A dynamic action potential model analysis of shock-induced aftereffects in ventricular muscle by reversible breakdown of cell membrane

2002 ◽  
Vol 49 (1) ◽  
pp. 18-30 ◽  
Author(s):  
K. Ohuchi ◽  
Y. Fukui ◽  
I. Sakuma ◽  
N. Shibata ◽  
H. Honjo ◽  
...  
Keyword(s):  
Cell Membrane ◽  
Action Potential ◽  
Potential Model ◽  
Model Analysis ◽  
Ventricular Muscle ◽  
Dynamic Action

A model analysis of aftereffects of high-intensity DC stimulation on action potential of ventricular muscle

1998 ◽  
Vol 45 (2) ◽  
pp. 258-267 ◽  
Author(s):  
I. Sakuma ◽  
T. Haraguchi ◽  
K. Ohuchi ◽  
Y. Fukui ◽  
I. Kodama ◽  
...  
Keyword(s):  
Action Potential ◽  
High Intensity ◽  
Model Analysis ◽  
Ventricular Muscle

Cell Membrane Potential Model Circuit Lab

2018 ◽  
Vol 56 (8) ◽  
pp. 540-543
Author(s):  
Mickey D. Kutzner ◽  
J. Michael Bryson
Keyword(s):  
Membrane Potential ◽  
Cell Membrane ◽  
Potential Model ◽  
Cell Membrane Potential ◽  
Model Circuit

scholarly journals Choline Permeability in Cardiac Muscle Cells of the Cat

1970 ◽  
Vol 55 (5) ◽  
pp. 602-619 ◽  
Author(s):  
S. Bosteels ◽  
A. Vleugels ◽  
E. Carmeliet
Keyword(s):  
Cell Membrane ◽  
Cardiac Muscle ◽  
Paper Chromatography ◽  
Heart Muscle ◽  
Muscle Cells ◽  
Heart Cells ◽  
Ventricular Muscle ◽  
Cardiac Cell ◽  
Cardiac Muscle Cells ◽  
Rapid Phase

Permeability of the cardiac cell membrane to choline ions was estimated by measuring radioactive choline influx and efflux in cat ventricular muscle. Maximum values for choline influx in 3.5 and 137 mM choline were respectively 0.56 and 9 pmoles/cm2·sec. In 3.5 mM choline the intracellular choline concentration was raised more than five times above the extracellular concentration after 2 hr of incubation. In 137 mM choline, choline influx corresponded to the combined loss of intracellular Na and K ions. Paper chromatography of muscle extracts indicated that choline was not metabolized to any important degree. The accumulation of intracellular choline rules out the existence of an efficient active pumping mechanism. By measuring simultaneously choline and sucrose exchange, choline efflux was analyzed in an extracellular phase, followed by two intracellular phases: a rapid and a slow one. Efflux corresponding to the rapid phase was estimated at 16–45 pmoles/cm2·sec in 137 mM choline and at 1.3–3.5 pmoles/cm2·sec in 3.5 mM choline; efflux in 3.5 mM choline was proportional to the intracellular choline concentration. The absolute figures for unidirectional efflux were much larger than the net influx values. The data are compared to Na and Li exchange in heart cells. Possible mechanisms for explaining the choline behavior in heart muscle are discussed.

Excitability and electrical response of ischemic heart muscle

1960 ◽  
Vol 198 (6) ◽  
pp. 1143-1147 ◽  
Author(s):  
Chandler McC. Brooks ◽  
Jerome L. Gilbert ◽  
Martin E. Greenspan ◽  
Gertrude Lange ◽  
Hector M. Mazzella
Keyword(s):  
Action Potential ◽  
Blood Supply ◽  
Heart Muscle ◽  
Action Potentials ◽  
Electrical Response ◽  
Left Ventricular ◽  
Ischemic Heart ◽  
Monophasic Action Potential ◽  
Ventricular Muscle ◽  
Refractory Periods

Measurements were made of the changes in the monophasic action potential, excitability, durations of the refractory periods and conduction times in an area of left ventricular muscle during the development of ischemia subsequent to ligation of the ramus descendens anterior. The degree and duration of the ischemia produced varied greatly and effects were related thereto. It was found that action potentials shortened as did the refractory periods; thresholds fell momentarily and then rose progressively as tissue responsiveness failed due to continuing ischemia. Latency of responses increased, the action potentials decreased in amplitude and alternation occurred before the tissue became completely unresponsive. Early re-establishment of a blood supply caused a reversal of the abnormalities. The significance of these changes to the origin of arrhythmias is discussed.

