Coronary occlusion and reperfusion: effects on subendocardial cardiac fibers

1980 ◽  
Vol 238 (4) ◽  
pp. H581-H593 ◽  
Author(s):  
H. S. Karaguezian ◽  
J. J. Fenoglio ◽  
M. B. Weiss ◽  
A. L. Wit
Keyword(s):  
Action Potential ◽  
Action Potentials ◽  
Coronary Flow ◽  
Transmembrane Potential ◽  
Coronary Occlusion ◽  
Muscle Cells ◽  
Purkinje Fibers ◽  
Transmembrane Potentials ◽  
Purkinje System ◽  
Potential Parameters

Coronary flow and transmembrane potentials of Purkinje and muscle fibers in reperfused infarcts and infarcts caused by permanent coronary occlusion were compared. Purkinje fibers in permanently occluded infarcts at 24 h had markedly reduced resting potentials. Action potential amplitudes, and Vmax were reduced and duration markedly prolonged. In reperfused infarcts, changes in Purkinje fiber transmembrane potentials were not as marked. Action potential duration in 3-day-old permanently occluded infarcts were longer than at 24 h, but in reperfused infarcts durations had returned to normal. Premature impulses conducted more rapidly in the reperfused infarct Purkinje system than in the permanently occluded. Other transmembrane potential parameters of Purkinje fibers in 3-day-old and 9- to 10-day-old reperfused and permanently occluded infarcts were not significantly different from each other. The ventricular muscle cells that survived in reperfused infarcts at all times also had reduced resting potentials and action potentials with decreased amplitudes, reduced Vmax, and prolonged durations. Almost no muscle cells survived in permanently occluded infarcts. Therefore, reperfusion salvages subendocardial fibers and prevents some but not all of the electrophysiological abnormalities.

Effects of temperature on cardiac transmembrane potentials in hibernation

1976 ◽  
Vol 230 (2) ◽  
pp. 403-409 ◽  
Author(s):  
HK Jacobs ◽  
FE South
Keyword(s):  
Membrane Potential ◽  
Action Potential ◽  
Papillary Muscle ◽  
Action Potentials ◽  
Resting Membrane Potential ◽  
Prolonged Action ◽  
Transmembrane Potentials ◽  
Effects Of Temperature ◽  
And Control ◽  
Potential Parameters

Resting and action potential parameters were measured from papillary muscle isolated from hibernating and control hamsters and from rats. The temperature range of the study was 12-38 degrees C. The decrease in resting membrane potential (Em) with decreasing temperature was significantly less in the hibernation preparations (HH), down to 20 degrees C, than in either the control hamsters or rats. Below 20 degrees C the declines in Em of all preparations were indistinguishable. Action potential magnitude was adequately maintained in HH to 12 degrees C while both control hamster and rat action potentials declined markedly as temperatures were reduced. Both types of hamster preparations showed greatly prolonged action potentials with reduced temperatures as contrasted to a limited prolongation of rat action potentials. The data are suggestive of a membrane modication in hibernation.

Effects of autonomic neurohumors on transmembrane potentials of atrial plateau fibers

1975 ◽  
Vol 229 (5) ◽  
pp. 1351-1356 ◽  
Author(s):  
LD Davis
Keyword(s):  
Action Potential ◽  
Action Potentials ◽  
Transmembrane Potential ◽  
Plateau Phase ◽  
Transmembrane Potentials ◽  
Discernible Effect ◽  
Diastolic Potential

