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Coronary vessel alterations following chronic carbon monoxide exposure in the adult rat
Author(s) -
Penney David G.,
Giraldo Alvaro A.,
Van Egmond Eve M.
Publication year - 1994
Publication title -
journal of applied toxicology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.784
H-Index - 87
eISSN - 1099-1263
pISSN - 0260-437X
DOI - 10.1002/jat.2550140110
Subject(s) - ventricle , interventricular septum , medicine , cardiology , anatomy , artery , coronary arteries
Adult male rats were exposed to 500 ppm CO continuously for 30 days, while litter‐mate controls remained in room air (AIR). Heart weight‐to‐body weight ratio and hematocrit were increased significantly. Right ventricle (RV) free wall thickness was increased significantly as was right to left heart diameter and average heart diameter. Cross‐sectional areas of the left ventricle (LV) free wall, interventricular septum (S) and RV midway between the apex and base were increased significantly. Morphometric analysis of the CO‐exposed and AIR hearts revealed no significant differences in the number of small (27–114 μm) or larger (>114 μm) blood vessels in any region; however, there was a trend towards an increased number of the smaller vessels, both arterioles and venules, in the CO‐exposed rats. The larger arteries in the S and RV were significantly larger in the CO‐exposed rats. There was a significant overall effect of CO on larger artery diameter across all heart regions, consistent with the appearance of heart radiographs taken. There were no differences in the diameter of the small vessels in any region of the heart between the CO‐exposed and AIR rats. The vessel cross‐sectional area of the larger vessels tended to be increased in all regions of the heart. The cross‐sectional area of the large arteries in the LV was increased significantly. Arterial wall thickness was decreased significantly in RV and there was a significant overall effect of CO in decreasing wall thickness and the ratio of wall thickness‐to‐vessel luminal diameter in these vessels. No vascular pathology was observed. The results of this study suggest changes in coronary vessel architecture during chronic CO‐induced cardiac hypertrophy and are consistent with earlier hemodynamic and morphometric studies of CO‐exposed hearts.