The metabolic effect of carbon monoxide on the heart

Hattori, Hiroyuki; Sugawara, Norisuke; Nakamura, Kazuyuki; Furuno, Junji

doi:10.1007/bf00219969

Cited by 4 publications

(3 citation statements)

References 25 publications

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“…Thus, induction of iNOS mRNA in macrophages and hepatocytes requires ongoing protein synthesis. In contrast, we recently reported that CHX actually induces iNOS mRNA in rat vascular smooth muscle cells (VSM) (19). Additionally, the induction of iNOS mRNA by LPS is substantially potentiated by CHX in VSM (19).…”

Section: Discussionmentioning

confidence: 81%

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Effect of cycloheximide on the expression of LPS‐inducible iNOS, IFN‐β, and IRF‐1 genes in J774 macrophages

et al. 1996

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The effect of cycloheximide (CHX) on the gene expression for inducible NO synthase (iNOS), interferon (IFN)-~ and IFN regulatory factor (IRF)-I was examined in LPSstimulated J774 macrophages. LPS caused increased expression of mRNAs specific for iNOS, IFN-I~, and IRF-1 with different kinetics. Addition of CHX resulted in inhibition of the LPSinduced iNOS gene expression and parallel decrease in NO production. In contrast, expression of IFN-I~ and IRF-1 genes in response to LPS was potentiated in the presence of CHX. These results indicate that de novo protein synthesis is not required for IFN-13 and IRF-1 gene expression and that ongoing protein synthesis including IFN-13 and IRF-1 may be involved in the induction process of iNOS in mouse macrophages.We report here that J774 macrophages respond to LPS treatment by increased expression of mRNAs specific for IFN-I~, IRF-1 and iNOS with the kinetics unique for each gene. Addition of protein synthesis inhibitor cycloheximide (CHX) inhibits the LPS-induced iNOS gene expression while expression of IFN-fl and IRF-1 genes in response to LPS is clearly increased in the presence of CHX. These findings may suggest that LPS acts to induce iNOS via synthesis or release of intermediary cytokines and/or regulatory proteins in J774 macrophages. MATERIALS AND METHODSCell culture: The mouse macrophage cell line J774 was cultured and prepared as described previously (12). J774 macrophages were seeded into 96-well plates for nitrite assay and cytotoxic assay and into 10-era dishes for RNA preparation. To induce NO synthase in the cells, fresh culture medium containing LPS (E. coli, serotype No. 0127: B8, Sigma Chemical Co., Saint Louis, MO, USA)) was added at a concentration of 1 yg/ml. To assess the effects of cyeloheximide (CHX: 0.01 -10/~g/ml, Sigma Chemical Co.), the agent was added to the cells simultaneously with LPS except time-cx)urse study of CHX addition.

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Section: Discussionmentioning

confidence: 81%

“…In contrast, we recently reported that CHX actually induces iNOS mRNA in rat vascular smooth muscle cells (VSM) (19). Additionally, the induction of iNOS mRNA by LPS is substantially potentiated by CHX in VSM (19). Thus, a fundamental difference appears to exist in the regulation of iNOS mRNA among cell types.…”

Section: Discussionmentioning

confidence: 85%

Effect of cycloheximide on the expression of LPS‐inducible iNOS, IFN‐β, and IRF‐1 genes in J774 macrophages

et al. 1996

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“…The frequent occurrence of cardiac disturbances during or after exposure to CO, such as increased frequency of anginal attacks, arrhythmia, and increased levels of cardiac enzymes, has led to a search for morphological changes that could be attributed to CO, especially because the myocardium has been shown to bind more CO than skeletal muscle [4,5]. There is a decreased oxidative phosphorylation [6,7] with a parallel decrease of heart rate, pulse pressure [8,9,10,11] and increased coronary blood flow [8,12] with a relative subendocardial underperfusion [13] whereby vasodilatation is the major response to CO hypoxia [14]. The cardiac electrical instability is not influenced by CO exposure in both normal and ischemic dog hearts, without any effect on coronary blood flow and platelet aggregation [15], a finding which apparently contrasts with other studies both in animals and in human coronary artery disease [12,16].…”

Section: Introductionmentioning

confidence: 99%

Myocardial findings in fatal carbon monoxide poisoning: a human and experimental morphometric study

Fineschi

Agricola

Baroldi

et al. 2000

International Journal of Legal Medicine

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The aim of this study was to define the status of the myocardium in selected human cases of acute, fatal carbon monoxide intoxication and the myocardial changes in rats exposed to carbon monoxide in relation to the type of cardiac arrest and the effects of reoxygenation following pre-fatal CO intoxication. The human study consisted of 26 cases (17 accidental and 9 suicide) of acute, fatal CO intoxication, without evidence of obstructive coronary atherosclerosis or history of ischemic heart disease which were compared with 45 cases of fatal head trauma in subjects who died instantaneously (26 cases) or within 1-12 h (19 cases). Inhalation of a lethal dose of CO in rats was compared with sub-lethal doses plus reoxygenation with and without pre-treatment by a betablocker. In all human and experimental histological sections, changes were normalised per mm2 area. In the human cases the myocardium did not show any ischemic types of changes or other lesions. Only in "three accidental" cases a few, small foci of coagulative myocytolysis were detected. In the case of spontaneous death in 31 rats following CO intoxication, no pathological myocardial changes were seen. Of the 15 "reoxygenated" rats, 2 of the 7 spontaneous deaths presented coagulative myocytolysis with 15 +/- 6 foci and 381 +/- 255 necrotic myocells. All the eight rats sacrificed at 3 h had coagulative myocytolysis with 5 +/- 4 foci and 60 +/- 47 myocells. Of the 24 reoxygenated rats pre-treated with a betablocker, 5 died spontaneously after a short survival and 2 of these showed 11 +/- 9 foci and 21 +/- 20 myocells. The 19 rats sacrificed after 3 h all presented coagulative myocytolysis with figures of 75 +/- 43 and 356 +/- 301 with 0.5 mg/kg of propranolol hydrochloride and 55 +/- 45 and 253 +/- 216 with 2 mg/kg, respectively.

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Cardiovascular effects of subchronically low/high carbon monoxide exposure in rats

Barbé¹,

Rochetaing²,

Kreher³

1999

Environmental Toxicology and Pharmacology

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The metabolic effect of carbon monoxide on the heart

Cited by 4 publications

References 25 publications

Effect of cycloheximide on the expression of LPS‐inducible iNOS, IFN‐β, and IRF‐1 genes in J774 macrophages

Effect of cycloheximide on the expression of LPS‐inducible iNOS, IFN‐β, and IRF‐1 genes in J774 macrophages

Myocardial findings in fatal carbon monoxide poisoning: a human and experimental morphometric study

Cardiovascular effects of subchronically low/high carbon monoxide exposure in rats

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