Based on the records of carboxyhemoglobin in blood samples stored for recent years, the stability of carboxyhemoglobin in these samples could be affected by the containers, the storage temperatures, the volumes of air above the blood, the saturation of the initial carboxyhemoglobin and preservatives added in these blood samples, among which the storage temperatures, the volumes of air above the blood and the saturation of the initial carboxyhemoglobin are the major influence factors.
Air ; Blood Preservation ; Carbon Monoxide/chemistry* ; Carbon Monoxide Poisoning/blood* ; Carboxyhemoglobin/analysis* ; Drug Stability ; Forensic Medicine ; Humans ; Specimen Handling/methods* ; Temperature

Pulverized coal reburning, ammonia injection and advanced reburning in a pilot scale drop tube furnace were investigated. Premix of petroleum gas, air and NH3 were burned in a porous gas burner to generate the needed flue gas. Four kinds of pulverized coal were fed as reburning fuel at constant rate of 1g/min. The coal reburning process parameters including 15% approximately 25% reburn heat input, temperature range from 1100 degrees C to 1400 degrees C and also the carbon in fly ash, coal fineness, reburn zone stoichiometric ratio, etc. were investigated. On the condition of 25% reburn heat input, maximum of 47% NO reduction with Yanzhou coal was obtained by pure coal reburning. Optimal temperature for reburning is about 1300 degrees C and fuel-rich stoichiometric ratio is essential; coal fineness can slightly enhance the reburning ability. The temperature window for ammonia injection is about 700 degrees C approximately 1100 degrees C. CO can improve the NH3 ability at lower temperature. During advanced reburning, 72.9% NO reduction was measured. To achieve more than 70% NO reduction, Selective Non-catalytic NO(x) Reduction (SNCR) should need NH3/NO stoichiometric ratio larger than 5, while advanced reburning only uses common dose of ammonia as in conventional SNCR technology. Mechanism study shows the oxidization of CO can improve the decomposition of H2O, which will rich the radical pools igniting the whole reactions at lower temperatures.
Air Pollutants ; chemistry ; isolation & purification ; Carbon Monoxide ; chemistry ; Coal ; Computer Simulation ; Hot Temperature ; Models, Chemical ; Nitrogen Oxides ; chemistry ; isolation & purification ; Oxidation-Reduction ; Temperature

In this study, products of psoralen pyrolysis were detected using a solid pyrolysis apparatus and synchrotron radiation vacuum ultraviolet photoionization mass spectrum (SVUV-PIMS). The pyrolytic kinetics of psoralen was also studied by calculating its initial pyrolytic route in quantum chemistry. According to the findings with SVUV-PIMS, three pyrolytic products were observed, CO, C9H6O and C10H6O2. Theoretically, three fragment pathways were calculated for psoralen, in which the major primary decomposition route was de-CO, and the major secondary decomposition reaction was de-CO reaction of de-CO products.
Carbon Monoxide ; chemistry ; Ficusin ; chemistry ; Hot Temperature ; Kinetics ; Mass Spectrometry ; instrumentation ; methods ; Models, Chemical ; Molecular Structure ; Organic Chemicals ; chemistry ; Synchrotrons ; Ultraviolet Rays ; Vacuum

OBJECTIVETo compare the distribution of heme oxygenase-2 and concentration of carbon monoxide in rat penile tissue of 8, 16 and 24 months and investigate the relationship between the system of HO-2/CO and aging.

METHODSUsing SABC immunohistochemistry staining, image analysis system and the method of carboxyhemoglobin standard curve, the distribution of heme oxygenase-2 and concentration of carbon monoxide in different month rat penile tissues were investigated.

RESULTSThe penile arteries were surrounded by HO-2 positive cells, which were also seen in the trabecular meshwork of smooth muscle. Compared with other part of penile, the penile arteries adventitia and the endothelial cells of cavernous exhibited darker staining. With the increasing of rat's living month the staining of penile tissues turned faint and the concentration of carbon monoxide in tissue decreased( P < 0.05 ). The imaging analysis system showed that the older the rat was the less HO-2 positive compositions contained (P < 0.05).

