Discontinuities in Action Potential Propagation Along Chains of Single Ventricular Myocytes in Culture: Multiple Site Optical Recording of Transmembrane Voltage (MSORTV) Suggests Propagation Delays at the Junctional Sites Between Cells

1992 ◽  
Vol 183 (2) ◽  
pp. 342-343 ◽  
Author(s):  
S. Rohr ◽  
B. M. Salzberg
Keyword(s):  
Action Potential ◽  
Ventricular Myocytes ◽  
Optical Recording ◽  
Multiple Site ◽  
Action Potential Propagation ◽  
Transmembrane Voltage ◽  
Propagation Delays ◽  
Single Ventricular Myocytes

scholarly journals Characterization of impulse propagation at the microscopic level across geometrically defined expansions of excitable tissue: multiple site optical recording of transmembrane voltage (MSORTV) in patterned growth heart cell cultures.

1994 ◽  
Vol 104 (2) ◽  
pp. 287-309 ◽  
Author(s):  
S Rohr ◽  
B M Salzberg
Keyword(s):  
Action Potential ◽  
Optical Recording ◽  
Neonatal Rat ◽  
Two Dimensional ◽  
Multiple Site ◽  
Patterned Growth ◽  
Excitable Tissue ◽  
Impulse Propagation ◽  
Transmembrane Voltage ◽  
Narrow Cell

Impulse propagation across sudden expansions of excitable tissue has been shown to exhibit various forms of conduction disturbance on a macroscopic scale, ranging from small delays to unidirectional or complete conduction block. With the present study, we attempted to characterize systematically the dependence of impulse propagation on the geometry of the underlying excitable tissue on a microscopic scale by investigating the spatio-temporal pattern of transmembrane voltage changes associated with impulse propagation from a narrow cell strand to a large cell area using multiple site optical recording of transmembrane voltage (MSORTV) in conjunction with patterned growth of neonatal rat heart cells in culture. While action potential propagation was smooth in the case of funneled expansions, delays of variable size occurred during propagation into rectangular or incised expansions. Close to the abrupt expansion, which functionally represented an increased electrical load to the narrow cell strand, the delays were accompanied by marked distortions of the action potential upstroke, exhibiting, in extreme cases, an initial depolarization to 50% followed by a delayed secondary depolarization to 100% of the full-signal amplitude. These distortions, which were based on bidirectional electrotonic interactions across the transition, were maximal immediately downstream from the expansion. The maximal slowing of impulse conduction across abrupt expansions was, in agreement with recently published results obtained from two-dimensional computer simulations, always situated in the expanded region. At high stimulation rates, the delays sometimes turned into intermittent unidirectional blocks, as revealed by reverse stimulation. These blocks were always characterized by a marked abbreviation of the action potentials upstream from the region causing the block which might, in an appropriate network, facilitate reentry because of the associated shortening of the refractory period. Because the patterns were composed of cells having identical membrane properties, the results show that the local action potential shape can be modulated profoundly by the two-dimensional architecture of the underlying cell ensemble alone.

scholarly journals Optical recording of action potential propagation in demyelinated frog nerve

1987 ◽  
Vol 51 (2) ◽  
pp. 351-355 ◽  
Author(s):  
P. Shrager ◽  
S.Y. Chiu ◽  
J.M. Ritchie ◽  
D. Zecevic ◽  
L.B. Cohen
Keyword(s):  
Action Potential ◽  
Optical Recording ◽  
Action Potential Propagation

Antagonism of forskolin effects by adenosine in isolated hearts and ventricular myocytes

1986 ◽  
Vol 250 (5) ◽  
pp. H769-H777
Author(s):  
G. A. West ◽  
G. Isenberg ◽  
L. Belardinelli
Keyword(s):  
Action Potential ◽  
Ventricular Myocytes ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Ventricular Pressure ◽  
Dibutyryl Camp ◽  
Isolated Hearts ◽  
Ventricular Tissue ◽  
Single Ventricular Myocytes ◽  
Isolated Ventricular Myocytes

Adenosine is known to antagonize the effects of catecholamine stimulation in atrial and ventricular tissue; however, its mechanism of action is unknown. Forskolin is an inotropic agent that causes an increase in cyclic AMP (cAMP) levels independent of receptor stimulation. We sought to test whether adenosine could attenuate the effects of forskolin in isolated perfused guinea pig hearts and isolated single ventricular myocytes. In isolated perfused hearts (n = 18), forskolin caused a concentration-dependent increase in left ventricular pressure and dP/dt. Adenosine (5 microM) antagonized the forskolin (0.35 microM)-induced increase in left ventricular pressure and dP/dt by 96 +/- 2 and 92 +/- 4% (means +/- SE), respectively. In contrast, in four hearts, adenosine was ineffective in attenuating the inotropic response to dibutyryl cAMP. In isolated ventricular myocytes (n = 10) 150 nM forskolin caused a significant increase in action potential duration and plateau. In voltage-clamp experiments (n = 8), 150 nM forskolin caused a 39 +/- 3% increase in the calcium current, which was antagonized by adenosine (50 microM) by 80%. Forskolin also caused an increase in contractility, as estimated by sarcomere shortening of the cell. Adenosine, and its analogue N6-R-phenylisopropyladenosine (L-PIA), antagonized the effects of 150 nM forskolin on the action potential and on sarcomere shortening. Dibutyryl cAMP had similar effects as forskolin, but they were not antagonized by adenosine. At higher concentrations of forskolin, above 300 nM, delayed after depolarizations and sustained spontaneous activity occurred that could be abolished by L-PIA. Forskolin caused a concentration-dependent increase in cAMP, measured in isolated ventricular myocytes.(ABSTRACT TRUNCATED AT 250 WORDS)

Electrophysiological effects of L-palmitoylcarnitine in single ventricular myocytes

1990 ◽  
Vol 258 (4) ◽  
pp. H931-H938 ◽  
Author(s):  
J. Meszaros ◽  
A. J. Pappano
Keyword(s):  
Guinea Pig ◽  
Action Potential ◽  
Action Potential Duration ◽  
Ventricular Myocytes ◽  
Membrane Depolarization ◽  
Time Dependent ◽  
Resting Potential ◽  
Neuraminidase Treatment ◽  
Single Ventricular Myocytes ◽  
Electrophysiological Effects

In isolated guinea pig ventricular myocytes, L-palmitoylcarnitine (L-PC) produced concentration- and time-dependent changes of resting potential (RP) and action potential duration at 50% repolarization (APD50). At 10(-8) to 10(-6) M, L-PC increased APD50 without changing RP. At 10(-5) M, the amphiphile initially increased (0-10 min) and eventually decreased (greater than 10 min) APD50; the membrane depolarized when APD50 decreased. Additionally, transient depolarizations (TDs) were consistently induced in 10(-5) M L-PC within 10 min, and TD amplitude progressively increased with continued exposure to L-PC. The TDs induced in L-PC were augmented by membrane depolarization, elevated extracellular Ca2+ concentration ([Ca2+]o), and increased number of stimuli. Elevated [Ca2+]o or neuraminidase treatment also allowed TDs. In neuraminidase, the changes of RP, APD50, and TD amplitude were qualitatively similar to those seen with L-PC. These results are consistent with the hypothesis that 10(-5) M L-PC causes intracellular Ca2+ overload. The blockade of L-PC and neuraminidase-induced TDs by ryanodine is consistent with the intracellular Ca2+ overload hypothesis.

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