Increase In Carbon Monoxide Levels Research Articles

Ambient Air Pollution and Incident Cardiovascular Disease in People with Type 2 Diabetes Mellitus: A cohort study.

We aimed to assess the effect of air pollution on incident cardiovascular disease (CVD) in people with type 2 diabetes mellitus (T2DM). We tracked 486 T2DM patients from 2012 to 2021. Cox regression models were applied to assess the hazard of exposure to particulate matter, carbon monoxide (CO), ozone, nitrogen dioxide, and sulfur dioxide (SO2) on incident CVD, revealing hazard ratios (HRs). CVD incidents occurred in 73 individuals. Among men, each 1-ppm increase in CO levels raised the risk of CVD (HR: 2.66 (95% CI: 1.30-5.44). For women, a 5-ppb rise in SO2 increased CVD risk (HR: 1.60 (95% CI: 1.11-2.30). No notable impact of particulate pollutants was found. Persistent exposure to gaseous air pollutants, specifically CO and SO2, is linked to the development of CVD in men and women with T2DM.

A Field Study of Carbon Monoxide Levels in Snow Caves During Short-Term Stove Use.

While the use of camping stoves in poorly ventilated areas is discouraged, the need to address dehydration challenges in harsh arctic conditions has led to their unconventional use inside snow caves for snow melting, subjecting occupants to unknown carbon monoxide (CO) levels. This study, located at sea level in northeastern Greenland, aimed to assess CO levels and dynamics during short cooking sessions in newly constructed emergency snow caves. In 5 snow caves, constructed according to the same design principles by 4 different individuals, a single MSR Whisperlite multifuel burner, primed with ethanol and burning white gas, was used to melt snow. CO concentrations were monitored every minute until all the snow in a 5-L pot was converted to water and CO levels returned to below 10 ppm. A total of 16 experiments conducted showed that the priming phase generated the highest CO peaks, with a maximum of 120 ppm. Time-weighted averages ranged from 14 ppm to 67 ppm, with trial durations of 15 to 21 min. A single trial with a dirty burner resulted in up to a 10-fold increase in CO levels. While single, short cooking sessions of less than 10 min burn time in newly constructed snow caves may be tolerated under specific conditions, the study highlighted substantial variation between caves and the importance of using clean burners, emphasizing the need for further research to gain a comprehensive understanding of CO exposure dynamics in snow caves.

Exploring the therapeutic potential of a nano micelle containing a carbon monoxide-releasing molecule for metabolic-associated fatty liver disease by modulating hypoxia-inducible factor-1α.

Metabolic-associated fatty liver disease (MAFLD) encompasses a spectrum of chronic liver diseases, including steatohepatitis, cirrhosis, and liver cancer. Despite the increasing prevalence and severity of MAFLD, no approved pharmacological interventions are currently available. Hypoxia-inducible factor-1α (HIF-1α) has emerged as a crucial early mediator in the pathogenesis of MAFLD. Previously, we demonstrated the potent anti-inflammatory properties of the nano-designed carbon monoxide (CO) donor, styrene maleic acid copolymer (SMA) encapsulating CO-releasing molecule (SMA/CORM2), which effectively suppressed HIF-1α in various inflammatory disorders. Here, we investigated the therapeutic potential of SMA/CORM2 in a mouse model of MAFLD induced by a high-fat methionine- and choline-deficient (HF-MCD) diet. Following 4 weeks of HF-MCD diet consumption, we observed pronounced hepatic lipid accumulation accompanied by disrupted lipid metabolism, polarization of macrophages towards the pro-inflammatory M1 phenotype, activation of the NLRP3 inflammasome, and upregulation of the TGF-β fibrosis signaling pathway. Notably, the early and upstream event driving these pathological changes was the upregulation of HIF-1α. Treatment with SMA/CORM2 (10mg/kg, three times per week) led to a significant increase in CO levels in both the circulation and liver, resulting in remarkable suppression of HIF-1α expression even before the onset of apparent pathological changes induced by the HF-MCD diet. Consequently, SMA/CORM2 administration exerted a significantly protective and therapeutic effect on MAFLD. In vitro studies using hepatocytes treated with high concentrations of fatty acids further supported these findings, as knockdown of HIF-1α using short hairpin RNA (shRNA) elicited similar effects to SMA/CORM2 treatment. Collectively, our results highlight the therapeutic potential of SMA/CORM2 in the management of MAFLD through suppression of HIF-1α. We anticipate that SMA/CORM2, with its ability to modulate HIF-1α expression, may hold promise for future applications in the treatment of MAFLD. STATEMENT OF SIGNIFICANCE: Carbon monoxide (CO) is a crucial gaseous signaling molecule that plays a vital role in maintaining homeostasis and is a potential target for treating many inflammatory diseases. Developing drug delivery systems that can deliver CO stably and target specific tissues is of great interest. Our team previously developed a nano micellar CO donor, SMA/CORM2, which exhibits superior bioavailability to native CORM2 and shows therapeutic potential in many inflammatory disease models. In this study, we showed that SMA/CORM2, through controlled CO release, significantly ameliorated steatohepatitis and liver fibrosis induced by an HF-MCD diet by suppressing an HIF-1α mediated inflammatory cascade. These findings provide new insight into the anti-inflammatory function of CO and a promising approach for controlling metabolic-associated fatty liver disease.

