Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0004153 (atherosclerosis)
77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The acute and chronic effects of carbon monoxide (CO) are reviewed. Direct effects of CO-induced hypoxia on arterial metabolism may facilitate deposition of cholesterol in the intimal surface and exacerbate existing atherosclerosis. Other studies indicate that CO may alter hepatic metabolism so as to inhibit both the secretion of very low density lipoproteins and the clearance of chylomicron remnants. The former change would diminish and the latter enhance atherogenesis. These findings are considered and avenues of future investigation suggested.
Atherosclerosis 1977 Feb
PMID:Metabolic effects of carbon monoxide in relation to atherogenesis. 18 82

Two experiments are described. In the first, 3 pairs of groups of 20 female White Carneau pigeons were fed on diets containing 0.5%, 1% or 2% cholesterol. Birds in one group from each pair were exposed to 150 ppm carbon monoxide (CO) for 6 h on 5 days of each week for 52 weeks, sufficient to raise their carboxyhaemoglobin (COHb) levels to approximately 10%, while those in the other group were sham-exposed under similar conditions. In the second experiment, 3 groups of 40 female pigeons were each fed on a diet containing 1% cholesterol, one group being exposed to CO to give COHb levels of 20%, one to give COHb levels of 10% and one being sham exposed. In addition, 20 birds in the second experiment were fed on the 1% cholesterol diet but were neither exposed to CO nor sham-exposed. Cholesterol enriched diets caused mean plasma cholesterol values in each group to rise sharply within 4 weeks of starting them, but the levels reached were as high with diets containing 0.5% cholesterol as for diets containing 1% or 2% added cholesterol. Exposure to CO increased plasma and aortic cholesterol levels, though this increase was only statistically significant for aortic levels in the second experiment. In both experiments combined exposure to the 1% cholesterol diet and CO resulted in a significant decrease in aortic triglyceride content. The incidence and severity of coronary artery atherosclerosis was associated with increasing dietary cholesterol. It was also associated with exposure to CO in birds given 0.5% or 1%, but not 2%, dietary cholesterol; the increase in birds given 1% was related to the dose of CO. Possible mechanisms are discussed for this effect of CO, which is not found in normally fed birds.
Atherosclerosis 1979 Dec
PMID:Atherogenesis in the White Carneau pigeon. Further studies of the role of carbon monoxide and dietary cholesterol. 51 46

Smoking habits and random measurements of the proportion of haemoglobin bound to carbon monoxide (COHb%) were examined for their association with atherosclerotic diseases in 1068 men aged 55 to 74 years from rural areas of Finland. COHb% and smoking history were similarly associated with claudication and coronary heart disease. Random measurements of COHb% did not show a better overall relation to the prevalence of atherosclerotic diseases than smoking history, though COHb% showed a stronger association with a probable previous myocardial infarction. Further studies are needed to clarify the role of carbon monoxide in atherosclerosis.
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PMID:Smoking, carbon monoxide, and atherosclerotic diseases. 62 Mar 2

The elevated carbon monoxide level found in tobacco smokers has been suggested as one etiologic factor linking it with atherosclerosis. Unquestionably carbon monoxide does induce some arterial wall hypoxia, which has been established as an atherogenic factor, but without knowing the extent and location of this hypoxia the importance of this mechanism could not previously be assessed. Carbon monoxide acts both by inducing hypoxemia and shifting the oxyhemoglobin equilibrium curve, with these effects acting on the oxygen transport system from both the luminal blood and the vasa vasorum. We have studied this system using a computer simulation of the human arterial wall and found significant, mid-medial hypoxia with blood carbon monoxide levels routinely found in smokers. Because these levels fluctuate, the hypoxia they induce would be expected to be uncompensated by increased vascularization and therefore potentially represent a much more significant factor in atherogenesis than chronic hypoxia alone.
Atherosclerosis 1978 May
PMID:Carbon monoxide-induced arterial wall hypoxia and atherosclerosis. 67 10

Non-cholesterol-fed rabbits were exposed to carbon monoxide at concentrations in air of either 200, 2000, or 4000 parts per million (=0.02, 0.2 or 0.4%, vol/vol). Using the same criteria for intimal damage as in earlier morphological studies, no histotoxic effect on intimal/subintimal morphology of coronary arteries or the aorta could be demonstrated, when light-microscopic evaluation was performed blindly.
Atherosclerosis 1978 Aug
PMID:Effect of carbon monoxide exposure on aortic and coronary intimal morphology in the rabbit. A revaluation. 70 90

Twenty patients with a mean age of 79 years were followed over a period of 6 months after intra-arterial insufflation of CO2 in the lower extremity. All patients had severe peripheral occlusive arterial disease caused by atherosclerosis and were scheduled for amputation. A significant increase of the distal perfusion pressure was obtained in the majority of the cases resulting in pain relief and healing of ulcers and gangrenes.
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PMID:Effect of intra-arterial CO2 insuffflation on occlusive arterial disease in the lower leg. 73 39