Isolated canine atrial plateau fibers were treated with acetylcholine or norepinephrine to note the effects on the transmembrane potential. Acetylcholine, 1.0 or 2.0 mug/ml, consistently reduced the slope of inherent phase 4 depolarization. Increases in maximum diastolic potential and rising velocity occurred along with a decrease in overshoot. The plateau phase disappeared. Pretreatment with atropine, 1.0 mug/ml, prevented these responses, and alone this drug had no discernible effect. Norepinephrine consistently increased the slope of phase 4 depolarization. Frequently plateau fibers generated action potentials by the normal pacemaker mechanism. "Arrhythmias" characterized by spontaneous excitations were induced in 92% of the norepinephrine experiments. Norepinephrine also enhanced the plateau phase of the action potential and decreased the rising velocity and overshoot. Racemic propranolol, 1.0 mug/ml, blocked all the above effects including arrhythmias. Dextropropranolol, 1.0 mug/ml, did not block effects produced by norepinephrine. Acetylcholine, applied to fibers under treatment with norepinephrine, reduced the slope of norepinephrine-induced phase 4 depolarization and terminated induced arrhythmias.

Time course of infarct growth toward the endocardium after coronary occlusion

1979 ◽  
Vol 236 (2) ◽  
pp. H356-H370 ◽  
Author(s):  
J. J. Fenoglio ◽  
H. S. Karagueuzian ◽  
P. L. Friedman ◽  
A. Albala ◽  
A. L. Wit
Keyword(s):  
Action Potential ◽  
Time Course ◽  
Coronary Occlusion ◽  
Muscle Fibers ◽  
Muscle Cells ◽  
Progressive Increase ◽  
Resting Potential ◽  
Ventricular Muscle ◽  
Purkinje Fibers ◽  
Endocardial Surface

Transmembrane potentials and ultrastructure of subendocardial Purkinje and ventricular muscle fibers, isolated 1, 3, 5, 6, 14, and 24 h after coronary occlusion were investigated. Action potentials were recorded from progressively fewer layers of muscle cells as the age of the infarct increased. At 14 h little viable muscle remained. The decrease in the number of electrophysiologically viable muscle fibers correlated with structural evidence that the infarct moved with time toward the endocardial surface until only viable Purkinje fibers remained. Purkinje and surviving ventricular muscle fibers demonstrated a progressive decrease in resting potential, action potential amplitude, and Vmax and a progressive increase in action potential duration. Spontaneous diastolic depolarizations were found in Purkinje fibers only in 24-h infarcts and occasionally in cells deep to the endocardial surface, which may have been muscle cells. We hypothesize that during the first 24 h after coronary occlusion arrhythmias originate near the interface of infarcted and ischemic myocardium. As this interface moves toward the endocardium, this site of origin of arrhythmias moves with it until the Purkinje network is reached.

Basis for tetrodotoxin and lidocaine effects on action potentials in dog ventricular myocytes

1988 ◽  
Vol 254 (6) ◽  
pp. H1157-H1166 ◽  
Author(s):  
J. A. Wasserstrom ◽  
J. J. Salata
Keyword(s):  
Action Potential ◽  
Action Potentials ◽  
Ventricular Myocytes ◽  
Ionic Currents ◽  
Detectable Effect ◽  
Na Channel ◽  
Na Current ◽  
Voltage Range ◽  
Purkinje Fibers ◽  
Ventricular Cells

We studied the effects of tetrodotoxin (TTX) and lidocaine on transmembrane action potentials and ionic currents in dog isolated ventricular myocytes. TTX (0.1-1 x 10(-5) M) and lidocaine (0.5-2 x 10(-5) M) decreased action potential duration, but only TTX decreased the maximum rate of depolarization (Vmax). Both TTX (1-2 x 10(-5) M) and lidocaine (2-5 x 10(-5) M) blocked a slowly inactivating toward current in the plateau voltage range. The voltage- and time-dependent characteristics of this current are virtually identical to those described in Purkinje fibers for the slowly inactivating inward Na+ current. In addition, TTX abolished the outward shift in net current at plateau potentials caused by lidocaine alone. Lidocaine had no detectable effect on the slow inward Ca2+ current and the inward K+ current rectifier, Ia. Our results indicate that 1) there is a slowly inactivating inward Na+ current in ventricular cells similar in time, voltage, and TTX sensitivity to that described in Purkinje fibers; 2) both TTX and lidocaine shorten ventricular action potentials by reducing this slowly inactivating Na+ current; 3) lidocaine has no additional actions on other ionic currents that contribute to its ability to abbreviate ventricular action potentials; and 4) although both agents shorten the action potential by the same mechanism, only TTX reduces Vmax. This last point suggests that TTX produces tonic block of Na+ current, whereas lidocaine may produce state-dependent Na+ channel block, namely, blockade of Na+ current only after Na+ channels have already been opened (inactivated-state block).