Ontogeny of Carbon Monoxide-Related Gene Expression in a Deep-Diving Marine Mammal.

Marine mammals such as northern elephant seals (NES) routinely experience hypoxemia and ischemia-reperfusion events to many tissues during deep dives with no apparent adverse effects. Adaptations to diving include increased antioxidants and elevated oxygen storage capacity associated with high hemoprotein content in blood and muscle. The natural turnover of heme by heme oxygenase enzymes (encoded by HMOX1 and HMOX2) produces endogenous carbon monoxide (CO), which is present at high levels in NES blood and has been shown to have cytoprotective effects in laboratory systems exposed to hypoxia. To understand how pathways associated with endogenous CO production and signaling change across ontogeny in diving mammals, we measured muscle CO and baseline expression of 17 CO-related genes in skeletal muscle and whole blood of three age classes of NES. Muscle CO levels approached those of animals exposed to high exogenous CO, increased with age, and were significantly correlated with gene expression levels. Muscle expression of genes associated with CO production and antioxidant defenses (HMOX1, BVR, GPX3, PRDX1) increased with age and was highest in adult females, while that of genes associated with protection from lipid peroxidation (GPX4, PRDX6, PRDX1, SIRT1) was highest in adult males. In contrast, muscle expression of mitochondrial biogenesis regulators (PGC1A, ESRRA, ESRRG) was highest in pups, while genes associated with inflammation (HMOX2, NRF2, IL1B) did not vary with age or sex. Blood expression of genes involved in regulation of inflammation (IL1B, NRF2, BVR, IL10) was highest in pups, while HMOX1, HMOX2 and pro-inflammatory markers (TLR4, CCL4, PRDX1, TNFA) did not vary with age. We propose that ontogenetic upregulation of baseline HMOX1 expression in skeletal muscle of NES may, in part, underlie increases in CO levels and expression of genes encoding antioxidant enzymes. HMOX2, in turn, may play a role in regulating inflammation related to ischemia and reperfusion in muscle and circulating immune cells. Our data suggest putative ontogenetic mechanisms that may enable phocid pups to transition to a deep-diving lifestyle, including high baseline expression of genes associated with mitochondrial biogenesis and immune system activation during postnatal development and increased expression of genes associated with protection from lipid peroxidation in adulthood.

Predictors of Nicotine Dependence Among Adult Male Midwakh and Cigarette Smokers.

ObjectivesMidwakh is a popular form of smoking in the Middle East. This study aimed to assess the predictors of nicotine dependence among cigarette or midwakh smokers in the United Arab Emirates (UAE).MethodsThis cross-sectional study was conducted from September to December 2015 in Ajman, UAE. A convenience sampling strategy was implemented to recruit adult male smokers aged ≥18 years who exclusively smoked either cigarettes or midwakh. A validated self-administered questionnaire was used to collect data from the participants, with nicotine dependence assessed using the Modified Fagerström Test for Nicotine Dependence. In addition, the levels of salivary cotinine and exhaled breath carbon monoxide (CO) were measured.ResultsOf the 88 adult male smokers included in the study, 40 (45.5%) were cigarette smokers and 48 (54.5%) smoked midwakh. The majority of participants were 26–35 years of age (48.9%), followed by 18–25 years (30.7%) and >35 years (20.5%). Midwakh use was associated with more than a three-fold increase in the risk of moderate-to-high nicotine dependence compared to cigarette smoking. Moreover, for each unit increase in CO level, there was a 10% increase in the risk of nicotine dependency. There was also a significant association between nicotine dependence level and depth of inhalation (P = 0.023).ConclusionType of smoking and CO level were found to be significant predictors of nicotine dependence among adult male smokers. In particular, greater dependency was observed among midwakh smokers than cigarette smokers.

