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Carbon monoxide and coronary heart disease

Journal Article:

Abstract

Studies on the relationship between increased carboxyhemoglobin levels in the blood and coronary heart disease in smokers and city dwellers are reviewed. The evidence of myocardial infarction is significantly higher in smokers than in nonsmokers which is due, apart from nicotine which promotes coronary arteriosclerosis, to inhaled carbon monoxide which leads to increased carboxyhemoglobin levels and most likely plays a role in the risk of arteriosclerosis and the coronary heart disease. Apart from combining with hemoglobin, CO increases the circulation rate and the coronary blood flow, and reduces the coronary arteriovenous oxygen difference, which is indicative of a reduced rate of oxygen extraction by the myocardium against an increased myocardial oxygen demand. The reduction of the oxygen extraction correlates with the increased COHb level. Inhaled CO lowers the threshold of angina pectoris due to the reduced myocardial oxygen tension. Also, considerable reduction of the oxygen diffusion from the capillaries toward the mitochondria due to the combination of CO with myoglobin is observed. Chronically increased CO levels in the blood and tissues not only accelerate the development of arteriosclerosis, but also induce a process directly injurious to the myocardial metabolism. (Air Pollut. Abstr.)
Authors:
Publication Date:
Jan 01, 1974
Product Type:
Journal Article
Reference Number:
EDB-76-087996
Resource Relation:
Journal Name: Herz Kreislauf; (Germany, Federal Republic of); Journal Volume: 6:1
Subject:
54 ENVIRONMENTAL SCIENCES; 59 BASIC BIOLOGICAL SCIENCES; 63 RADIATION, THERMAL, AND OTHER ENVIRON. POLLUTANT EFFECTS ON LIVING ORGS. AND BIOL. MAT.; AIR POLLUTION; BIOLOGICAL EFFECTS; CARBON MONOXIDE; CARDIOVASCULAR DISEASES; ENVIRONMENTAL EFFECTS; HEART; PUBLIC HEALTH; TOBACCO SMOKES; TOXICITY; URBAN AREAS; URBAN POPULATIONS; AEROSOLS; BODY; CARBON COMPOUNDS; CARBON OXIDES; CARDIOVASCULAR SYSTEM; CHALCOGENIDES; COLLOIDS; DISEASES; DISPERSIONS; HUMAN POPULATIONS; ORGANS; OXIDES; OXYGEN COMPOUNDS; POLLUTION; POPULATIONS; RESIDUES; SMOKES; SOLS; 500200* - Environment, Atmospheric- Chemicals Monitoring & Transport- (-1989); 550500 - Metabolism; 560306 - Chemicals Metabolism & Toxicology- Man- (-1987); 560301 - Chemicals Metabolism & Toxicology- Cells- (-1987)
OSTI ID:
7156340
Country of Origin:
Germany
Language:
German
Other Identifying Numbers:
Journal ID: CODEN: HZKLA
Submitting Site:
APA
Size:
Pages: 16-17
Announcement Date:
Sep 01, 1976

Journal Article:

Citation Formats

Scheidemandel, V. Carbon monoxide and coronary heart disease. Germany: N. p., 1974. Web.
Scheidemandel, V. Carbon monoxide and coronary heart disease. Germany.
Scheidemandel, V. 1974. "Carbon monoxide and coronary heart disease." Germany.
@misc{etde_7156340,
title = {Carbon monoxide and coronary heart disease}
author = {Scheidemandel, V}
abstractNote = {Studies on the relationship between increased carboxyhemoglobin levels in the blood and coronary heart disease in smokers and city dwellers are reviewed. The evidence of myocardial infarction is significantly higher in smokers than in nonsmokers which is due, apart from nicotine which promotes coronary arteriosclerosis, to inhaled carbon monoxide which leads to increased carboxyhemoglobin levels and most likely plays a role in the risk of arteriosclerosis and the coronary heart disease. Apart from combining with hemoglobin, CO increases the circulation rate and the coronary blood flow, and reduces the coronary arteriovenous oxygen difference, which is indicative of a reduced rate of oxygen extraction by the myocardium against an increased myocardial oxygen demand. The reduction of the oxygen extraction correlates with the increased COHb level. Inhaled CO lowers the threshold of angina pectoris due to the reduced myocardial oxygen tension. Also, considerable reduction of the oxygen diffusion from the capillaries toward the mitochondria due to the combination of CO with myoglobin is observed. Chronically increased CO levels in the blood and tissues not only accelerate the development of arteriosclerosis, but also induce a process directly injurious to the myocardial metabolism. (Air Pollut. Abstr.)}
journal = {Herz Kreislauf; (Germany, Federal Republic of)}
volume = {6:1}
journal type = {AC}
place = {Germany}
year = {1974}
month = {Jan}
}