COHb % values detected in this case which fell within the lethal range reported for other species, along with the gross lesions and unique histological findings in the heart suggest a helpful criteria for diagnosis of CO intoxication associated death in cats. This case demonstrates that since pets share the same environment as human beings and often are a part of their activities, they can be useful adjuncts in potential forensic investigations to help solve human cases.

The impact of hydrogen sulfide on the heme oxygenase-1/carbon monoxide system in Coxsackie virus B3-induced myocarditis in mice

Objective: To explore the impact of hydrogen sulfide (H(2)S) on the heme oxygenase-1/carbon monoxide pathway in Coxsackie virus B3 (CVB3)-induced murine myocarditis (VMC) model. Method: A total of 70 inbred male Balb/c mouse (4-6 weeks old) were randomized into the following four groups: Normal, VMC, PAG and NaHS (n=10 for Normal, n=20 for VMC, PAG and NaHS groups). Mice in Normal group were non-infected mice treated with intraperitoneal injection of sterile phosphate-buffered saline daily for 10 days.Mice in VMC group received intraperitoneal CVB3 injection (0.1 ml 10(-5.69)TCID(50)m·ml(-1)·d(-1) and PBS for 10 days), and mice in PAG group received additional intraperitoneal DL-proparglygylcine injection (40 mg·kg(-1)·d(-1) for 10 days), mice in NaHS group received additional intraperitoneal NaHS injection (50 μmol·kg(-1)·d(-1) for 10 days). All mice were sacrificed on day 10th, and body weight and heart weight, the ratio of heart weight to body weight were compared among groups.Pathological changes of heart tissues were observed microscopically by HE and the histopathologic scores were valued.The content of COHb was tested after the gathering of blood specimens while reverse transcription-polymerase chain reaction was used to detect myocardial HO-1 mRNA expression. Results: (1) Pathological findings in myocardium: hearts sections in Normal group were normal and no inflammatory cells and necrosis were found.A notable cellular infiltration, interstitial edema, vascular hyperemia and necrosis were observed in heart section of VMC, PAG and NaHS group.Extensive inflammations and larger area of myocardial cells necrosis were evidenced in PAG group and above changes were significantly reduced in NaHS group.(2) Comparison of the ratio of heart weight to body weight and histological scores of myocardium: the ratio was significantly higher in the VMC, PAG, NaHS groups than in Normal group (P<0.05), which was higher in PAG group and lower in NaHS group as compared with VMC group (both P<0.05). The histopathologic scores of all CVB3 innoculation groups were higher than in the Normal group, which was higher in PAG group and lower in NaHS group as compared to VMC group (both P<0.05). (3) The content of blood COHb in VMC, PAG or NaHS group was significantly higher than that in Normal group (P<0.05), which was significantly lower in PAG group, and higher in NaHS group as compared to VMC group (both P<0.05). (4) The mRNA expression of myocardial HO-1 detected by RT-PCR: weak expression was observed in Normal group, which was significantly upregulated in VMC, PAG and NaHS groups (P<0.05), which was downregulated in PAG group and upregulated in NaHS group as compared to VMC group (both P<0.05). (5) Correlation analysis: blood COHb concentration was positively correlated with myocardial HO-1 mRNA expression(r=0.927, P=0.000), negatively correlated with histopathologic scores(r=-0.753, P=0.000)and the histopathologic scores were negatively correlated with the myocardial HO-1 mRNA expression (r=-0.754, P=0.000). Conclusions: H(2)S could play a protective role in murine CVB3 myocarditis model through inducing HO-1 expression and upregulating HO-1/CO pathway.

Carbon monoxide poisoning from waterpipe smoking: a retrospective cohort study

Objective: Waterpipe smoking may increasingly account for unintentional carbon monoxide poisoning, a serious health hazard with high morbidity and mortality. We aimed at identifying waterpipe smoking as a cause for carbon monoxide poisoning in a large critical care database of a specialty care referral center.Methods: This retrospective cohort study included patients with a history of exposure to waterpipe smoking and carbon monoxide blood gas levels >10% or presence of clinical symptoms compatible with CO poisoning admitted between January 2013 and December 2016. Patients’ initial symptoms and carbon monoxide blood levels were retrieved from records and neurologic status was assessed before and after hyperbaric oxygen treatment.Results: Sixty-one subjects with carbon monoxide poisoning were included [41 males, 20 females; mean age 23 (SD ± 6) years; range 13–45] with an initial mean carboxyhemoglobin of 26.93% (SD ± 9.72). Most common symptoms included syncope, dizziness, headache, and nausea; 75% had temporary syncope. Symptoms were not closely associated with blood COHb levels.Conclusion: CO poisoning after waterpipe smoking may present in young adults with a wide variability of symptoms from none to unconsciousness. Therefore diagnosis should be suspected even in the absence of symptoms.