Effect of environmental pollution PM2.5, carbon monoxide, and ozone on the incidence and mortality due to SARS-CoV-2 infection in London, United Kingdom

ObjectivesCOVID-19 pandemic raised several queries on the relationship between the environment pollution and occurrence of new cases and deaths. This study aims to explore the effect of environmental pollution, particulate matter (PM 2.5 μm), carbon monoxide (CO) and Ozone (O3) on daily cases and daily deaths due to Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) infection in a largest metropolitan city London, United Kingdom. MethodsFor this study, we selected London, one of the highly populated capitals, and markedly affected due to COVID-19 pandemic. The data on the SARS-CoV-2 daily new cases and deaths were recorded from UK-gov Web "Coronavirus COVId-19 in the UK, 2020". The daily environmental pollutants PM 2.5 μm, CO and O3 were recorded from the metrological web "(London Air Pollution, Air Quality Index- AQI, 2020)". The daily cases, deaths, PM 2.5 μm, CO and O3 were documented from the date of the occurrence of the first case of SARS-CoV-2 in London, February 24 to November 2, 2020. ResultsThe SARS-CoV-2 cases and deaths were positively related with environmental pollutants, PM2.5, O3 and CO levels. Additionally, with 1 µm increase in PM2.5 the number of cases and deaths significantly increased by 1.1% and 2.3% respectively. A 1 unit increase in CO level significantly increased the number of cases and deaths by 21.3% and 21.8% respectively. A similar trend was observed in O3, with 1-unit increase, the number of cases and deaths were significantly increased respectively by 0.8% and 4.4%. ConclusionsEnvironmental pollutants, PM2.5, CO and O3 have a positive association with an increased number of SARS-CoV-2 daily cases and daily deaths in London, UK. Environmental pollution management authorities must implement necessary policies and assist in planning to minimize the environmental pollution and COVID-19 pandemic.

Global Associations between Air Pollutants and Chronic Obstructive Pulmonary Disease Hospitalizations. A Systematic Review.

Exacerbations are key events in chronic obstructive pulmonary disease (COPD), affecting lung function decline and quality of life. The effect of exposure to different air pollutants on COPD exacerbations is not clear. To carry out a systematic review, examining associations between air pollutants and hospital admissions for COPD exacerbations. MEDLINE, Embase, BIOSIS, Science Citation Index, and the Air Pollution Epidemiology Database were searched for publications published between 1980 and September 2015. Inclusion criteria were focused on studies presenting solely a COPD outcome defined by hospital admissions and a measure of gaseous air pollutants and particle fractions. The association between each pollutant and COPD admissions was investigated in metaanalyses using random effects models. Analyses were stratified by geographical clusters for investigation of the consistency of the evidence worldwide. Forty-six studies were included, and results for all the pollutants under investigation showed marginal positive associations; however, the number of included studies was small, the studies had high heterogeneity, and there was evidence of small-study bias. Geographical clustering of the effects of pollution on COPD hospital admissions was evident and reduced heterogeneity significantly. The most consistent association was between a 1-mg/m3 increase in carbon monoxide level and COPD-related admissions (odds ratio, 1.02; 95% confidence interval, 1.01-1.03). The heterogeneity was moderate, and there was a consistent positive association in both Europe and North America, although levels were clearly below World Health Organization guideline values. There is mixed evidence on the effects of environmental pollution on COPD exacerbations. Limitations of previous studies included the low spatiotemporal resolution of pollutants, inadequate control for confounding factors, and the use of aggregated health data that ignored personal characteristics. The need for more targeted exposure estimates in a large number of geographical locations is evident.

Effects of convection and long-range transport on the distribution of carbon monoxide in the troposphere over India

Variability in the tropospheric distributions of carbon monoxide (CO) over five selected regions of India has been studied using the MOPITT data for the period of 2001–2014. The average seasonal profiles show highest mixing ratios at 900 hPa in the boreal winter and lowest in the Indian summer monsoon over all the study regions. We observe a slight increase in CO levels from 500 hPa to 200 hPa over all the locations. The CO mixing ratios are found to be higher by about 10–40% around 300–200 hPa as compared to 900 hPa over Ahmedabad, Hyderabad and Trivandrum during monsoon period. This could be due to lifting of polluted air by convection and getting trapped in the anticyclonic winds over the Indian region during the monsoon. Most of the 7 day back trajectories over these regions show transport of the polluted air mass from the major biomass burning regions of central Africa and SE Asia. The results show dominance of the seasonal amplitude at 900 hPa over all the regions, while inter-annual variability dominates mostly over Ahmedabad, Hyderabad and Trivandrum at 300 hPa. In order to check the ability of different models in capturing the observed variability, the results have been compared with simulations from two chemistry transport models (MOZART and EMAC). This comparison shows that both the models perform reasonably well in simulating the basic features such as annual variation as well as increase in CO around 300–200 hPa due to convection during the monsoon season.

