The myocardial collagenous connective tissue in experimental cardiac hypertrophy induced by swimming exercise and hypertension

Abstract

Summary As a result of the studies carried out on the myocardial collagenous connective tissue in 107 rats with different forms of cardiac hypertrophy - caused by renal hypertension (n = 48), by spontaneous hypertension (n = 9) and by swimming exercise (n = 50) that were compared with 66 controls, the following conclusions can be drawn: 1. In the presence of severe forms of renal hypertension associated with a systolic blood pressure rapidly rising to values around 200 mm Hg, the histologically most striking structural changes (interstitial fibrosis, microscars, infarction callosities) as well as a significant increase in the hydroxyproline content in the right ventricle (5.7 ± 1.5 µg hydroxyproline per mg dry weight as against 2.6 ± 0.4 in normotensive controls) are found. These histological and chemical findings can be demonstrated already in the presence of moderate renal hypertension with systolic pressure values around 160 mm Hg, though being less pronounced (4.0 ± 0.9 µg hydroxyproline per mg dry weight). The left ventricle shows slight to moderate structural changes of the myocardium that also depend on the blood pressure level, but there is no rise in the hydroxyproline concentration. 2. In the genesis of these changes post-ischaemic reparative processes and tissue extension resulting from a rise in pressure act together thereby stimulating the collagen synthesis of myocardial connective tissue cells as is demonstrated autoradiographically by an increased 3 H-proline incorporation. In our opinion, the smaller extravasal resistance in the right ventricle of the rat is the cause of the preferential localisation of severe obliterating alterations of the intramural coronary arteries in this part of the heart. 3. In the early phase of the slowly developing spontaneous hypertension no structural changes of the interstitial myocardial connective tissue can be detected histologically. Histoautoradiographically, a stimulation of the mesenchymal protein metabolism manifests itself in both ventricles of the hypertrophied hearts as an increased 3 H-leucine uptake by the interstitial cells. 4. As a result of both short-term (20 hours) and long-term (180 hours) swimming exercise there develops cardiac hypertrophy without any changes in the histological structure of the myocardial connective tissue and in the hydroxyproline concentration being detectable. Also, the specific hydroxyproline activity following application of 14 C-proline, and the fraction of the DNA-synthesizing connective tissue cells remain unaltered. If, however, the animals undergo a 20-hour swimming programme combined with an additional weight load, there is a slight, but significant rise in the number of 3 H-thymidine-labelled cells of the interstitium. This finding is interpreted as a stress-provoked increase in cell turnover.