Why the study?
Does chronic thyroxine treatment induce coronary angiogenesis in senescent rats similarly to young adult rats?
Does chronic thyroxine treatment induce coronary angiogenesis in senescent rats similarly to young adult rats?
In a rat model of thyroxine-induced cardiac hypertrophy, coronary vessel growth parallels the increase in ventricular mass and is not compromised by senescence.
Thyroxine-induced hypertrophy preserves perfusion per mass in aged rats; extends animal models but leaves open human translation.
We tested the hypothesis that coronary angiogenesis in response to chronic thyroxine (T4) treatment is not limited by age. Male Fischer 344 rats aged either 8 (young adult) or 24 (senescent) mo were studied after receiving either L-thyroxine (0.2 mg/kg sc) or vehicle for 2 mo. Heart weight-to-body weight ratio, compared with age-matched controls, increased by 47 and 44% in 8- and 24-mo T4 groups, respectively. Maximal myocardial perfusion per unit mass, measured in diastole-arrested, maximally dilated, isolated hearts, was similar in T4 rats and their age group controls; however, flow tended to be lower in senescent than in young adult rats. Thus the cross-sectional area of the coronary vessels grew in proportion to the increase in cardiac mass. Morphometric analyses, based on image analysis, showed that capillary length density was slightly lower in the midmyocardium but not the epimyocardium of the 24-mo T4 group compared with their age group controls. However, volume density, surface density, and intercapillary distance were not influenced by T4 treatment and the presence of cardiac hypertrophy. We conclude that in this model of cardiac hypertrophy 1) coronary vessel growth parallels the increase in ventricular mass, 2) capillaries grow by proliferation and an increase in diameter, and 3) vascular growth is not notably compromised during senescence.
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Tomanek et al. (1995) studied this question.
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