Role of acetylcholine in induction of repetitive activity in human atrial fibers

1989 ◽  
Vol 256 (1) ◽  
pp. H74-H84
Author(s):  
Z. Y. Hou ◽  
C. I. Lin ◽  
M. Vassalle ◽  
B. N. Chiang ◽  
K. K. Cheng
Keyword(s):  
Action Potential ◽  
Muscarinic Receptor ◽  
Action Potentials ◽  
Oscillatory Potentials ◽  
Contractile Force ◽  
Intracellular Level ◽  
Transmembrane Potentials ◽  
Rebound Increase

The actions of acetylcholine and its interactions with epinephrine were studied in human atrial tissues by recording transmembrane potentials and contractile force. Acetylcholine (0.55-5.5 microM) reduced force, shortened the duration and shifted to more negative values the plateau of action potentials, abolished phase 4 depolarization, and suppressed the activity of spontaneous fibers. During the recovery, often there was a rebound increase in some parameters of the action potential and in force. Epinephrine (0.3-2.8 microM) induced oscillatory potentials and aftercontractions and acetylcholine abolished them. However, during the washout of acetylcholine in the presence of epinephrine, the oscillatory potentials and aftercontractions were larger than before acetylcholine, and repetitive activity was often induced. The inhibitory and excitatory effects of acetylcholine were mimicked by methacholine (5.1 microM) and abolished by atropine (1.5 microM). The postacetylcholine rebound was also potentiated by theophylline (0.6-2 mM) but was not blocked by propranolol (1-3.4 microM), prazosin (1 microM), and diltiazem (0.1 microM). It is concluded that in human atrial fibers acetylcholine has inhibitory as well as excitatory effects that are exaggerated in the presence of epinephrine and are mediated by the activation of the muscarinic receptor. The interaction between acetylcholine and epinephrine involves an antagonism at an intracellular level.

Effect of Several Cations on Transmembrane Potentials of Cardiac Muscle

1956 ◽  
Vol 186 (2) ◽  
pp. 317-324 ◽  
Author(s):  
Brian F. Hoffman ◽  
E. E. Suckling
Keyword(s):  
Action Potential ◽  
Cardiac Muscle ◽  
Action Potentials ◽  
Time Course ◽  
Pacemaker Activity ◽  
Transmembrane Potentials ◽  
High K ◽  
Intracellular Microelectrodes ◽  
Simultaneous Decrease ◽  
Low K

The effects of changes in the extracellular concentrations of Ca, K and Mg on the transmembrane resting and action potentials of single fibers of the auricle, ventricle and specialized conducting system of the dog heart have been studied by means of intracellular microelectrodes. With respect to Ca, the three tissues exhibit quite different sensitivities. Changes in concentration of this ion alter the time course of the action potential recorded from auricle and ventricle but have little effect on the action potential configuration of the Purkinje fiber. In the latter tissue, on the other hand, pacemaker activity is most strongly enhanced by Ca depletion and excitability is lost at Ca concentrations permitting normal propagation in papillary muscle. The effect of K on the resting transmembrane potential is dependent on the simultaneous Ca concentration. The interrelationship is such that the depolarizing effect of high K is decreased by elevated Ca and the depolarization produced by low K is diminished by low levels of Ca. Changes in the concentration of Mg have little effect on the transmembrane potentials of cardiac muscle unless the level of Ca is low. Under this condition a simultaneous decrease in Mg gives rise to a marked prolongation of the action potential duration of both auricle and ventricle. Some evidence for the basic similarity of the processes underlying repolarization in these three tissues is presented and it is thought the normally encountered differences in their action potentials may be related to the sensitivity of each tissue to extracellular Ca.