Chronic carbon monoxide inhalation during pregnancy augments uterine artery blood flow and uteroplacental vascular growth in mice

End-tidal breath carbon monoxide (CO) is abnormally low in women with preeclampsia (PE), while women smoking during pregnancy have shown an increase in CO levels and a 33% lower incidence of PE. This effect may be, in part, due to lowered sFLT1 plasma levels in smokers, and perhaps low-level CO inhalation can attenuate the development of PE in high-risk women. Our previous work showed maternal chronic CO exposure (<300 ppm) throughout gestation had no maternal or fetal deleterious effects in mice. Our current study evaluated the uteroplacental vascular effects in CD-1 maternal mice that inhaled CO (250 ppm) both chronically, gestation day (GD) 0.5 to 18.5, and acutely, 2.5 h on each of GD 10.5 and 14.5. We demonstrated, using microultrasound measurements of blood velocity and microcomputed tomography imaging of the uteroplacental vasculature, that chronic maternal exposure to CO doubled uterine artery blood flow and augmented uteroplacental vascular diameters and branching. This finding may be of benefit to women with PE, as they exhibit uteroplacental vascular compromise. The ratio of VEGF protein to its FLT1 receptor was increased in the placenta, suggesting a shift to a more angiogenic state; however, maternal circulating levels of VEGF, sFLT1, and their ratio were not significantly changed. Doppler blood velocities in the maternal uterine artery and fetal umbilical artery and vein were unaltered. This study provides in vivo evidence that chronic inhalation of 250 ppm CO throughout gestation augments uterine blood flow and uteroplacental vascular growth, changes that may protect against the subsequent development of preeclampsia.

Role of Carbon Monoxide in Blood Pressure Regulation

Carbon monoxide (CO) is an odorless, colorless, tasteless gas that is generated in the environment as the result of combustion from stoves and engines among other sources. Approximately 500 people per year in the United States are victims of nonfire-associated CO poisoning according to the Centers for Disease Control and Prevention. CO poisoning is often fatal because of its interaction with hemoglobin, which renders it incapable of carrying oxygen-causing organs to become severely hypoxic. CO inhalation is believed to be fatally toxic at concentrations as little as 800 parts per million (ppm) or 0.08% in the air. Despite the lethal nature of this gas, several recent studies suggest that CO inhalation at low doses (≤250 ppm), as well as increases in CO levels using CO releasing molecules (CORMs), offers protection against ischemic injury in the heart, liver, and kidney.1–4 CO is endogenously produced in the body as a result of the metabolism of heme by heme oxygenase (HO), as well as from lipid peroxidation.5,6 The catabolism of heme by HO also produces an equimolar amount of biliverdin, which is rapidly converted in the cell to bilirubin by the enzyme biliverdin reductase.7 There are 2 major isoforms of HO responsible for CO production. HO-1 is expressed at very low levels under normal conditions but is highly induced by several stimuli, including heavy metals, ultraviolet light, endotoxin, shear stress, hypoxia, and oxidants.8 HO-2 is the constitutively expressed form of the enzyme with the highest levels observed in the brain and testes.9 Experimental evidence has demonstrated that systemic induction of HO has several beneficial actions on the cardiovascular system, including lowering of blood pressure, protection against myocardial infarction, and prevention of atherosclerosis.10–12 Although the cardiovascular actions of HO induction have been established, the role of CO in …

Effects of acute tyrosine/phenylalanine depletion on the selective processing of smoking-related cues and the relative value of cigarettes in smokers

