The effects of carbon monoxide on respiratory chemoreflexes in humans

Vesely, Alex; Somogyi, Ron B.; Sasano, Hiroshi; Sasano, Nobuko; Fisher, Joseph A.; Duffin, James

doi:10.1016/s0013-9351(03)00107-5

Cited by 6 publications

(2 citation statements)

References 32 publications

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“…For instance, CO inhalation at doses that exhibit preclinical efficacy in murine models of cancer (250–500 ppm for 1 h) has already been tested in humans 129–132 and appears to be well tolerated, at least in short-term regimens.…”

Section: Carbon Monoxidementioning

confidence: 99%

Gasotransmitters in cancer: from pathophysiology to experimental therapy

Szabó

2015

Nat Rev Drug Discov

573

424

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The three endogenous gaseous transmitters — nitric oxide (NO), carbon monoxide (CO) and hydrogen sulfide (H2S) — regulate a number of key biological functions. Emerging data identify several new mechanisms of each of these three gasotransmitters in tumour biology. It is now appreciated that they show bimodal pharmacological character in cancer, in that not only the inhibition of their biosynthesis, but also elevation of the concentration of each gasotransmitter beyond a certain threshold can exert anticancer effects. This Review discusses the role of each gasotransmitter in cancer and the effects of compounds — some of which are in early-stage clinical studies — that modulate the levels of each gasotransmitter. A clearer understanding of the pharmacological character of these three gases and their underlying biological mechanisms is expected to guide further clinical translation.

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Section: Carbon Monoxidementioning

confidence: 99%

Gasotransmitters in cancer: from pathophysiology to experimental therapy

Szabó

2015

Nat Rev Drug Discov

573

424

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“… Cardiovascular effects (cardiac output, heart rate, artery diameter, electrocardiogram changes) [ 25 , 29 , 33 , 49 , 89 , 90 ] 2.4 [ 33 ] 15 ppm for 10 days (continuous exposure) Electrocardiogram changes, specifically to p -waves, observed among three out of 15 subjects. Respiratory effects [ 22 , 25 , 36 , 45 , 46 , 89 , 91 ] 3.95 (SD: 1.87) [ 25 ] 5000 ppm for 2.5–3.5 min Decrease in mean (sd) inspiratory capacity from 3655 (415) ml to 3380 (419) ml ( p < 0.05), and total lung capacity from 7705 (1083) ml to 7545 (993) ml ( p < 0.02). Cognitive function [ 24 , 26 , 28 , 34 , 37 , 38 , 43 , 47 ] 5.1 (SD: 0.57) [ 34 ] 74.1 ppm for 4 h Decreases in performance of visual tracking exercises among high exposure group, compared with low exposure and control groups ( p < 0.01).…”

Section: Resultsmentioning

confidence: 99%

A review of the experimental evidence on the toxicokinetics of carbon monoxide: the potential role of pathophysiology among susceptible groups

Barn¹,

Giles²,

Héroux³

et al. 2018

Environ Health

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BackgroundAcute high level carbon monoxide (CO) exposure can cause immediate cardio-respiratory arrest in anyone, but the effects of lower level exposures in susceptible persons are less well known. The percentage of CO-bound hemoglobin in blood (carboxyhemoglobin; COHb) is a marker of exposure and potential health outcomes. Indoor air quality guidelines developed by the World Health Organization and Health Canada, among others, are set so that CO exposure does not lead to COHb levels above 2.0%, a target based on experimental evidence on toxicodynamic relationships between COHb and cardiac performance among persons with cardiovascular disease (CVD). The guidelines do not consider the role of pathophysiological influences on toxicokinetic relationships. Physiological deficits that contribute to increased CO uptake, decreased CO elimination, and increased COHb formation can alter relationships between CO exposures and resulting COHb levels, and consequently, the severity of outcomes. Following three fatalities attributed to CO in a long-term care facility (LTCF), we queried whether pathologies other than CVD could alter CO-COHb relationships. Our primary objective was to inform susceptibility-specific modeling that accounts for physiological deficits that may alter CO-COHb relationships, ultimately to better inform CO management in LTCFs.MethodsWe reviewed experimental studies investigating relationships between CO, COHb, and outcomes related to health or physiological outcomes among healthy persons, persons with CVD, and six additional physiologically susceptible groups considered relevant to LTCF residents: persons with chronic obstructive pulmonary disease (COPD), anemia, cerebrovascular disease (CBD), heart failure, multiple co-morbidities, and persons of older age (≥ 60 years).ResultsWe identified 54 studies published since 1946. Six studies investigated toxicokinetics among healthy persons, and the remaining investigated toxicodynamics, mainly among healthy persons and persons with CVD. We identified one study each of CO dynamics in persons with COPD, anemia and persons of older age, and no studies of persons with CBD, heart failure, or multiple co-morbidities. Considerable heterogeneity existed for exposure scenarios and outcomes investigated.ConclusionsLimited experimental human evidence on the effects of physiological deficits relevant to CO kinetics exists to support indoor air CO guidelines. Both experimentation and modeling are needed to assess how physiological deficits influence the CO-COHb relationship, particularly at sub-acute exposures relevant to indoor environments. Such evidence would better inform indoor air quality guidelines and CO management in indoor settings where susceptible groups are housed.

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Carbon Monoxide Transport and Actions in Blood and Tissues

Thom

2011

Comprehensive Physiology

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This chapter will discuss the transport of carbon monoxide (CO) from the environment to the tissues of the body and physiological effects on blood-borne cells and perivascular tissues. It will review the physiology of CO exchange between alveolar gas and pulmonary capillary blood, dynamics of hemoglobin transport, the effects of CO on blood elements, and the effects of CO on extravascular tissues at the capillary bed. Effects of CO from exogenous and endogenous sources on the activities of different proteins will be reviewed. Because CO binds competitively to heme-containing proteins its effects depend on CO concentration relative to alternative ligands. Therefore, some discussion is devoted to how nitric oxide and hydrogen sulfide influence CO effects.

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The effects of carbon monoxide on respiratory chemoreflexes in humans

Cited by 6 publications

References 32 publications

Gasotransmitters in cancer: from pathophysiology to experimental therapy

Gasotransmitters in cancer: from pathophysiology to experimental therapy

A review of the experimental evidence on the toxicokinetics of carbon monoxide: the potential role of pathophysiology among susceptible groups

Carbon Monoxide Transport and Actions in Blood and Tissues

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