CONCLUSIONWith aging the decreasing concentration of HO-2 leads to the downfgt-regulation in rat penile tissue.

Aging ; metabolism ; Animals ; Carbon Monoxide ; analysis ; metabolism ; Down-Regulation ; Heme Oxygenase (Decyclizing) ; analysis ; metabolism ; Image Processing, Computer-Assisted ; Immunohistochemistry ; Male ; Penis ; chemistry ; metabolism ; Rats ; Rats, Wistar ; Staining and Labeling

Hypoxic pulmonary vasoconstriction (HPV), a unique response of pulmonary circulation, is critical to prevent hypoxemia under local hypoventilation. Hypoxic inhibition of K+ channel is known as an important O2-sensing mechanism in HPV. Carbon monoxide (CO) is suggested as a positive regulator of Ca2+-activated K+ channel (BK(Ca)), a stimulator of guanylate cyclase, and an O2-mimetic agent in heme moiety-dependent O2 sensing mechanisms. Here we compared the effects of CO on the HPV (Po2, 3%) in isolated pulmonary artery (HPV(PA)) and in blood-perfused/ventilated lungs (HPV(lung)) of rats. A pretreatment with CO (3%) abolished the HPV(PA) in a reversible manner. The inhibition of HPV(PA) was completely reversed by 1H-[1,2,4]oxadiazolo-[4,3-a]quinoxalin-1-one (ODQ), a guanylate cyclase inhibitor. In contrast, the HPV(lung) was only partly decreased by CO. Moreover, the partial inhibition of HPV(lung) by CO was affected neither by the pretreatment with ODQ nor by NO synthase inhibitor (L-NAME). The CO-induced inhibitions of HPV(PA) and HPV(lung) were commonly unaffected by tetraethylammonium (TEA, 2 mM), a blocker of BK(Ca). As a whole, CO inhibits HPV(PA) via activating guanylate cyclase. The inconsistent effects of ODQ on HPV(PA) and HPV(lung) suggest that ODQ may lose its sGC inhibitory action when applied to the blood-containing perfusate.
Animals ; Anoxia/*physiopathology ; Carbon Monoxide/*pharmacology ; Guanylate Cyclase/antagonists & inhibitors/metabolism ; NG-Nitroarginine Methyl Ester/chemistry/pharmacology ; Nitric Oxide Synthase/antagonists & inhibitors/metabolism ; Oxadiazoles/chemistry/pharmacology ; Pulmonary Artery/*physiopathology ; Quinoxalines/chemistry/pharmacology ; Rats ; Tetraethylammonium/chemistry/pharmacology ; Vasoconstriction/*drug effects/physiology

Carbon monoxide intoxication is the most prevalent cause of death from carbon monoxide poisoning. We herein report the case of a 56-year-old man who was found unconscious and smelled of smoke after exposure to carbon monoxide from a heater. He scored 5 on the Glasgow Coma Scale, and had respiratory insufficiency and elevated troponin I, creatine kinase-MB fraction and carboxyhaemoglobin levels. He was treated by mechanical ventilation. After regaining consciousness, brain magnetic resonance imaging showed diffusion restriction in the left occipital lobe; there was a loss of vision (right temporal hemianopsia), which improved by the follow-up session. Carbon monoxide intoxication may cause neurologic and cardiac sequelae, and the initial treatment includes oxygen therapy. Acute carbon monoxide poisoning can cause serious injury to the brain, heart and other organs; the most severe damages that could be inflicted to the brain include cerebral ischaemia and hypoxia, oedema, and neural cell degeneration and necrosis.
Brain ; physiopathology ; Brain Ischemia ; physiopathology ; Carbon Monoxide ; chemistry ; Carbon Monoxide Poisoning ; physiopathology ; Carboxyhemoglobin ; chemistry ; Creatine Kinase, MB Form ; blood ; Diffusion ; Glasgow Coma Scale ; Humans ; Hyperbaric Oxygenation ; Hypoxia ; Magnetic Resonance Imaging ; Male ; Middle Aged ; Myocardial Ischemia ; physiopathology ; Stroke ; physiopathology ; Troponin I ; blood

