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1 Laboratory for Physiology, Institute for Cardiovascular Research (ICaR-VU), VU University, Amsterdam, The Netherlands
2 Facultad de Ciencias Medicas de La Plata, Centro de Investigaciones Cardiovasculares, La Plata, Argentina
* To whom correspondence should be addressed. E-mail: Lamberts{at}physiol.med.vu.nl.
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 diastolic and developed tension-length relations in isometric contracting perfused rat papillary muscles (perfusion pressure 60 cm H2O) before and after acute and specific removal of small collagen-struts using purified collagenase type I. At 95%Lmax, diastolic tension increased 20.4 ± 8.1% (p<0.05, n=6) and developed tension increased 15.0 ± 6.7% after collagenase treatment compared to time-controls. Treatment increased the diastolic muscle diameter by 7.1 ± 3.4% at 95%Lmax, whereas the change in diameter due to contraction was not changed. Diastolic coronary flow and normalized coronary arterial flow impediment did not changed after collagenase treatment. Electron microscopy revealed that the number of small collagen-struts, interconnecting myocytes and capillaries, was reduced to ~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, while 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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