Abstract
Rabbits were fed chow plus 2% cholesterol and 12 of 24 were exposed to 170 ppM CO for 8 wks and 350 ppM CO for the 2 following wks. COHb was 15 to 19% through the 8th wk and 33% in the 10th wk. Hemoglobin in exposed rabbits rose from 10.1 to 12.2 and then to 13.5 in response to increasing CO. Degree of visible atheromatosis and content of total cholesterol in aortic tissue were significantly higher in CO-exposed rabbits. Rise in serum cholesterol was also greater in this group. Mean heart weights were higher; 7 of 12 had small multiple subendocardial and subpericardial hemorrhages; 8 of 12 had focal degenerative changes (only 1 control had such changes). Microscopic findings supported the above differentiation between control and CO-exposed animals: fibrosis, valvular edema, vascular lipoidal infiltration. Hypoxia per se is an important pathogenetic factor as well as decreased activity of certain CO-bound enzymes.
Citation Formats
Astrup, P, Kjeldsen, K, and Wanstrup, J.
Enhancing influence of carbon monoxide on the development of atheromatosis in cholesterol-fed rabbits.
Netherlands: N. p.,
1967.
Web.
Astrup, P, Kjeldsen, K, & Wanstrup, J.
Enhancing influence of carbon monoxide on the development of atheromatosis in cholesterol-fed rabbits.
Netherlands.
Astrup, P, Kjeldsen, K, and Wanstrup, J.
1967.
"Enhancing influence of carbon monoxide on the development of atheromatosis in cholesterol-fed rabbits."
Netherlands.
@misc{etde_6380807,
title = {Enhancing influence of carbon monoxide on the development of atheromatosis in cholesterol-fed rabbits}
author = {Astrup, P, Kjeldsen, K, and Wanstrup, J}
abstractNote = {Rabbits were fed chow plus 2% cholesterol and 12 of 24 were exposed to 170 ppM CO for 8 wks and 350 ppM CO for the 2 following wks. COHb was 15 to 19% through the 8th wk and 33% in the 10th wk. Hemoglobin in exposed rabbits rose from 10.1 to 12.2 and then to 13.5 in response to increasing CO. Degree of visible atheromatosis and content of total cholesterol in aortic tissue were significantly higher in CO-exposed rabbits. Rise in serum cholesterol was also greater in this group. Mean heart weights were higher; 7 of 12 had small multiple subendocardial and subpericardial hemorrhages; 8 of 12 had focal degenerative changes (only 1 control had such changes). Microscopic findings supported the above differentiation between control and CO-exposed animals: fibrosis, valvular edema, vascular lipoidal infiltration. Hypoxia per se is an important pathogenetic factor as well as decreased activity of certain CO-bound enzymes.}
journal = []
volume = {7}
journal type = {AC}
place = {Netherlands}
year = {1967}
month = {Jan}
}
title = {Enhancing influence of carbon monoxide on the development of atheromatosis in cholesterol-fed rabbits}
author = {Astrup, P, Kjeldsen, K, and Wanstrup, J}
abstractNote = {Rabbits were fed chow plus 2% cholesterol and 12 of 24 were exposed to 170 ppM CO for 8 wks and 350 ppM CO for the 2 following wks. COHb was 15 to 19% through the 8th wk and 33% in the 10th wk. Hemoglobin in exposed rabbits rose from 10.1 to 12.2 and then to 13.5 in response to increasing CO. Degree of visible atheromatosis and content of total cholesterol in aortic tissue were significantly higher in CO-exposed rabbits. Rise in serum cholesterol was also greater in this group. Mean heart weights were higher; 7 of 12 had small multiple subendocardial and subpericardial hemorrhages; 8 of 12 had focal degenerative changes (only 1 control had such changes). Microscopic findings supported the above differentiation between control and CO-exposed animals: fibrosis, valvular edema, vascular lipoidal infiltration. Hypoxia per se is an important pathogenetic factor as well as decreased activity of certain CO-bound enzymes.}
journal = []
volume = {7}
journal type = {AC}
place = {Netherlands}
year = {1967}
month = {Jan}
}