| pubmed-article:3411477 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:3411477 | lifeskim:mentions | umls-concept:C0034493 | lld:lifeskim |
| pubmed-article:3411477 | lifeskim:mentions | umls-concept:C0027061 | lld:lifeskim |
| pubmed-article:3411477 | lifeskim:mentions | umls-concept:C0018837 | lld:lifeskim |
| pubmed-article:3411477 | lifeskim:mentions | umls-concept:C1879547 | lld:lifeskim |
| pubmed-article:3411477 | pubmed:dateCreated | 1988-10-13 | lld:pubmed |
| pubmed-article:3411477 | 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. | lld:pubmed |
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| pubmed-article:3411477 | pubmed:language | eng | lld:pubmed |
| pubmed-article:3411477 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:3411477 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:3411477 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:3411477 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:3411477 | pubmed:month | Jan | lld:pubmed |
| pubmed-article:3411477 | pubmed:issn | 0022-3751 | lld:pubmed |
| pubmed-article:3411477 | pubmed:author | pubmed-author:GibbsC LCL | lld:pubmed |
| pubmed-article:3411477 | pubmed:author | pubmed-author:LoiselleD SDS | lld:pubmed |
| pubmed-article:3411477 | pubmed:author | pubmed-author:WendtI RIR | lld:pubmed |
| pubmed-article:3411477 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:3411477 | pubmed:volume | 395 | lld:pubmed |
| pubmed-article:3411477 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:3411477 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:3411477 | pubmed:pagination | 115-30 | lld:pubmed |
| pubmed-article:3411477 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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| pubmed-article:3411477 | pubmed:meshHeading | pubmed-meshheading:3411477-... | lld:pubmed |
| pubmed-article:3411477 | pubmed:year | 1988 | lld:pubmed |
| pubmed-article:3411477 | pubmed:articleTitle | Activation heat in rabbit cardiac muscle. | lld:pubmed |
| pubmed-article:3411477 | pubmed:affiliation | Department of Physiology, Monash University, Clayton, Victoria, Australia. | lld:pubmed |
| pubmed-article:3411477 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:3411477 | pubmed:publicationType | In Vitro | lld:pubmed |
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