The effects of chronic hypoxia on the myocardial cell of normotensive and hypertensive rats.

Abstract

AbstractMyocardial cellular and subcellular adaptations associated with chronic hypoxia were determined in 16 week old male normotensive Wistar‐Kyoto, spontaneously hypertensive and aortic constricted rats. The animals were exposed to six weeks of hypobaric hypoxia at a simulated altitude of 6,100 (m), and their glutaraldehyde perfuse‐fixed hearts compared to normoxic controls.Exposure to hypoxia abolished the hypertension associated with the spontaneously hypertensive and aortic constricted groups and reduced the mean heart rate in all three hypoxic groups. The magnitude of hypertrophy was significant and comparable in all three groups, based on heart weight and left ventricular fiber diameter measurements. While capillary density was significantly reduced in the spontaneously hypertensive and aortic constricted rats, exposure to hypoxia facilitated an absolute increase in the number of capillaries of the hypoxic spontaneously hypertensive and aortic constricted rats. In the hypoxic control group, the capillary density was maintained despite a 20% increase in the muscle fiber diameter, indicating a proliferation of the capillary bed in proportion to the increase in muscle mass. The myocytes in all hypoxic groups were characterized by deep invaginations of the cell membrane and an increase in the number of pinocytotic vesicles. Stereological analyses of the myocytes revealed a statistically significant decrease in the mitochondria/myofibril volume ratio in animals with pressure overload. This ratio was not significantly altered when the animals were subjected to chronic hypoxia. However, there was an increase in the number of mitochondrial profiles and a decrease in the size of individual profiles in all hypoxic groups when compared to the control group.These findings suggest that cardiac hypertrophy associated with chronic hypobaric hypoxia, unlike hypertrophy due to pressure overload, is associated with a number of structural adaptations which may aid the heart in functioning in the hypoxic environment.