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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
 
 
 
 

Myocardial mechanics in allylamine-induced myocardial fibrosis.

To examine the effect of fibrosis on myocardial mechanics, we studied isolated left ventricular papillary muscles from 18 rats given 0.1% allylamine, an agent known to cause myocardial fibrosis, in drinking water for 4-8 wk. Six control rats were given tap water. Left ventricular hydroxyproline concentration was higher in the allylamine-treated group [3.47 +/- 2.12 vs. 2.10 +/- 0.66 (SD) micrograms/mg dry wt; P less than 0.01]. Because of variable and heterogeneous involvement of the ventricle by fibrosis, preparations from allylamine-fed rats were divided into two subgroups; data from four papillary muscles with more than 25% fibrosis by point counting (AL-B group) were compared with eight control muscles from nonallylamine-treated rats. A third subgroup of nine muscles from allylamine-treated rats but with normal left ventricular hydroxyproline concentration and fibrosis as determined by point counting served as another control group (AL-A) for the evaluation of effects of allylamine not due to fibrosis. Myocardial fiber diameters of AL-B preparations were significantly larger than other groups (controls, 12.1 +/- 1.7 microns; AL-A group, 12.7 +/- 1.7 microns; AL-B group, 18.0 +/- 1.2 microns; P less than 0.01). Passive and active stiffness constants in AL-B muscles were significantly increased compared with control and AL-A preparations (P less than 0.05). Electromechanical delay plus time to peak tension and the time for tension to fall from its peak to one-half of that value at the peak of the length-tension curve were significantly prolonged in AL-B muscles.(ABSTRACT TRUNCATED AT 250 WORDS)[1]

References

  1. Myocardial mechanics in allylamine-induced myocardial fibrosis. Nakamura, Y., Wiegner, A.W., Aslanis, J.T., Apstein, C.S., Bing, O.H. Am. J. Physiol. (1986) [Pubmed]
 
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