Postextrasystolic Potentiation of Contraction in Cardiac Muscle

1956 ◽  
Vol 185 (1) ◽  
pp. 95-102 ◽  
Author(s):  
Brian F. Hoffman ◽  
Elliot Bindler ◽  
E. E. Suckling
Keyword(s):  
Right Ventricle ◽  
Action Potentials ◽  
Transmembrane Potential ◽  
Isometric Tension ◽  
Papillary Muscles ◽  
Postextrasystolic Potentiation ◽  
Single Fibers ◽  
Transmembrane Potentials ◽  
Diastolic Interval ◽  
The Right

The phenomenon of postextrasystolic potentiation of contraction has been studied in papillary muscles isolated from the right ventricle of dog and cat hearts. Isometric tension has been recorded by means of an electronic transducer (RCA #5734) and electrical activity of single fibers by means of an intracellular microelectrode. The degree of potentiation of contraction resulting from a single extrasystole is directly related to the degree of prematurity of this beat. Evidence has been obtained which indicates that the potentiation is maximally effective immediately after the extrasystole and decays at a progressively slower rate during the course of seven to ten beats. The appearance of postextrasystolic potentiation is not dependent upon the changes in frequency of contraction, diastolic interval or presystolic tension which result from the premature contraction. Studies of the transmembrane potentials of single fibers reveal no change in amplitude and little change in configuration of the action potentials associated with potentiated beats. Studies of the resting transmembrane potential and the effects of changes in extracellular concentrations of K and Ca fail to support the concept that potentiation is related solely to changes in the fiber K content. It is concluded that postextrasystolic potentiation results from mechanisms which remain unknown.

Calcium action potentials in single freshly isolated smooth muscle cells

1980 ◽  
Vol 239 (5) ◽  
pp. C162-C174 ◽  
Author(s):  
J. V. Walsh ◽  
J. J. Singer
Keyword(s):  
Smooth Muscle ◽  
Action Potential ◽  
Smooth Muscle Cells ◽  
Action Potentials ◽  
Maximum Rate ◽  
Muscle Cells ◽  
Membrane Resistance ◽  
Inward Current ◽  
Visceral Smooth Muscle ◽  
Maximum Rate Of Rise

The ionic basis of the action potential was investigated using intracellular microelectrodes in single smooth muscle cells freshly isolated from the stomach of the toad Bufo marinus. When [Ca2+]0 was elevated (> 8mM), action potentials were readily elicited, which had similar characteristics to those found in many tissue preparations of visceral smooth muscle. There was a decrease in membrane resistance at the peak of the action potential and during the undershoot. The following evidence indicated that the inward current is carried by Ca2+: 1) Raising [Ca2+]0 from 15 to 49.6 mM in the presence of 18.2 mM tetraethylammonium chloride (TEA) increased the maximum rate of rise and the overshoot amplitude, the latter by 15 mV, i.e., 29.5 mV/10-fold change in [Ca2+]0. Changing [Na2+]0 from 11.8 to 81.8 mM had no significant effect on the maximum rate of rise or the overshoot. 2) The action potentials were blocked by 8 mM Mn2+ ([Ca2+]0 = 14.6 mM) but not by 14.3 microM tetrodotoxin (TTX) ([Na2+]0 = 100 mM). 3) Action potentials could be elicited when [Ba2+]0 or [Sr2+]0 were present in high concentrations ([Ca2+]0 less than or equal to 31 microM,[Na2+]0 = 11.8 mM). Both the maximum rate of rise and overshoot amplitude of the action potential increased as the membrane potential became more negative, suggesting increased activation of the inward current. Both TEA and Ba2+ prolonged the action potential, suggesting that a K+ current is responsible for repolarization. Action potentials could also be elicited on anode break at elevated [K+]0 (91 mM).

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