Ischemic preconditioning translocates PKC-δ and -ε, which mediate functional protection in isolated rat heart

1998 ◽  
Vol 275 (6) ◽  
pp. H2266-H2271 ◽  
Author(s):  
Shuji Kawamura ◽  
Ken-Ichi Yoshida ◽  
Toshiro Miura ◽  
Yoichi Mizukami ◽  
Masunori Matsuzaki

Protein kinase C (PKC) plays an important role in mediating ischemic preconditioning (PC). However, the relationship between PKC isoforms and PC is still uncertain. We analyzed subcellular localization of PKC isoforms by Western blot analysis in isolated rat heart and demonstrate that PKC-α, -δ, and -ε were translocated to the membrane fraction associated with the improvement of cardiac function. Translocation of PKC-δ and -ε persisted after a 30-min period following PC, but the translocation of PKC-α was transient. Under low Ca2+ perfusion (0.2 mmol/l), PC improved the cardiac function associated with the translocation of PKC-δ. Chelerythrine (1.0 μmol/l) suppressed the translocation of all PKC isoforms associated with the loss of improvement of the cardiac function. On the other hand, bisindolylmaleimide (0.1 μmol/l) did not inhibit the improvement of cardiac function induced by PC, which was associated with the translocation of PKC-ε. These results indicate that the effect of PC on cardiac function is mediated by the translocation of either PKC-δ or -ε independently in rat hearts.

Life Sciences ◽  
2003 ◽  
Vol 72 (16) ◽  
pp. 1859-1870 ◽  
Author(s):  
Jean-François Bouchard ◽  
Philippe Lépicier ◽  
Daniel Lamontagne

1962 ◽  
Vol 202 (4) ◽  
pp. 636-640 ◽  
Author(s):  
F. L. Meijler

Variation in amplitude of isotonic contractions of intact isolated rat hearts, following changes in cycle length, were studied. It was found that a staircase-like phenomenon resembling the original Bowditch effect cannot be evoked in a intact mammalian heart without special measures, such as adding acetylcholine to the perfusion fluid. A steady state relation of rate to amplitude of isotonic contractions was demonstrated. Potentiation of contractility can be originated by sudden changes in stimulation rate. A rest period preceding the changes in stimulation rate does not change the potentiation found originally. At a constant rate the amplitude of a contraction is determined by the preceding cycle length. This relation has been called restitution. Theoretical evidence is presented in an attempt to demonstrate that restitution and potentiation are due to the same process. It can be concluded that Bowditch's staircase does not play a role in the relationship between cycle length and contractility in intact hearts and the statement that restitution and potentiation are due to the same process offers an opportunity to describe all effects of changes in cycle length on isotonic contractions as one phenomenon.


2006 ◽  
Vol 8 (1) ◽  
pp. 55-66 ◽  
Author(s):  
Autumn M. Schumacher ◽  
Joseph P. Zbilut ◽  
Charles L. Webber ◽  
Dorie W. Schwertz ◽  
Mariann R. Piano

Cardiac variability can be assessed from two perspectives: beat-to-beat performance and continuous performance during the cardiac cycle. Linear analysis techniques assess cardiac variability by measuring the physical attributes of a signal, whereas nonlinear techniques evaluate signal dynamics. This study sought to determine if recurrence quantification analysis (RQA), a nonlinear technique, could detect pharmacologically induced autonomic changes in the continuous left ventricular pressure (LVP) and electrographic (EC) signals from an isolated rat heart—a model that theoretically contains no inherent variability. LVP and EC signal data were acquired simultaneously during Langendorff perfusion of isolated rat hearts before and after the addition of acetylcholine (n = 11), norepinephrine (n = 12), or no drug (n = 12). Two-minute segments of the continuous LVP and EC signal data were analyzed by RQA. Findings showed that%recurrence,%determinism, entropy, maxline, and trend from the continuous LVP signal significantly increased in the presence of both acetylcholine and norepinephrine, although systolic LVP significantly increased only with norepinephrine. In the continuous EC signal, the RQA trend variable significantly increased in the presence of norepinephrine. These results suggest that when either the sympathetic or parasympathetic division of the autonomic nervous system overwhelms the other, the dynamics underlying cardiac variability become stationary. This study also shows that information concerning inherent variability in the isolated rat heart can be gained via RQA of the continuous cardiac signal. Although speculative, RQA may be a tool for detecting alterations in cardiac variability and evaluating signal dynamics as a nonlinear indicator of cardiac pathology.


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