| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
Experimental Research Laboratory, Division of Cardiology, University of Louisville and Jewish Hospital Heart and Lung Institute, Louisville, Kentucky 40292
In phase I of this study, the rate of protein synthesis was measured by the incorporation of [3H]leucine into the protein pool in the heart of conscious rabbits. At 2 h after ischemic preconditioning (PC) with six 4-min occlusion/4-min reperfusion (O/R) cycles (group II), the [3H]leucine content in the ischemic-reperfused region was increased by 82% compared with that in controls (group I), indicating increased protein synthesis. This increase was completely abrogated by pretreatment with cycloheximide (CH; group III). In phase II, rabbits underwent six O/R cycles for three consecutive days (days 1-3). Controls (group IV) exhibited late PC against myocardial stunning on days 2 and 3. In group V, which received CH 30 min before the 1st O/R cycle on day 1 (same dose as group III), late PC against stunning on day 2 was completely abrogated. In group VI, pretreatment with CH 24 h before the 1st sequence of O/R cycles had no effect on myocardial stunning on day 1, indicating that the absence of late PC on day 2 in group V cannot be ascribed to delayed toxicity of CH. Taken together, these results demonstrate that, in the conscious rabbit, ischemic PC causes a rapid increase in myocardial protein synthesis and that this increased protein synthesis (or at least a fraction of it) is necessary for the development of the protection against myocardial stunning 24 h later. The late phase of ischemic PC is therefore dependent on the formation of new proteins in intact animals.
cycloheximide; myocardial ischemia; myocardial reperfusion; [3H]leucine; systolic wall thickening
This article has been cited by other articles:
|
|
 |
|
  E. Murphy and C. Steenbergen Mechanisms Underlying Acute Protection From Cardiac Ischemia-Reperfusion Injury Physiol Rev, April 1, 2008; 88(2): 581 - 609. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 C. R. Hampton, A. Shimamoto, C. L. Rothnie, J. Griscavage-Ennis, A. Chong, D. J. Dix, E. D. Verrier, and T. H. Pohlman HSP70.1 and -70.3 are required for late-phase protection induced by ischemic preconditioning of mouse hearts Am J Physiol Heart Circ Physiol, July 11, 2003; 285(2): H866 - H874. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A. R. Lankford, A. M. Byford, K. J. Ashton, B. A. French, J. K. Lee, J. P. Headrick, and G. P. Matherne Gene expression profile of mouse myocardium with transgenic overexpression of A1 adenosine receptors Physiol Genomics, October 29, 2002; 11(2): 81 - 89. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 R. Bolli The Late Phase of Preconditioning Circ. Res., November 24, 2000; 87(11): 972 - 983. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
H. Takano, X.-L. Tang, and R. Bolli Differential role of KATP channels in late preconditioning against myocardial stunning and infarction in rabbits Am J Physiol Heart Circ Physiol, November 1, 2000; 279(5): H2350 - H2359. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
Y.-T. Xuan, X.-L. Tang, Y. Qiu, S. Banerjee, H. Takano, H. Han, and R. Bolli Biphasic response of cardiac NO synthase isoforms to ischemic preconditioning in conscious rabbits Am J Physiol Heart Circ Physiol, November 1, 2000; 279(5): H2360 - H2371. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
R. C. X. Li, P. Ping, J. Zhang, W. B. Wead, X. Cao, J. Gao, Y. Zheng, S. Huang, J. Han, and R. Bolli PKCepsilon modulates NF-kappa B and AP-1 via mitogen-activated protein kinases in adult rabbit cardiomyocytes Am J Physiol Heart Circ Physiol, October 1, 2000; 279(4): H1679 - H1689. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 G. L. Semenza HIF-1 and human disease: one highly involved factor Genes & Dev., August 15, 2000; 14(16): 1983 - 1991. [Full Text]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| Visit Other APS Journals Online |
