Hypoxia: Unique myocardial morphology?

Abstract

Objective The objective of this study was to investigate the effects of chronic and intermittent hypoxia on myocardial morphology. Methods Rats randomly divided into 3 groups (n = 14 per group) were exposed to room air (F io 2 = 0.21), chronic hypoxia (F io 2 = 0.10), and intermittent hypoxia (chronic hypoxia with 1 hour per day of room air) for 2 weeks. Weight, blood gas analysis, hematocrit, hemoglobin, red cells, and right and left ventricular pressures were measured. Hearts excised for morphologic examination were randomly divided into 2 groups (9 per group for gross morphologic measurements and 5 per group for histologic and morphometric analysis). The weight ratio of right to left ventricles plus interventricular septum, myocyte diameter, cross-sectional area, and free wall thickness in right and left ventricles were measured. Results Despite the same polycythemia, the right ventricle pressure ( P < .05) and ratio of right to left ventricle pressures ( P < .02) were higher after chronic hypoxia than intermittent hypoxia. The ratio of heart weight to total body weight and the ratio of right to left ventricles plus interventricular septum was higher ( P < .01) in chronic and intermittent hypoxia than in normoxia. Myocyte diameter was not different between the right and left ventricles in normoxia, whereas right ventricle myocytes were larger than left ventricle myocytes in chronic hypoxia ( P < .05) and intermittent hypoxia ( P < .0005). There was marked dilatation of right ventricle size ( P < .001) and marked reduction of left ventricle ( P < .001) size in chronic and intermittent hypoxia compared with normoxia. The total ventricular area (right ventricle plus left ventricle area) remained the same in all groups. The wall thickness ratio in chronic hypoxia and intermittent hypoxia was increased ( P < .001) compared with normoxia in the right ventricle but not in the left ventricle. Conclusions Intermittent reoxygenation episodes do not induce a lesser ventricular hypertrophic response than observed with chronic hypoxia. The functional myocardial preconditioning consequence of intermittent reoxygenation is not supported by structural differences evident with the available techniques.