Myocardial Dysfunction and Potential Cardiac Hypoxia in Rats Induced by Carbon Monoxide Inhalation

Favory, Raphaël; Lancel, Steve; Tissier, Stéphanie; Mathieu, Daniel; Decoster, Brigitte; Nevière, Rémi

doi:10.1164/rccm.200601-117oc

Cited by 39 publications

(23 citation statements)

References 40 publications

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“…Indeed, it is today well known that NO play a major role in the coronary vasomotor response of the myocardium. Therefore, we can note that a myocardial dysfunction and a potential cardiac hypoxia in heart of rats inhaling CO for 90 min at 250 ppm was previously reported (Favory et al, 2006). In this model, myocardial hypoxia was explained by coronary endothelium dependent abnormalities.…”

Section: Co In Urban Environmentsupporting

confidence: 64%

Carbon Monoxide Urban Air Pollution: Cardiac Effects

Meyer¹,

Tanguy²,

Obert³

et al. 2011

Advanced Topics in Environmental Health and Air Pollution Case Studies

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Section: Co In Urban Environmentsupporting

confidence: 64%

Carbon Monoxide Urban Air Pollution: Cardiac Effects

Meyer¹,

Tanguy²,

Obert³

et al. 2011

Advanced Topics in Environmental Health and Air Pollution Case Studies

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“…It is not clear whether CO mediates this effect directly or indirectly through NO production. At least one study suggests that CO-related increases in coronary perfusion pressure are related to both endothelium-dependent and -independent mechanisms, suggesting more than one mechanism of action for CO. 20 The trend toward decreased pO 2 during the basal phase in the CO and nitrogen control groups cannot be explained. However, statistically the difference in pO 2 was not significant and the pO 2 decreased during the experimental phase and returned to baseline levels in the recovery in these groups ( Figure 5).…”

Section: Discussionmentioning

confidence: 90%

Carbon Monoxide Has Direct Toxicity on the Myocardium Distinct from Effects of Hypoxia in an Ex Vivo Rat Heart Model

Suner

Jay

2008

Academic Emergency Medicine

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Objectives: Carbon monoxide (CO) toxicity causes significant central nervous system and cardiac injury. Although the neurological damage caused by CO toxicity is extensively described, the mechanisms underlying myocardial insult are unclear. The authors used an externally perfused isolated rat heart model to examine the effects of a physiological saline solution (Krebs Henseleit HEPES, KHH) aerated with CO on cardiac function.Methods: Fifteen rats were equally divided into three groups: the control group (KHH + 100% O 2 ), the nitrogen control group (KHH + 70% O 2 , 30% N 2 ), and the CO group (KHH + 70% oxygen, 30% CO). Left ventricular peak systolic pressure (LVPsP), end diastolic pressure (LVEdP), and coronary perfusion pressure were measured while the isolated heart was paced and perfused on a modified Langendorf apparatus.Results: Left ventricular generated pressure (LVGP = LVPsP ) LVEdP) decreased in the nitrogen control and CO groups compared to the control group. There was higher LVGP in the recovery phase between the nitrogen control group compared to the CO group. Both groups had increased lactic acid levels in the experimental phase.Conclusions: Carbon monoxide with hypoxia and hypoxemic hypoxia both result in similar depression of cardiac function. Hearts poisoned with CO with hypoxia do not recover function to the extent that hearts rendered hypoxic with nitrogen do when perfused with 100% oxygen after the insult. This suggests that CO causes direct myocardial toxicity distinct from the effects of hypoxia.ACADEMIC EMERGENCY MEDICINE 2008; 15:59-65 ª

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“…In this regard, a recent human study, representing a first step in this direction, failed to demonstrate antiinflammatory effects of CO inhalation, although the study encompassed only a limited dose and kinetic regimen (90). Furthermore, a recent study demonstrated cardiac dysfunction in rats after treatment with CO at 250 ppm, a dose that was associated with tissue protection in oxidative lung injury models (91). Clearly, rigorous pharmacokinetics and dosing studies in clinical trials are needed before routine use as a molecular medicine.…”

Section: Discussionmentioning

confidence: 99%

Carbon Monoxide and Bilirubin

Ryter

Morse

Choi

2007

Am J Respir Cell Mol Biol

149

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Heme oxygenase (HO)-1, an inducible, low-molecular-weight stress protein, confers cellular and tissue protection in multiple models of injury and disease, including oxidative or inflammatory lung injury, ischemia/reperfusion (I/R) injuries, and vascular injury/disease. The tissue protection provided by HO-1 potentially relates to the endogenous production of the end products of its enzymatic activity: namely, biliverdin (BV)/bilirubin (BR), carbon monoxide (CO), and iron. Of these, CO and BV/BR show promise as possible therapeutic agents when applied exogenously in models of lung or vascular injury. CO activates intracellular signaling pathways that involve soluble guanylate cyclase and/or p38 mitogen-activated protein kinase. Although toxic at elevated concentrations, low concentrations of CO can confer antiinflammatory, antiapoptotic, antiproliferative, and vasodilatory effects. BV and BR are natural antioxidants that can provide protection against oxidative stress in cell culture and in plasma. Application of BV or BR protects against I/R injury in several organ models. Recent evidence has also demonstrated antiinflammatory and antiproliferative properties of these pigments. To date, evidence has accumulated for salutary effects of CO, BV, and/or BR in lung/vascular injury models, as well as in models of transplant-associated I/R injury. Thus, the exogenous application of HO end products may provide an alternative to pharmacologic or gene therapy approaches to harness the therapeutic potential of HO-1.

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Myocardial Dysfunction and Potential Cardiac Hypoxia in Rats Induced by Carbon Monoxide Inhalation

Cited by 39 publications

References 40 publications

Carbon Monoxide Urban Air Pollution: Cardiac Effects

Carbon Monoxide Urban Air Pollution: Cardiac Effects

Carbon Monoxide Has Direct Toxicity on the Myocardium Distinct from Effects of Hypoxia in an Ex Vivo Rat Heart Model

Carbon Monoxide and Bilirubin

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