In situ assessment of the rat heart during chronic carbon monoxide exposure using nuclear magnetic resonance imaging

Abstract

Ventricular hypertrophy induced in male Sprague-Dawley rats by inhalation of 500 ppm carbon monoxide (40% carboxyhemoglobin level) for 0-62 days was assessed by contiguous 2-mm thick axial cardiac cross-sections, using 32 accumulated averages of ungated fast-scan gradient-recalled nuclear magnetic resonance (NMR) images. Following final imaging, the rats were sacrificed and the hematocrit and heart mass were determined. The mean outside diameter of the left ventricle plus interventricular septum (LV + S) showed a strong correlation (r = 0.73, P less than 0.01) with the duration of CO exposure, while the correlation coefficients for the LV + S lumen diameter and wall thickness were marginally significant. The mean pleural space diameter also increased significantly (r = 0.64, P less than 0.05) with the duration of CO exposure. The ratio of the LV + S wall thickness and the lumen radius was 0.53 in the rats exposed to CO for 0-8 days; this value did not change with longer CO exposure. The LV + S outside and lumen diameter showed significant correlations to the hematocrit (r = 0.72, p less than 0.05 and r = 0.66, P less than 0.05, respectively), and the LV + S outside diameter correlated with the increase in the LV + S mass (r = 0.72, P less than 0.05). The results achieved with NMR imaging are consistent with past morphometric studies of CO-induced ventricular hypertrophy, where heart dimensions were determined in relaxed frozen tissue, and corroborate the eccentric nature of CO-induced ventricular hypertrophy.

Myocardial findings in fatal carbon monoxide poisoning: a human and experimental morphometric study

“…The latter may ensue in different conditions by a primary, still unknown, metabolic disorder in which the adrenergic system seems to play a role [39]. Again, the question is whether eccentric cardiomegaly with longer myocells and without an increase of their volume [48,49,50,51], a finding observed in congestive failure following any cardiac disease [36], is due to CO as a promoter of myocell growth [52,53,54,55] or to adrenergic stimulation. Two last points need to be emphasised.…”