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pubmed:abstractText |
1. Activation heat was estimated myothermically in right ventricular papillary muscles of rabbits using several different methods. 2. Gradual pre-shortening of muscles to a length (lmin) where no active force development took place upon stimulation led to relatively low estimates of activation heat (1.59 +/- 0.26-2.06 +/- 0.57 mJ g-1 blotted wet weight, mean +/- S.E.M., n = 10). 3. Quick releases applied during the latency period, before force development, from lmax to various muscle lengths allowed a heat-stress relation to be established. The zero-stress intercept of this relation estimated the activation heat to be 3.27 +/- 0.40 mJ g-1; this was close to the experimentally measured value of 3.46 +/- 0.39 mJ g-1 (mean +/- S.E.M., n = 23) found by quick release from lmax to lmin. 4. The magnitude of the activation heat measured by the quick-release technique is dependent upon the extracellular Ca2+ concentration and there is good correlation between activation heat magnitude and peak developed stress. 5. In agreement with expectations based on the aequorin data of Allen & Kurihara (1982) a prolonged period of time spent at a short length is shown to depress the subsequently determined activation heat. 6. Hyperosmotic solutions (2.5 x normal) only abolished active stress development at low stimulus rates (0.2 Hz) and the activation heat measured at lmax under these conditions was 2.03 +/- 0.12 mJ g-1 (mean +/- S.E.M., n = 6). This value was significantly lower than the latency release estimate of activation heat in the same preparations (2.93 +/- 0.39 mJ g-1). 7. The latency release method of estimating activation heat results in activation heat values that account for approximately 30% of total active energy flux per contraction; a fraction comparable to that found in skeletal muscle. Calculations based on the data suggest that, under our experimental conditions, total Ca2+ release per beat lies between 50 and 100 nmol g-1 wet weight which would produce less than half-maximal myofibrillar ATPase activity when allowance is made for the passive Ca2+-buffering capacity of the myocardial cell.
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