Carbon monoxide has been proved to be an important signal molecule in body. Transition metal carbonyl compounds are solidified form of carbon monoxide. Numerous studies have shown that Ruthenium carbonyl carbon monoxide releasing molecules have a strong pharmacological activity. In this paper, five Ruthenium (II) carbonyl CORMs 1-5 were synthesized and their toxicology, tissue distribution and interaction with blood endogenous substances were investigated. The results showed CORMs' IC50 to fibroblasts are ranged from 212.9 to 2089.2 micromol x L(-1). Their oral LD50 to mouse is between 800 to 1600 mg x kg(-1). After repeated administration, CORMs 1 and CORMs 5 haven't shown an obvious influence to rats' liver and kidney function, but caused the injury to liver and kidney cells. The in vivo distribution result revealed the majority of CORMs were distributed in blood, liver and kidney, only a small part of CORMs distributed in lung, heart and spleen. They could scarcely cross the blood-brain barrier and distribute to brain. The non-CO ligands in structure have an obvious relevance to their in vivo absorption and distribution. Interestingly, CORMs could enhance the fluorescence of bovine serum albumin, and this enhancement was in direct proportion with the concentration of CORMs. Under different conditions, interaction of CORMs with glutathione got different type of products, one is Ruthenium (II) tricarbonyl complexes, and Ruthenium (II) dicarbonyl complexes.
Animals ; Carbon Monoxide ; chemistry ; pharmacokinetics ; toxicity ; Fibroblasts ; drug effects ; Kidney ; drug effects ; Liver ; drug effects ; Mice ; Molecular Structure ; Organometallic Compounds ; chemical synthesis ; chemistry ; pharmacokinetics ; toxicity ; Rats ; Rats, Wistar ; Ruthenium ; chemistry ; pharmacokinetics ; toxicity ; Tissue Distribution

BACKGROUND: A large number of pollutants such as sulfur dioxide, nitric oxide, carbon monoxide, particulate matter, and ozone influence on the body. These pollutants put a burden on the lung and the sequelae resulting from the oxidative stress are thought to contribute to the development of fibrotic lung disease, emphysema, chronic bronchitis and lung cancer. Also, carbon monoxide generated from the incomplete combustion of carbon-containing compounds is an important component of air pollution caused by traffic exhaust fumes and has the toxic effect of tissue hypoxia and produce various systemic and neurologic complications. The objective of this study is to compare the difference of pulmonary function and serum carboxyhemoglobin(CO-Hb) level between the traffic policemen and clerk policemen. METHODS: Three hundred and twenty-nine of traffic policemen, and one hundred and thirty clerk policemen were included between 2001 May and 2002 August. The policemen who took part in this study were asked to fill out a questionnaire which included questions on age, smoking, drinking, years of working, work-related symptoms and past medical history. The serum CO-Hb level was measured by using carboxyoximeter. Pulmonary function test was done by using automated spirometer. Additional tests, such as elecrocardiogram, urinalysis, chest radiography, blood chemistry, and CBC, were also done. RESULTS: FEV1(%) was 97.1+/-0.85%, and 105.7+/-1.21%(p<0.05). FVC(%) was 94.6+/-0.67%, and 102.1+/-1.09%, respectively(p<0.05). Serum CO-Hb level was 2.4+/-0.06%, and 1.8+/-0.08%(p<0.05). After correction of confounding factors (age, smoking), significant variables were FVC(%), FEV1(%) and serum CO-Hb level(%)(p<0.05). CONCLUSION: Long exposure to air pollution may influence the pulmonary function and serum CO-Hb level. But, further prospective cohort study will be needed to elucidate detailed influences of specific pollutants on pulmonary function and serum carboxyhemoglobin level.
Air Pollution ; Anoxia ; Bronchitis, Chronic ; Carbon Monoxide ; Carboxyhemoglobin* ; Chemistry ; Cohort Studies ; Drinking ; Emphysema ; Lung ; Lung Diseases ; Lung Neoplasms ; Nitric Oxide ; Oxidative Stress ; Ozone ; Particulate Matter ; Surveys and Questionnaires ; Radiography ; Respiratory Function Tests ; Smoke ; Smoking ; Sulfur Dioxide ; Thorax ; Urinalysis

