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Heart volume and myocardial connective tissue during development and regression of thyroxine-induced cardiac
Insights
Thyroid hormone-induced cardiac hypertrophy in rats led to decreased myocardial collagen. This reduction in connective tissue may contribute to increased heart volume during hypertrophy.
Area of Science:
- Cardiology
- Biochemistry
- Pathology
Background:
- Cardiac hypertrophy is a significant cardiovascular adaptation.
- Understanding the role of myocardial connective tissue in hypertrophy is crucial.
Purpose of the Study:
- To investigate changes in heart volume and myocardial connective tissue during cardiac hypertrophy and regression.
- To determine the relationship between heart volume alterations and myocardial collagen content.
Main Methods:
- Cardiac hypertrophy was induced in rats using L-thyroxine administration.
- Heart volume was assessed using in vivo radiological estimations.
- Myocardial collagen (hydroxyproline) and glycosaminoglycans (uronic acid) were quantified.
Main Results:
- Thyroxine treatment significantly increased heart weight and heart volume relative to body weight.
- A significant decrease in myocardial hydroxyproline concentration was observed.
- Following thyroxine withdrawal, heart volume, heart weight, and collagen concentration normalized within 2 weeks, though total collagen remained reduced.
Conclusions:
- Thyroxine-induced cardiac hypertrophy involves changes in myocardial connective tissue composition.
- Reduced myocardial collagen concentration may contribute to increased heart volume in cardiac hypertrophy.
- The heart can recover volume and weight, but collagen levels may take longer to normalize.
Abstract:
To determine whether development and regression of cardiac hypertrophy are accompanied by changes in heart volume and to learn whether a change in heart volume is associated with changes in the myocardial connective tissue, cardiac hypertrophy was induced in rats by administration of thyroxine. Rats were given L-thyroxine for 4 weeks. Heart volume was estimated radiologically in vivo at the start of the experiment and at 1- or 2-week intervals for 7 weeks. At each of these stages a number of rats were killed, their hearts were weighed and determinations were made of the myocardial contents of DNA, of collagen measured as hydroxyproline, and of glycosaminoglycans, measured as uronic acid. After thyroxine treatment the ratio of left heart ventricle weight to body weight and of heart volume to body weight rose significantly. The increase in heart weight was greater than the increase in heart volume. At the same time, there was a significant decrease in the concentration of hydroxyproline. After discontinuation of thyroxine treatment heart volume, heart weight and the concentration of myocardial collagen returned to normal within 2 weeks. However, the total amount of myocardial collagen was still less than normal at 2 weeks. The results suggest that the decrease in the amount of myocardial collagen associated with thyroxine-induced cardiac hypertrophy--because it results in a weakening of the supporting properties of the myocardial connective tissue framework--might contribute to a slight increase in in vivo heart volume.