| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
|
|
|
|||||||
|
|||||||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
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.
This article has been cited by other articles:
|
|
 |
|
  S. Itoh, B. Ding, T. Shishido, N. Lerner-Marmarosh, N. Wang, N. Maekawa, B. C. Berk, Y. Takeishi, C. Yan, B. C. Blaxall, et al. Role of p90 Ribosomal S6 Kinase-Mediated Prorenin-Converting Enzyme in Ischemic and Diabetic Myocardium Circulation, April 11, 2006; 113(14): 1787 - 1798. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 Z. B. Popovic, A. Prasad, M. J. Garcia, A. Arbab-Zadeh, A. Borowski, E. Dijk, N. L. Greenberg, B. D. Levine, and J. D. Thomas Relationship among diastolic intraventricular pressure gradients, relaxation, and preload: impact of age and fitness Am J Physiol Heart Circ Physiol, April 1, 2006; 290(4): H1454 - H1459. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 P. O. Reger, M. F. Barbe, M. Amin, B. F. Renna, L. A. Hewston, S. M. MacDonnell, S. R. Houser, and J. R. Libonati Myocardial hypoperfusion/reperfusion tolerance with exercise training in hypertension J Appl Physiol, February 1, 2006; 100(2): 541 - 547. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. R. Libonati, Z. V. Kendrick, and S. R. Houser Sprint training improves postischemic, left ventricular diastolic performance J Appl Physiol, December 1, 2005; 99(6): 2121 - 2127. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 D. A. Kass, J. G.F. Bronzwaer, and W. J. Paulus What Mechanisms Underlie Diastolic Dysfunction in Heart Failure? Circ. Res., June 25, 2004; 94(12): 1533 - 1542. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
| Visit Other APS Journals Online |
