|
|
|
|
|
|
|
||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
The Journal of General Physiology, Vol 88, 437-473, Copyright © 1986 by The Rockefeller University Press
ARTICLES |
JH Bridge
Rabbit right ventricular papillary muscles were cooled from 30 to approximately 1 degree C immediately after discontinuing electrical stimulation (0.5 Hz). This produced a contracture that was 30-50% of the preceding twitch magnitude and required 20-30 s to develop. The contractures were identical in cooling solutions with normal (144 mM) or low (2.0 mM) Na. They were therefore not Na-withdrawal contractures. Contracture activation was considerably slower than muscle cooling (approximately 2.5 s to cool below 2 degrees C). Cooling contractures were suppressed by caffeine treatment (10.0 mM). Rapid cooling did not cause sufficient membrane depolarization (16.5 +/- 1.2 mV after 30 s of cooling) to produce either a voltage-dependent activation of contracture or a gated entry of Ca from the extracellular space. Contractures induced by treating resting muscles with 5 X 10(-5) M strophanthidin at 30 degrees C exhibited pronounced tension noise. The Fourier spectrum of this noise revealed a periodic component (2-3 Hz) that disappeared when the muscle was cooled. Cooling contractures decayed with rest (t1/2 = 71.0 +/- 9.3 s). This decay accelerated in the presence of 10.0 mM caffeine and was prevented and to some extent reversed when extracellular Na was reduced to 2.0 mM. 20 min of rest resulted in a net decline in intracellular Ca content of 1.29 +/- 0.38 mmol/kg dry wt. I infer that cooling contractures are principally activated by Ca from the sarcoplasmic reticulum (SR). The properties of these contractures suggest that they may provide a convenient relative index of the availability of SR Ca for contraction. The rest decay of cooling contractures (and hence the decay in the availability of activating Ca) is consistent with the measured loss in analytic Ca during rest. The results suggest that contraction in heart muscle can be regulated by an interaction between sarcolemmal and SR Ca transport.
CiteULike 
Complore 
Connotea 
Del.icio.us 
Digg 
Facebook 
Reddit 
Technorati 
Twitter What's this?
This article has been cited by other articles:
|
|
 |
|
  F. Protasi, A. Shtifman, F. J. Julian, and P. D. Allen All three ryanodine receptor isoforms generate rapid cooling responses in muscle cells Am J Physiol Cell Physiol, March 1, 2004; 286(3): C662 - C670. [Abstract] [Full Text]
|
|
|
|
 |
|
 J.-Y. Min, M. F. Sullivan, X. Yan, X. Feng, V. Chu, J.-F. Wang, I. Amende, J. P. Morgan, K. D. Philipson, and T. G. Hampton Overexpression of Na+/Ca2+ exchanger gene attenuates postinfarction myocardial dysfunction Am J Physiol Heart Circ Physiol, December 1, 2002; 283(6): H2466 - H2471. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 H.-P. Hermann, O. Zeitz, S. E Lehnart, B. Keweloh, N. Datz, G. Hasenfuss, and P. M.L Janssen Potentiation of beta-adrenergic inotropic response by pyruvate in failing human myocardium Cardiovasc Res, January 1, 2002; 53(1): 116 - 123. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 L. Hove-Madsen, A. Llach, and L. Tort The function of the sarcoplasmic reticulum is not inhibited by low temperatures in trout atrial myocytes Am J Physiol Regulatory Integrative Comp Physiol, December 1, 2001; 281(6): R1902 - R1906. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. Y. Boateng, R. U. Naqvi, M. U. Koban, M. H. Yacoub, K. T. MacLeod, and K. R. Boheler Low-dose ramipril treatment improves relaxation and calcium cycling after established cardiac hypertrophy Am J Physiol Heart Circ Physiol, March 1, 2001; 280(3): H1029 - H1038. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
H.-P. Hermann, O. Zeitz, B. Keweloh, G. Hasenfuss, and P. M. L. Janssen Pyruvate potentiates inotropic effects of isoproterenol and Ca2+ in rabbit cardiac muscle preparations Am J Physiol Heart Circ Physiol, August 1, 2000; 279(2): H702 - H708. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
P. M.L Janssen, O. Zeitz, B. Keweloh, U. Siegel, L. S Maier, P. Barckhausen, B. Pieske, J. Prestle, S. E Lehnart, and G. Hasenfuss Influence of cyclosporine A on contractile function, calcium handling, and energetics in isolated human and rabbit myocardium Cardiovasc Res, July 1, 2000; 47(1): 99 - 107. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 C. M N Terracciano, A. I De Souza, K. D Philipson, and K. T MacLeod Na+ -Ca2+ exchange and sarcoplasmic reticular Ca2+ regulation in ventricular myocytes from transgenic mice overexpressing the Na+ -Ca2+ exchanger J. Physiol., November 1, 1998; 512(3): 651 - 667. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
D.A Eisner, A.W Trafford, M.E Dnaz, C.L Overend, and S.C O'Neill The control of Ca release from the cardiac sarcoplasmic reticulum: regulation versus autoregulation Cardiovasc Res, June 1, 1998; 38(3): 589 - 604. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
L. S. Maier, R. Brandes, B. Pieske, and D. M. Bers Effects of left ventricular hypertrophy on force and Ca2+ handling in isolated rat myocardium Am J Physiol Heart Circ Physiol, April 1, 1998; 274(4): H1361 - H1370. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. A. Lahorra, D. F. Torchiana, G. Tolis Jr, C. A. Bashour, C. Hahn, J. S. Titus, G. A. Geffin, and W. M. Daggett Rapid Cooling Contracture With Cold Cardioplegia Ann. Thorac. Surg., May 1, 1997; 63(5): 1353 - 1360. [Abstract] [Full Text]
|
|
|
|
 |
|
 G. D. Buckberg Normothermic blood cardioplegiaAlternative or adjunct? J. Thorac. Cardiovasc. Surg., March 1, 1994; 107(3): 860 - 867. [Abstract] [Full Text]
|
|
|
|
|
|
T. K. Steigen, E. Aasum, T. Myrmel, and T. S. Larsen Effects of fatty acids on myocardial calcium control during hypothermic perfusion J. Thorac. Cardiovasc. Surg., January 1, 1994; 107(1): 233 - 241. [Abstract] [Full Text]
|
|
|
|