Acute tyrosine/phenylalanine depletion (ATPD) is a validated neurobiological challenge that results in reduced dopaminergic neurotransmission, allowing examination of the effects of a hypodopaminergic state on craving-related processes. We studied 16 nonabstaining smokers (>10 cigarettes/day; 9 males; age 20-33 years) to whom was administered a tyrosine/phenylalanine-free mixture (TYR/PHE-free) and a balanced amino acid mixture (BAL) in a double-blind, counterbalanced, crossover design. Subjective cigarette craving, attentional bias to smoking-related word cues, relative value of cigarettes, negative mood, and expired carbon monoxide (CO) levels were measured at various timepoints through 300 min. Participants smoked at hourly intervals to prevent acute nicotine withdrawal during testing. The TYR/PHE-free mixture, as compared to the BAL mixture, was associated with a greater increase in CO levels from baseline (p = 0.01). Adjusting for the potential confounding influence of between-condition differences in CO levels across time, TYR/PHE-free mixture was associated with increased demand for cigarettes (p = 0.01) and decreased attentional bias toward smoking-related words (p = 0.003). There were no significant differences between conditions in either subjective craving or depressed or anxious mood (p values > 0.05). Among nonabstaining daily smokers, acute dopaminergic depletion via ATPD may influence smoking behavior and indices of smoking-related motivation, such as attentional bias to smoking cues and relative cigarette value, which are not readily captured by subjective craving.

Role of Renal Medullary Heme Oxygenase in the Regulation of Pressure Natriuresis and Arterial Blood Pressure

Recent studies have demonstrated that inhibition of renal medullary heme oxygenase (HO) activity and carbon monoxide (CO) significantly decreases renal medullary blood flow and sodium excretion. Given the crucial role of renal medullary blood flow in the control of pressure natriuresis, the present study was designed to determine whether renal medullary HO activity and resulting CO production participate in the regulation of pressure natriuresis and thereby the long-term control of arterial blood pressure. In anesthetized Sprague-Dawley rats, increases in renal perfusion pressure induced significant elevations of CO concentrations in the renal medulla. Renal medullary infusion of chromium mesoporphyrin (CrMP), an inhibitor of HO activity, remarkably inhibited HO activity and the renal perfusion pressure-dependent increases in CO levels in the renal medulla and significantly blunted pressure natriuresis. In conscious Sprague-Dawley rats, continuous infusion of CrMP into the renal medulla significantly increased mean arterial pressure (129+/-2.5 mm Hg in CrMP group versus 118+/-1.6 mm Hg in vehicle group) when animals were fed a normal salt diet (1% NaCl). After rats were switched to a high-salt diet (8% NaCl) for 10 days, CrMP-treated animals exhibited further increases in mean arterial pressure compared with CrMP-treated animals that were kept on normal salt diet (152+/-4.1 versus 130+/-4.2 mm Hg). These results suggest that renal medullary HO activity plays a crucial role in the control of pressure natriuresis and arterial blood pressure and that impairment of this HO/CO-mediated antihypertensive mechanism in the renal medulla may result in the development of hypertension.

Environmental tobacco smoke exposure among non-smoking waiters: measurement of expired carbon monoxide levels.

Exposure to environmental tobacco smoke is a health risk that is of concern to patrons and of particular concern to employees of restaurants and bars. To assess environmental tobacco smoke exposure (using expired carbon monoxide levels) in non-smoking waiters before and after a normal day's shift and to compare pre-exposure levels with non-smoking medical students. An observational study. Restaurants with more than 50 tables or 100 places in São Paulo. 100 non-smoking restaurant waiters and 100 non-smoking medical students in São Paulo, Brazil. Levels of expired carbon monoxide, measured with a Smokerlyser (Bedfont EC 50 Scientific), before and after a normal day's work. Waiters' pre-exposure expired carbon monoxide levels were similar to those of medical students, but after a mean of 9 hours exposure in the workplace, median levels more than doubled (2.0 ppm vs. 5.0 ppm, P <0.001). Post-exposure carbon monoxide levels were correlated with the number of tables available for smokers (Kendall's tau = 0.2, P <0.0001). Exposure to environmental tobacco smoke is the most likely explanation for the increase in carbon monoxide levels among these non-smoking waiters. These findings can be used to inform the ongoing public health debate on passive smoking.

