Increased Carbon Monoxide in Exhaled Air of Critically Ill Patients

Scharte, Marion; Bone, Hans-Georg; Aken, Hugo Van; Meyer, J.

doi:10.1006/bbrc.1999.1936

Cited by 77 publications

(49 citation statements)

References 20 publications

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“…Previous studies reported that there was an increase in ExCO-C in inflammatory airway diseases, such as asthma, chronic obstructive pulmonary disease and cystic fibrosis (26)(27)(28). It has also been reported that ExCO-C was increased in systemic inflammatory diseases such as sepsis and critical illness (15,(29)(30)(31). Our findings in this study have additionally shown that I/R during LDLT led to an increase in ExCO-C, and indicate that I/R in LDLT is a significant oxidative stress on the grafted liver.…”

Section: Discussionmentioning

confidence: 96%

Increased exhaled carbon monoxide concentration during living donor liver transplantation

Matsusaki

Morimatsu²,

Takahashi³

et al. 2008

Int J Mol Med

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Section: Discussionmentioning

confidence: 96%

Increased exhaled carbon monoxide concentration during living donor liver transplantation

Matsusaki

Morimatsu²,

Takahashi³

et al. 2008

Int J Mol Med

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“…18 Further, the role of CO in attenuating vasodilatation in response to NO is demonstrated in bovine pulmonary artery where induction of HO with two to fourfold increase in its activity by either cobalt chloride or Co-protoporphyrin IX resulted in decreased cGMP production and attenuation of pulmonary artery relaxation to the NO-donor spermine-NONOate. 25 Moreover, excess endogenous CO, even at low levels, can reflect underlying inflammatory and oxidative stress in critical illness 26 and vascular pathology. 27 HO expression is increased in patients with OSA 28 with elevated endogenous blood levels of CO. 29 The role of CO in vascular function and its relationship to hypertension in patients with OSA is unknown.…”

mentioning

confidence: 99%

Activation of Heme Oxygenase and Suppression of cGMP Are Associated With Impaired Endothelial Function in Obstructive Sleep Apnea With Hypertension

Jafari

Mohsenin

2012

Am J Hypertens

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Obstructive sleep apnea (OSA) is a highly prevalent disorder characterized by recurrent upper airway obstruction during sleep. These episodes are terminated by arousals and are commonly associated with hypoxemia. The acute hemodynamic and autonomic perturbations that accompany obstructive apneas can lead to sustained diurnal hypertension. [1][2][3] In a cross-sectional study of a sleep clinic patients 60% of men and women with severe OSA had hypertension. 4 In populationbased prospective studies, patients with severe OSA had three times the risk of developing hypertension within 5 years, independent of other risk factors. 1 Current evidence suggests that sympathoexcitation, inflammatory processes, oxidative stress, and endothelial dysfunction play important roles in the pathogenesis of hypertension and vascular complications in OSA. [5][6][7][8][9] However, the exact mechanisms of hypertension and varying susceptibility to endothelial dysfunction among patients with OSA are not well understood.Endothelial-dependent vasodilatory capacity is primarily regulated by local production of nitric oxide (NO) and modulated by carbon monoxide (CO). 10-12 CO is predominantly released during heme metabolism by heme oxygenase (HO), generating iron and biliverdin. Biliverdin is further metabolized to bilirubin by biliverdin reductase. HO has been reported to be present in all tissues and colocalizes with NO synthase in the vasculature. 13,14 Like NO, the ability of CO to relax blood vessels occurs through soluble guanylate cyclase with increases in guanosine 3′,5′-cyclic monophosphate (cGMP) and activation of calcium-gated potassium channels. 15,16 The activation of potassium channels inhibits calcium entry from BackgroundObstructive sleep apnea (Osa) is a highly prevalent disorder that increases the risk of systemic hypertension and cardiovascular diseases. Heme oxygenase (HO) has been shown to be upregulated in patients with Osa and its overexpression in mice causes hypertension. End products of HO are carbon monoxide (CO) and bilirubin. CO exerts a pleiotropic action on vasoregulation. Despite high prevalence and incident of hypertension in Osa, its pathophysiology is not well-understood, particularly in regard to varying susceptibility of patients to hypertension. We investigated the role of HO in endothelial dysfunction and hypertension in Osa.

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“…Indeed, it has been demonstrated that exhaled CO levels are increased in asthma (23,86), cystic fibrosis (59), diabetes (58), and critically ill patients (64). It is presumed that the exhaled CO reflects increased activity of HO due to a disease process.…”

Section: Exhaled Markermentioning

confidence: 99%

Carbon Monoxide and Human Disease

Morse

Sethi

2002

Antioxidants & Redox Signaling

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Carbon monoxide is produced endogenously in humans through the breakdown of hemoglobin by heme oxygenase. Although originally thought to be a superfluous by-product of heme catabolism, carbon monoxide is now known to play a central role in many aspects of human health and disease. The functions of carbon monoxide that have been described to date are myriad, including blood pressure regulation, maintenance of organ-specific vascular tone, neurotransmission, stress response, platelet activation, and smooth muscle relaxation. This review outlines what is known to date about carbon monoxide as it relates to human disease.

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Increased Carbon Monoxide in Exhaled Air of Critically Ill Patients

Cited by 77 publications

References 20 publications

Increased exhaled carbon monoxide concentration during living donor liver transplantation

Increased exhaled carbon monoxide concentration during living donor liver transplantation

Activation of Heme Oxygenase and Suppression of cGMP Are Associated With Impaired Endothelial Function in Obstructive Sleep Apnea With Hypertension

Carbon Monoxide and Human Disease

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