Regression of LV hypertrophy with captopril normalizes membrane currents in rabbits

1998 ◽  
Vol 275 (4) ◽  
pp. H1216-H1224 ◽  
Author(s):  
Seth J. Rials ◽  
Xiaoping Xu ◽  
Ying Wu ◽  
Roger A. Marinchak ◽  
Peter R. Kowey
Keyword(s):  
Cell Membrane ◽  
Action Potential ◽  
Renal Artery ◽  
Current Density ◽  
Action Potential Duration ◽  
Left Ventricular ◽  
Membrane Current ◽  
Membrane Capacitance ◽  
Membrane Currents ◽  
Cell Membrane Capacitance

Recent studies indicate that regression of left ventricular hypertrophy (LVH) normalizes the in situ electrophysiological abnormalities of the left ventricle. This study was designed to determine whether regression of LVH also normalizes the abnormalities of individual membrane currents. LVH was induced in rabbits by renal artery banding. Single ventricular myocytes from rabbits with LVH at 3 mo after renal artery banding demonstrated increased cell membrane capacitance, prolonged action potential duration, decreased inward rectifier K+ current density, and increased transient outward K+ current density compared with myocytes from age-matched controls. Additional rabbits were randomized at 3 mo after banding to treatment with either vehicle or captopril for an additional 3 mo. Myocytes from LVH rabbits treated with vehicle showed persistent membrane current abnormalities. However, myocytes isolated from LVH rabbits treated with captopril had normal cell membrane capacitance, action potential duration, and membrane current densities. Captopril had no direct effect on membrane currents of either control or LVH myocytes. These data support the hypothesis that the action potential prolongation and membrane current abnormalities of LVH are reversed by regression. Normalization of membrane currents probably explains the reduced vulnerability to ventricular arrhythmia observed in this LVH model after treatment with captopril.

Analysis of catecholamine effects in single atrial trabeculae of the frog heart

1977 ◽  
Vol 197 (1128) ◽  
pp. 333-362 ◽  
Keyword(s):  
Cell Membrane ◽  
Action Potential ◽  
Time Course ◽  
Drug Exposure ◽  
Drug Application ◽  
Latency Period ◽  
Frog Heart ◽  
Phosphodiesterase Activity ◽  
Inward Current ◽  
Calcium Inward Current

A study was made of the time course of the effects of adrenaline and isoprenaline on both twitch tension and the intracellular action potential of single atrial trabeculae from frog heart, under a variety of experimental conditions. Twitch tension and overshoot of action potentials rose and subsided in a parallel fashion during build-up and decline of catecholamine action. Cessation of stimulation during drug application had little effect on the tension responses to the drugs. These, and also results obtained with step changes of external calcium concentration during drug exposure, suggest that tension enhancement is a direct consequence of the increased calcium inward current produced by the catecholamines. Exceptional results from trabeculae of ‘hypodynamic’ hearts are described and interpreted on the basis of previous findings obtained in the ‘hypo-dynamic’ condition. Under suitable conditions, including the use of brief periods of drug exposure (≤20 s), three phases of ( β -catecholamine action were discernible: (1) a latency period, of up to 15 s, which preceded tension and potential rise after drug application. Results are presented suggesting that this latency mainly reflects the time which it takes for drug-combined receptors to activate adenylate cyclase in the cell membrane. (2) A sub­sequent phase was critically dependent, in both its magnitude and time course, on phosphodiesterase activity, as was shown by the application of the specific inhibitors papaverine, ICI 63 197, and Ro 20-1724. This phase is probably controlled by the build-up and decline of cAMP within the cells and the subsequent activation and deactivation of a protein kinase. (3) A third phase, associated with the final portion of the decline of catecholamine action, was relatively insensitive to moderate inhi­bition of phosphodiesterase activity. It is attributed to a change of phosphorylation of sites at the internal surface of the cell membrane, the process which, it is assumed, determines the size of calcium inward current during an action potential. Tension decline after a short staircase occurred with a time course closely similar to that of the final phase of the declining catecholamine response. A common final step in the sequential cellular processes under­ lying the two responses is proposed. In some 40% of the trabeculae examined, adrenaline responses were of ‘mixed’ origin: in addition to the relatively slow β -adrenergic action, an initial rapid tension change was present, and experimental tests suggest that this is mediated by α -type receptors.

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