Transient carbon monoxide inhibits the ventilatory responses to hypoxia through peripheral mechanisms in the rat

Zhuang, Jianguo; Xu, Fadi; Campen, Matthew J.; Hernandez, Joseph P.; Shi, Shaojun; Wang, Rurong

doi:10.1016/j.lfs.2005.10.037

Cited by 5 publications

(4 citation statements)

References 34 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Moreover, carbon monoxide determines a cardiac inotropic effect with augmented oxygen demand and diminished coronary perfusion, a situation that can rapidly precipitate toward cardiac ischemia [30]. An increase of the pulmonary pressure was reported in cases of CO poisoning [31,32], possibly as a consequence of the severe cerebral hypoxia following intoxication [33,34].…”

Section: Discussionmentioning

confidence: 99%

Immunohistochemical expression of fibronectin and C5b-9 in the myocardium in cases of carbon monoxide poisoning

et al. 2010

View full text Add to dashboard Cite

Even if there is clinical evidence that carbon monoxide poisoning determines cardiac damage, the literature on the cardiac pathomorphology in such cases is scarce. We investigated the immunohistochemical expression of two known markers of fresh cardiac damage, fibronectin and the terminal complement complex C5b-9, in both cardiac ventricles in 26 cases of CO intoxication (study group, 15 ♀, 11 ♂, mean age 47 years, mean COHb level 65.9%, min. 51%, max. 85%) compared to a group of 23 cases of hanging (n = 23, 4♀, 19♂, mean age 42 years) as well as to 25 cases of myocardial infarction (n = 25, 13♀, 12♂, mean age 64 years). Fresh cardiac damage was detected with the antibody fibronectin in cases of CO poisoning and was prevalently localised at the right ventricle.

show abstract

Section: Discussionmentioning

confidence: 99%

Immunohistochemical expression of fibronectin and C5b-9 in the myocardium in cases of carbon monoxide poisoning

et al. 2010

View full text Add to dashboard Cite

show abstract

“…The carotid bodies can also be adversely affected by tobacco exposure. Smoke exposure can lead to abnormal maturation and neurotransmitter levels such as dopamine, leaving infants more vulnerable to hypoxic states (58,(79)(80)(81). These findings may further explain the impaired arousal observed in smoke-exposed infants in response to hypoxia (24,25).…”

Section: Autonomic Nervous System (Ans)mentioning

confidence: 99%

The Role of Maternal Smoking in Sudden Fetal and Infant Death Pathogenesis

2020

View full text Add to dashboard Cite

Maternal smoking is a risk factor for both sudden infant death syndrome (SIDS) and sudden intrauterine unexplained death syndrome (SIUDS). Both SIDS and SIUDS are more frequently observed in infants of smoking mothers. The global prevalence of smoking during pregnancy is 1.7% and up to 8.1% of women in Europe smoke during pregnancy and worldwide 250 million women smoke during pregnancy. Infants born to mothers who smoke have an abnormal response to hypoxia and hypercarbia and they also have reduced arousal responses. The harmful effects of tobacco smoke are mainly mediated by release of carbon monoxide and nicotine. Nicotine can enter the fetal circulation and affect multiple developing organs including the lungs, adrenal glands and the brain. Abnormalities in brainstem nuclei crucial to respiratory control, the cerebral cortex and the autonomic nervous system have been demonstrated. In addition, hypodevelopment of the intermediolateral nucleus in the spinal cord has been reported. It initiates episodic respiratory movements that facilitate lung development. Furthermore, abnormal maturation and transmitter levels in the carotid bodies have been described which would make infants more vulnerable to hypoxic challenges. Unfortunately, smoking cessation programs do not appear to have significantly reduced the number of pregnant women who smoke.

show abstract

“…Although CO mainly exerts its effects at the level of the central nervous system, in vitro and in vivo effects on peripheral arterial chemoreceptors have also been reported. Exogenous CO exposure reduces the hypoxic ventilatory response in rats, and this effect has been ascribed to the peripheral chemoreceptors (Zhuang et al 2006), based upon evidence that CO exposure inhibits CB sensory discharge in hypoxia in the cat (Lahiri et al 1993) and reverses hypoxic inhibition of the K + channels of CB chemoreceptors in the rat (Riesco-Fagundo et al 2001). Substance abuse.…”

Section: Continuousmentioning

confidence: 99%

“…Exogenous CO exposure reduces the hypoxic ventilatory response in rats, and this effect has been ascribed to the peripheral chemoreceptors (Zhuang et al . ), based upon evidence that CO exposure inhibits CB sensory discharge in hypoxia in the cat (Lahiri et al . ) and reverses hypoxic inhibition of the K + channels of CB chemoreceptors in the rat (Riesco‐Fagundo et al .…”

Section: Introductionmentioning

confidence: 99%

Central and peripheral chemoreceptors in sudden infant death syndrome

Porzionato

Macchi

2018

The Journal of Physiology

View full text Add to dashboard Cite

The pathogenesis of sudden infant death syndrome (SIDS) has been ascribed to an underlying biological vulnerability to stressors during a critical period of development. This paper reviews the main data in the literature supporting the role of central (e.g. retrotrapezoid nucleus, serotoninergic raphe nuclei, locus coeruleus, orexinergic neurons, ventral medullary surface, solitary tract nucleus) and peripheral (e.g. carotid body) chemoreceptors in the pathogenesis of SIDS. Clinical and experimental studies indicate that central and peripheral chemoreceptors undergo critical development during the initial postnatal period, consistent with the age range of SIDS (<1 year). Most of the risk factors for SIDS (gender, genetic factors, prematurity, hypoxic/hyperoxic stimuli, inflammation, perinatal exposure to cigarette smoke and/or substance abuse) may structurally and functionally affect the developmental plasticity of central and peripheral chemoreceptors, strongly suggesting the involvement of these structures in the pathogenesis of SIDS. Morphometric and neurochemical changes have been found in the carotid body and brainstem respiratory chemoreceptors of SIDS victims, together with functional signs of chemoreception impairment in some clinical studies. However, the methodological problems of SIDS research will have to be addressed in the future, requiring large and highly standardized case series. Up-to-date autopsy protocols should be produced, involving substantial, and exhaustive sampling of all potentially involved structures (including peripheral arterial chemoreceptors). Morphometric approaches should include unbiased stereological methods with three-dimensional probes. Prospective clinical studies addressing functional tests and risk factors (including genetic traits) would probably be the gold standard, allowing markers of intrinsic or acquired vulnerability to be properly identified.

show abstract

Transient carbon monoxide inhibits the ventilatory responses to hypoxia through peripheral mechanisms in the rat

Cited by 5 publications

References 34 publications

Immunohistochemical expression of fibronectin and C5b-9 in the myocardium in cases of carbon monoxide poisoning

Immunohistochemical expression of fibronectin and C5b-9 in the myocardium in cases of carbon monoxide poisoning

The Role of Maternal Smoking in Sudden Fetal and Infant Death Pathogenesis

Central and peripheral chemoreceptors in sudden infant death syndrome

Contact Info

Product

Resources

About