Use this URL to cite or link to this record in EThOS: https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.258480
Title: Experimental studies on carbon monoxide and atherosclerosis
Author: Ibrahim, Bahlul A.
ISNI:       0000 0001 3585 9315
Awarding Body: University of Surrey
Current Institution: University of Surrey
Date of Award: 1981
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Abstract:
New Zealand White California cross rabbits were used to investigate the toxic effect of 200 p.p.m. CO in air on the intimal/subintimal morphology of the aorta and of the coronary, renal and common iliac arteries of normally-fed rabbits. The effects of CO on the removal of serum cholesterol, HDL-cholesterol and LDL + VLDL-cholesterol was also studied in rabbits fed on a diet containing 2% cholesterol. For morphological studies, groups of rabbits were exposed for periods of 4 and 24 hours, and 3, 7 and 14 days. Light and transmission electron microscopy was used to study the intimal/subintimal morphology of the arterial wall. Exposures of 2, 4, 6, 8 and 11 days were used to study the removal of serum cholesterol and the relationship between CO and aortic wall cholesterol level in 2% cholesterol-fed rabbits. Also, exposure of 8 days was used to study the removal of HDL-cholesterol and LDL + VLDL-cholesterol in 2% cholesterol-fed rabbits. In addition, normally—fed rabbits exposed for 3 or 14 days were used to study the effect of CO on serum cholesterol level. Blood CO concentration was measured as COHb%. Light and transmission electron microscopy was used in blind trials to evaluate the morphological effects. No change was found in the intimal or subintimal morphology of coronary arteries, aorta, renal arteries, or common iliac arteries. However, CO raised serum cholesterol in normally-fed rabbits and inhibited serum cholesterol removal in cholesterol-fed rabbits. Increased amount of aortic wall cholesterol was also observed. CO had a slight effect on HDL-cholesterol removal in this study, when compared with the control rabbits, and inhibited the removal of LDL + VLDL-cholesterol. Also, CO significantly increased the ratio of LDL + VLDL-cholesterol to HDL-cholesterol. These findings are discussed with particular reference to the claim that CO is an agent in tobacco smoke, causal to the association of smoking with atherosclerosis.
Supervisor: Not available Sponsor: Not available
Qualification Name: Thesis (Ph.D.) Qualification Level: Doctoral
EThOS ID: uk.bl.ethos.258480  DOI: Not available
Keywords: Medicine
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