Studies on the mechanism of carbon monoxide toxicity

Orellano, T; Dergal, E; Alijani, M.R.; Briggs, Charles S.; Vásquez, Javier; Goldbaum, Leo R.; Absolon, Karel B.

doi:10.1016/0022-4804(76)90125-6

Cited by 23 publications

(11 citation statements)

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“…Also heart fiber microscopic changes were found [55). On the contrary, no functional and / or pathological change of heart and blood vessels was reported by other investigations [59][60]. Similar findings on different animals showed electrocardiographic changes after carbon monoxide exposure [61].…”

Section: Carbon Monoxidesupporting

confidence: 79%

Biochemical Markers of Cardiovascular Damage from Tobacco Smoke

Leone¹

2005

CPD

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There is growing evidence that several biochemical constituents of cigarette smoking play a significant role in the development and progression of heart and blood vessel damage, especially atherosclerotic lesions. Some biochemical markers of tobacco smoke may be determined in blood and urine samples. They are also the main responsible factors of cardiovascular harm. Nicotine and its major metabolite, cotinine, carbon monoxide, and thiocyanate seem to be specific markers. Ischaemic heart disease, cardiac arrhythmias, and endothelial dysfunction are the most common evidence of both active and passive smoking exposure. Dosage of cotinine in urine is of easier determination than that of other metabolites in assessing exposure to smoking, although carboxyhaemoglobin levels seem to be a qualitative, but not quantitative factor to estimate either the degree of cardiovascular damage or the level of exposure. Cigarette smoking is addictive because of nicotine, and it is nicotine withdrawal that causes many side effects of quitting smoking as well as the nicotine itself may exacerbate cardiac lesions. Also haematologic changes are a consequence of cigarette smoking exposure. Increased white blood cells, platelet aggregation and adhesiveness, fibrinogen level, and changes in serum lipids characterise the response to smoking. Anatomical and ultrastructural alterations of the heart and blood vessels are also described as a consequence of negative effects of biochemical markers of cigarette smoking. These alterations are known as "Smoke cardiomyopathy" in experimental pathology.

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Section: Carbon Monoxidesupporting

confidence: 79%

Biochemical Markers of Cardiovascular Damage from Tobacco Smoke

Leone¹

2005

CPD

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“…Exchange transfusion with blood containing 80% CO-Hgb to otherwise healthy dogs resulted in no toxic effects, however, despite resultant CO-Hgb levels of 57% to 64%, suggesting that CO toxicity is not dependent on CO-Hgb formation. Other studies have corroborated the findings of morbidity and mortality due to CO poisoning independent of hypoxia or CO-Hgb formation [45][46][47][48][49].…”

Section: Direct Cellular Toxicitymentioning

confidence: 77%

Carbon monoxide poisoning

Kao¹,

Nañagas²

2004

Emergency Medicine Clinics of North America

170

171

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“…However, exchange transfusion with blood containing 80% CO-Hgb to otherwise healthy dogs resulted in no toxic effects, despite resultant CO-Hgb levels of 57% to 64%, suggesting that CO toxicity is not dependent on CO-Hgb formation. Other studies have corroborated the findings of morbidity and mortality due to CO poisoning independent of hypoxia or CO-Hgb formation [38][39][40][41][42].…”

Section: Direct Cellular Toxicitymentioning

confidence: 77%