How reliable are parenchymal tissues for the evaluation of carbon monoxide poisoning? A pilot study.

Dealing with burnt bodies, the forensic pathologist must first of all answer the question whether the victim was alive at the moment of the fire. This study aims at clarifying whether some human solid tissues may be reliably used for the forensic diagnosis of Co poisoning on burnt bodies providing no collectable blood during the autopsy. From 34 selected cases, both cardiac blood and parenchymal samples were collected to perform CO-oxymeter, spectrophotometry, and gas chromatography tests: blood CO estimations (blood COHb% and blood[CO]) and parenchymal[CO] values have been compared with special focus on R values. The solid tissues having the best correlations with blood CO amount turned out to be the lung (R 0.84), the liver (R 0.83), the kidney (R 0.79), and the spleen (R 0.92).

Transfusion of hemoglobin-based oxygen carriers in the carboxy state is beneficial during transient focal cerebral ischemia

Exchange transfusion of large volumes of hemoglobin (Hb)-based oxygen carriers can protect the brain from middle cerebral artery occlusion (MCAO). Hb in the carboxy state (COHb) may provide protection at relatively low volumes by enhancing vasodilation. We determined whether transfusion of rats with 10 ml/kg PEGylated COHb [polyethylene glycol (PEG)-COHb] at 20 min of 2-h MCAO was more effective in reducing infarct volume compared with non-carbon monoxide (CO) PEG-Hb. After PEG-COHb transfusion, whole blood and plasma COHb was <3%, indicating rapid release of CO. PEG-COHb transfusion significantly reduced infarct volume (15 ± 5% of hemisphere; mean ± SE) compared with that in the control group (35 ± 6%), but non-CO PEG-Hb did not (24 ± 5%). Chemically dissimilar COHb polymers were also effective. Induction of MCAO initially produced 34 ± 2% dilation of pial arterioles in the border region that subsided to 10 ± 1% at 2 h. Transfusion of PEG-COHb at 20 min of MCAO maintained pial arterioles in a dilated state (40 ± 5%) at 2 h, whereas transfusion of non-CO PEG-Hb had an intermediate effect (22 ± 3%). When transfusion of PEG-COHb was delayed by 90 min, laser-Doppler flow in the border region increased from 57 ± 9 to 82 ± 13% of preischemic baseline. These data demonstrate that PEG-COHb is more effective than non-CO PEG-Hb at reducing infarct volume, sustaining cerebral vasodilation, and improving collateral perfusion in a model of transient focal cerebral ischemia when given at a relatively low dose (plasma Hb concentration < 1 g/dl). Use of acellular Hb as a CO donor that is rapidly converted to an oxygen carrier in vivo may permit potent protection at low transfusion volumes.

Improved intraischemic perfusion and pial arteriolar dilation by transfusion of pegylated hemoglobin in the carbon monoxide state

Transfusion of chemically‐modifed, cell‐free hemoglobin (Hb) during middle cerebral artery occlusion (MCAO) can reduce infarct volume, but large amounts are typically required. We tested the concept that transfusion of Hb in the CO state would promote vasodilation during MCAO without requiring large amounts of Hb to be transfused. Transfusion of 10 ml/kg of a 4% solution of pegylated COHb (PEG‐COHb) in anesthetized rats resulted in rapid release of CO and equilibration of CO with red cell‐based Hb (2–3% COHb in whole blood and plasma). Plasma [Hb] was ~0.5 g/dL. Induction of MCAO initially produced 37±8% (±SD) dilation of pial arterioles in the MCA border region that gradually subsided to 7±7% at 2 h in controls. Transfusion of PEG‐COHb at 20 min of MCAO maintained pial arterioles in a dilated state (40±13%) at 2 h, whereas transfusion of albumin (25±13%) or PEG‐Hb without CO (22±8%) had intermediate effects. When transfusion of PEG‐COHb was delayed by 90 min, penumbral laser‐Doppler flow increased from 58% to 80% of pre‐ischemic baseline, whereas transfusion of albumin or PEG‐Hb produced no significant change. We conclude that PEG‐COHb can serve as a CO donor that effectively prevents time‐dependent loss of pial arteriolar dilation during MCAO and improves blood flow in the penumbral region to levels above the threshold typically associated with eventual infarction. (Supported by NIH NS38684).