{'fraction_non_alphanumeric': 0.016403785488958992, 'fraction_numerical': 0.0, 'mean_word_length': 5.580912863070539, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
[Cardiac relaxation in experimental chronic myocardial hypertrophy: role of the sarcoplasmic reticulum].

The relaxation phase was studied in normal rat hearts submitted to chronic myocardial pressure and/or volume overload (stenosis of the abdominal aorta, aortic regurgitation, aorto-caval fistula) and in spontaneously hypertensive rats, some of which also had aorto-caval fistulae. Four indices were chosen to quantify the relaxation phase: maximal velocity of relaxation during contraction with preload alone, the negative peak of the derivative of isometric tension, and two other indices testing the sensitivity of the relaxation phase to other conditions of load. The first two indices were found to be depressed during chronic myocardial overload, especially with aorto-caval fistulae and mixed overload. On the other hand, the other two indices of the degree of sensitivity to the relaxation load by two different methods showed no significant difference between chronically overloaded and control hearts, though changes were observed after acute hypoxia. These two indices are related to morphological development and to the functional state of the sarcoplasmic reticulum. These results suggest that the rate of calcium uptake by the sarcoplasmic reticulum is reduced during chronic myocardial overload but that the myocardium retains its ability to regulate the relaxation phase with respect to time and the degree of total load. This property disappears temporarily after hypoxia when the heart behaves like frog myocardium which has practically no sarcoplasmic reticulum.