The luminal surface of fatty lesions of atherosclerosis was viewed by scanning electron microscopy (SEM). Endothelial cells were outlined by staining intercellular junctions with silver and the aortas were fixed in situ at physiological pressure. When aortas were dehydrated by passage through organic solvents followed by critical point drying from liquid CO2, there was considerable disruption of the luminal surface and it was not possible to correctly interpret the morphological integrity of the endothelium. In contrast, simple air-drying of aortas, without solvent dehydration after fixation, allowed the integrity of the cell layer overlying the lesion to be evaluated. The success of this technique was attributed to the retention of arterial lipids during dehydration of the tissue.
Atherosclerosis 1976 Oct
PMID:Scanning electron microscopy in the evaluation of endothelial integrity of the fatty lesion in atherosclerosis. 79 Dec 98

(1) Twenty-four female New Zealand White rabbits were fed commercial diet plus 2% cholesterol. Twelve of these animals were exposed to carbon monoxide for 4 hours per day, seven days per week for 10 weeks. The carbon monoxide exposure was such that the mean blood carboxy-haemoglobin was raised to approximately 20% during each exposure period. Twelve control animals breathed atmospheric air under the same conditions of confinement as the carbon monoxide-exposed group. (2) No significant differences in the plasma levels of cholesterol, triglycerides or glutamate oxalacetate transaminase were observed between the two groups during the experiment. (3) When the animals were sacrificed at the end of the experiment no significant differences were observed between the two groups in the aortic content of triglycerides, cholesterol or phospholipids. (4) The extent of coronary artery atherosclerosis was statistically significantly higher in the carbon monoxide group than in the control group. (5) Ultracentrifugal analysis of plasma lipoproteins revealed that there was significantly more cholesterol in the d less than l.006 fraction from the CO-exposed rabbits. (6) These findings, are discussed with particular reference to the claim that the causal agent in tobacco smoke associated arterial disease is carbon monoxide.
Atherosclerosis 1976 Sep
PMID:The effect of intermittent carbon monoxide exposure on experimental atherosclerosis in the rabbit. 97 51

Smooth muscle cells from the tunica media of piglet aortae grown under hypoxic conditions undergo the following changes: First, they become modified by partial loss of myofilaments and proliferation of organelles, which are characteristics of young primitive cells. Second, an increase in number of pinocytotic vesicles at and below the cell surface, indicating increased extracellular uptake of material, can be detected. This is followed by accumulation of Oil Red O positive intracytoplasmic granules and vacuoles as well as the subsequent formation of mount-like protrusions. The latter consist of a core of extracellular material and necrotic debris covered with a cap of viable cells. A third feature of the cells subjected to hypoxia is a conspicuous rise in the number of lysosomes. This is considered to be a manifestation of a defense mechanism of the cells to remove undesirable material from cytoplasm. Cells exposed to an atmosphere rich in carbon monoxide exhibit basically the same alterations as those grown under hypoxic conditions; however, formation of mound-like aggregates is less prominent, while the rise in the number of lysosomes is more evident than in the hypoxic cells. The above alterations are similar to changes observed in smooth muscle cells of rabbit with experimental atherosclerosis. It is suggested that whereever the arterial smooth muscle cell is subjected to adverse conditions basically the same mechanism, consisting of dedifferentiation, increased permeability and lysosomal defense reaction, takes place.
Atherosclerosis 1976 Oct
PMID:Light- and electron-microscopic characteristics of artrial smooth muscle cell cultures subjected to hypoxia or carbon monoxide. 98 93

The influence of variations of oxygen tension on the metabolism of bovine mesenteric arteries was studied in vitro. Glucose uptake, lactate production, glycogen content, adenosine triphosphate (ATP), creatine phosphate (CrP) and incorporation of [14C]leucine into protein were determined. The mesenteric arteries were suspended in Krebs-Henseleit bicarbonate buffer which was aerated with a gas mixture containing 5% CO2,O-95% O2 and N2 to 100%. Reduction of the O2 concentration of the gas phase from 95-20% resulted in little metabolic change. A further reduction from 20-0% O2 increased the lactate production 4-fold, indicating a marked Pasteur effect. At 0% O2 the glucose uptake was moderately increased and the glycogen content was decreased. The tissue level of CrP was reduced at a low oxygen tension and at 0% O2 the ATP content was also lowered. The incorporation of leucine into proteins was reduced at 0% O2.
Atherosclerosis
PMID:Influence of oxygen tension of the metabolism of vascular smooth muscle: demonstration of a Pasteur effect. 100 12


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