Literature DB >> 14576082

Acute and specific collagen type I degradation increases diastolic and developed tension in perfused rat papillary muscle.

Regis R Lamberts1, Maurice J J M F Willemsen, Néstor G Pérez, Pieter Sipkema, Nico Westerhof.   

Abstract

Collagen degradation is suggested to be responsible for long-term contractile dysfunction in different cardiomyopathies, but the effects of acute and specific collagen type I removal (main type in the heart muscle) on tension have not been studied. We determined the diastolic and developed tension length relations in isometric contracting perfused rat papillary muscles (perfusion pressure 60 cmH(2)O) before and after acute and specific removal of small collagen struts with the use of purified collagenase type I. At 95% of the maximal length (95%L(max)), diastolic tension increased 20.4 +/- 8.1% (P < 0.05, n = 6) and developed tension increased 15.0 +/- 6.7% after collagenase treatment compared with time controls. Treatment increased the diastolic muscle diameter by 7.1 +/- 3.4% at 95%L(max), whereas the change in diameter due to contraction was not changed. Diastolic coronary flow and normalized coronary arterial flow impediment did not change after collagenase treatment. Electron microscopy revealed that the number of small collagen struts, interconnecting myocytes, and capillaries was reduced to approximately 32% after treatment. We conclude that removal of the small collagen struts by acute and specific collagen type I degradation increases diastolic and developed tension in perfused papillary muscle. We suggest that diastolic tension is increased due to edema, whereas developed tension is increased because the removal of the struts poses a lower lateral load on the cardiac myocytes, allowing more myocyte thickening.

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Year:  2003        PMID: 14576082     DOI: 10.1152/ajpheart.00967.2001

Source DB:  PubMed          Journal:  Am J Physiol Heart Circ Physiol        ISSN: 0363-6135            Impact factor:   4.733


  5 in total

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Journal:  J Physiol       Date:  2005-02-17       Impact factor: 5.182

2.  Histone deacetylase activity governs diastolic dysfunction through a nongenomic mechanism.

Authors:  Mark Y Jeong; Ying H Lin; Sara A Wennersten; Kimberly M Demos-Davies; Maria A Cavasin; Jennifer H Mahaffey; Valmen Monzani; Chandrasekhar Saripalli; Paolo Mascagni; T Brett Reece; Amrut V Ambardekar; Henk L Granzier; Charles A Dinarello; Timothy A McKinsey
Journal:  Sci Transl Med       Date:  2018-02-07       Impact factor: 17.956

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4.  Fibronectin increases the force production of mouse papillary muscles via α5β1 integrin.

Authors:  Xin Wu; Sanjukta Chakraborty; Cristine L Heaps; Michael J Davis; Gerald A Meininger; Mariappan Muthuchamy
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Review 5.  Myocardial oedema: pathophysiological basis and implications for the failing heart.

Authors:  Francisco Vasques-Nóvoa; António Angélico-Gonçalves; José M G Alvarenga; João Nobrega; Rui J Cerqueira; Jennifer Mancio; Adelino F Leite-Moreira; Roberto Roncon-Albuquerque
Journal:  ESC Heart Fail       Date:  2022-02-11
  5 in total

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