The Generation of Nitric Oxide and Carbon Monoxide Produces Opposite Effects on the Release of Immunoreactive Interleukin-1 from the Rat Hypothalamus in Vitro: Evidence for the Involvement of Different Signaling Pathways

Both the cytokine, interleukin-1 (IL-1), and the gaseous neurotransmitters, nitric oxide (NO) and carbon monoxide (CO), have been implicated in the control of neuroendocrine functions, such as the release of CRH and luteotropic hormone-releasing hormone from the hypothalamus. Though increased levels of IL-1 in this brain region are unambiguously associated with enhanced CRH and reduced luteotropic hormone-releasing hormone release, the net effects of the two gases are still unclear, but in vivo and in vitro evidence suggests that the generation of NO and CO within the hypothalamus might counteract the stimulatory effects of IL-1 and bacterial lipopolysaccharide on the neuroendocrine stress axis. In this study, we have investigated the effects of NO and CO on the release of immunoreactive (ir)-IL-1β from the rat hypothalamus in vitro. It was observed that the NO donor, sodium nitroprusside (SNP), stimulates ir-IL-1β release under basal conditions, whereas the increase in CO levels obtained with hemin, the CO precursor through the heme oxygenase pathway, has no effect on basal ir-IL-1β release but inhibits release stimulated by high K+ concentrations. The opposite effects of the two gases on cytokine release seemed to be caused by the activation of different signaling pathways, because: 1) SNP, but not CO-saturated solutions, is able to increase cyclic GMP levels in hypothalamic tissue; 2) CO-saturated solutions increase PGE2 production and release from the hypothalamic explants, whereas SNP has no effect; 3) SNP-stimulated ir-IL-1β release is counteracted by a selective inhibitor of soluble guanylyl cyclase, LY 83583, but not by a cyclooxygenase inhibitor, indomethacin; and 4) conversely, indomethacin, but not LY 83583, reverses the inhibitory effect of hemin on K+-stimulated ir-IL-1β release. It is concluded that NO and CO signal in the rat hypothalamus via the activation of soluble guanylyl cyclase and cyclooxygenase, respectively.

The generation of nitric oxide and carbon monoxide produces opposite effects on the release of immunoreactive interleukin-1beta from the rat hypothalamus in vitro: evidence for the involvement of different signaling pathways.

Both the cytokine, interleukin-1 (IL-1), and the gaseous neurotransmitters, nitric oxide (NO) and carbon monoxide (CO), have been implicated in the control of neuroendocrine functions, such as the release of CRH and luteotropic hormone-releasing hormone from the hypothalamus. Though increased levels of IL-1 in this brain region are unambiguously associated with enhanced CRH and reduced luteotropic hormone-releasing hormone release, the net effects of the two gases are still unclear, but in vivo and in vitro evidence suggests that the generation of NO and CO within the hypothalamus might counteract the stimulatory effects of IL-1 and bacterial lipopolysaccharide on the neuroendocrine stress axis. In this study, we have investigated the effects of NO and CO on the release of immunoreactive (ir)-IL-1beta from the rat hypothalamus in vitro. It was observed that the NO donor, sodium nitroprusside (SNP), stimulates ir-IL-1beta release under basal conditions, whereas the increase in CO levels obtained with hemin, the CO precursor through the heme oxygenase pathway, has no effect on basal ir-IL-1beta release but inhibits release stimulated by high K+ concentrations. The opposite effects of the two gases on cytokine release seemed to be caused by the activation of different signaling pathways, because: 1) SNP, but not CO-saturated solutions, is able to increase cyclic GMP levels in hypothalamic tissue; 2) CO-saturated solutions increase PGE2 production and release from the hypothalamic explants, whereas SNP has no effect; 3) SNP-stimulated ir-IL-1beta release is counteracted by a selective inhibitor of soluble guanylyl cyclase, LY 83583, but not by a cyclooxygenase inhibitor, indomethacin; and 4) conversely, indomethacin, but not LY 83583, reverses the inhibitory effect of hemin on K+-stimulated ir-IL-1beta release. It is concluded that NO and CO signal in the rat hypothalamus via the activation of soluble guanylyl cyclase and cyclooxygenase, respectively.

Carbon monoxide exposure from commercial brand cigarettes under controlled smoking conditions

Carbon monoxide (CO) exposure from ultralow-, low- and high-CO delivery commerical cigarettes was examined under controlled smoking conditions. Seven chronic smokers of mid- to high-CO delivery commercial cigarettes served in the experiment. CO level increases of 2.10, 5.76 and 7.38 ppm were obtained from ultralow-yield (1.6 mg CO delivery), low-yield (5.9 mg CO delivery) and high-yield (14.3 mg CO delivery) cigarettes, respectively. Subjects achieved significantly higher increases in CO levels from both low- and high-yield cigarettes than from ultralow-yield cigarettes, but increased levels of CO from low-and high-yield cigarettes were not different from each other. The data suggest that degree of CO absorption by the lungs during a short period of time may limit increases in CO levels obtained from high-yield cigarettes.