OBJECTIVETo investigate the changes in the expression of HIF-1alpha in rat superior mesenteric artery (SMA) tissue after hypovolemic shock (HS), and its relationship with the pathogenesis of vascular hyporeactivity.

METHODSOne hundred and twelve SD rats were used in the study, and they were randomly divided into HS group (n = 56) and treatment group (n = 56, with intraperitoneal injection of 9 microg/kg oligomycin 4 h before the experiment). Arterial blood of the rats in each group were harvested at 0.0, 0.5, 1.0, 2.0, 3.0, 4.0, 6.0 post-injury hour (PIH), respectively,with 8 rats at each time-points. Then the rats were sacrificed and superior mesenteric arteries (SMA) were harvested. Other 8 rats without any treatment served as normal controls. The changes in mRNA expression of HIF-1alpha, inducible nitric oxide synthase (iNOS) and hemeoxygenase 1 (HO-1) were determined with RT-PCR. The contraction of vascular ring of SMA to gradient concentration of norepinephrine (NE) was measured with ex vitro vascular ring tension determination method. The plasma content of carbon monoxide and nitric oxide were measured with sodium dithionite reduction method and nitrate reductase method, respectively.

RESULTSCompared with normal controls, Vascular reactivity of SMA in HS group increased compensatorily during early stage of HS (0.0 -1.0 h), and peaked at 0.5 h. The pD2 ( - log[ NE] ) of NE decreased, but the maximal contraction (Emax) was above the normal level during 0.0 - 1.0 PIH (P < 0.01). During the middle and late shock stage, the vascular reactivity decreased gradually. The Emax decreased, pD2 increased, and the Emax was below the normal level at 4.0 PIH (P < 0.01). The increase of vascular reactivity in treatment group was partially inhibited during early stage after injury (P < 0.01). The Emax was (2.01 +/- 0. 22) g/mg at 0.5 PIH, which was obviously lower than that in HS group [(2.96 +/- 0.18) g/mg , P < 0.05]. In decompensated period of HS, the vascular reactivity was improved mildly, which exhibited obvious difference compared with that in HS group at 4.0 and 6.0 PIH (P < 0.05 or P < 0.01). HIF-1alpha mRNA expression in HS group exhibited a time-dependent increase following HS, and peaked at 4.0 PIH (P < 0.01), and the iNOS and HO-1 mRNA expression were also gradually increased, reaching the peak value at 2.0 and 4.0 PIH, respectively (P < 0.01). The plasma content of CO and NO in whole blood were gradually increased following the shock process when compared with those in normal control group, while the CO content in whole blood in treatment group maintained normal, and the plasma content of NO was obviously decreased compared with that in control group.

CONCLUSIONHS can elicit a dual-phase change in vascular reactivity as previously described. HIF-1alpha plays an important role in the occurrence of vascular hyporeactivity following HS.

Animals ; Blood Vessels ; metabolism ; Carbon Monoxide ; blood ; Heme Oxygenase-1 ; metabolism ; Hypoxia-Inducible Factor 1, alpha Subunit ; metabolism ; Nitric Oxide ; blood ; Nitric Oxide Synthase ; metabolism ; Plasma ; chemistry ; Rats ; Rats, Sprague-Dawley ; Shock, Hemorrhagic ; metabolism