Search

Carbonic anhydrase III and myoglobin concentrations were measured from vastus medialis muscle samples before and 6 weeks after postoperative leg immobilization following knee ligament reconstruction. Seven patients were immobilized with conventional cast so that the knee joint was fixed at 20 degrees flexion. Seven other patients used braces allowing a motion of 30-70 degrees. The atrophy of the medial part of musculus quadriceps was estimated by computer tomography. No difference in carbonic anhydrase III and myoglobin concentrations or muscle atrophy between the cast and brace groups was observed. The cross-sectional area of the medial part of musculus quadriceps decreased 38% during immobilization. The specific concentrations of carbonic anhydrase III and myoglobin remained unaltered. Due to the remarkable postoperative atrophy of the muscle the total carbonic anhydrase III and myoglobin contents, however, decreased significantly (37% and 31%, respectively). The results suggest that the net breakdown of carbonic anhydrase III and myoglobin during disuse atrophy occur at the same rate as the average net degradation of mixed muscle proteins and that the process is independent of the immobilization procedure.

The effect of angiotensin II-induced hypertension on selected biochemical parameters was studied in Sprague-Dawley rats. Angiotensin II infusion at rates of 41.7 micrograms h-1 kg-1 and 12.5 micrograms h-1 kg-1 for 2, 5, 10 and 15 days elevated the systolic blood pressure from 143 +/- 7 mmHg to 215-230 mmHg (P less than 0.001) and 185-195 mmHg (P less than 0.001), respectively. The left ventricular weight/body weight ratio increased 10-14% (P less than 0.05) and 23-32% (P less than 0.001) after 2-15 days in rats treated at the lower and higher infusion rates, respectively. Prolyl 4-hydroxylase (PH) activity, a marker of collagen synthesis, was evenly distributed in the left ventricle. PH activity increased by about 100% in both subendocardial and subepicardial layers of the left ventricular wall after angiotensin II infusion for 10 days at 41.7 micrograms h-1 kg-1, but remained unaltered at 12.5 micrograms h-1 kg-1. No change was observed in hydroxyproline concentration. Myosin isoenzymes (V1-V3), which reflect myocardial contractility, were unevenly distributed in the left ventricular wall: the proportion of the fast-turnover isoenzyme (V1) was smaller in the subendocardial layer than in the subepicardial layer. The proportion of V1 decreased after treatment in both layers. Alkaline phosphatase activity, a marker of capillary density, was evenly distributed transmurally in the left ventricular wall. Angiotensin II caused a slight decrease in this activity in both myocardial layers. The results suggest that the elevation of blood pressure leads to transmurally evenly distributed changes in biochemical parameters reflecting collagen synthesis, capillary density and contractile properties of the myocardium.