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Articles in PresS, published online ahead of print October 31, 2002
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.00286.2002
Submitted on April 3, 2002
Accepted on October 12, 2002
1 School of Medicine, Boston University, Boston, MA, USA; Cardiovascular Division, Harvard Medical School, Beth Israel Hospital, Boston, MA, USA
2 Cardiovascular Division, Harvard Medical School, Beth Israel Hospital, Boston, MA, USA
3 School of Medicine, Boston University, Boston, MA, USA
* To whom correspondence should be addressed. E-mail: nxv11{at}po.cwru.edu.
Increased diastolic stiffness (
DCS) during ischemia may result from increased diastolic calcium, rigor, or reduced velocity of relaxation (
). We tested these potential mechanisms, during severe ischemia, in isolated red-cell perfused, isovolumic, rabbit hearts. Ischemia (coronary flow reduced 83%) reduced LV contractility by 70%, which then remained stable. DCS progressively increased. When LVEDP had increased 5 mmHg: i) Myofilament calcium-responsiveness was altered using 50 mmol/L ammonium chloride, or 10 mmol/L butane-dione-monoxime. These affected contractility (ie a calcium-mediated force), but not DCS. ii) Quick-length-changes reversed DCS, supporting a rigor-mechanism. iii) Ischemia increased from 47±3 to 58±3ms (p<0.02) but concomitantly abbreviated the contraction-relaxation cycle ie pressure dissipation occurred earlier, without diastolic tetanization. (iv) To assess any link between rate of relaxation and DCS, hearts were exposed to 10 mmol/L calcium. Calcium doubled contractility and accelerated relaxation velocity, but without affecting DCS.
Conclusions DCS developed during ischemia despite severely reduced contractility, via a rigor (and not calcium-mediated) mechanism. Calcium resequestration capacity was preserved, and reduced relaxation velocity was not linked to DCS.
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