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P F Cranefield

Publications and source records attributed to P F Cranefield.

At least 37 records · Page 2Linked to original sources
PubMed1977

Action potentials, afterpotentials, and arrhythmias.

Triggered activity must be added to spontaneous activity and to circus movement as a cause for extrasystoles and tachycardias of either atrial or ventricular origin. The activity of a triggerable focus requires phase 4 depolarization caused by an afterpotential; this distinguishes it from the activity seen in circus movement. A triggerable focus becomes rhythmically active only if driven at a critical rate or by a critically timed premature impulse; this distinguishes it from a focus of spontaneous or automatic activity. The ease of triggering a triggerable focus increases in the presence of catecholamines; triggerable foci in the atrium become quiescent when exposed to acetylcholine. At the present time, fibers within the coronary sinus provide the most persuasive example of triggered activity as a possible cause of arrhythmias of clinical significance. It is possible that the coupled extrasystoles of digitalis toxicity may be triggered; there is every reason to believe that further examples of triggered arrhythmias of possible clinical significance will be discovered.

Action Potentials↗
PubMed1976

Triggered activity in cardiac muscle fibers of the simian mitral valve.

The action potential of cardiac fibers in the anterior mitral valve leaflet of the monkey heart is followed by an after-hyperpolarization. The addition of catecholamines causes a delayed after-depolarization to follow the after-hyperpolarization. The amplitude of the after-depolarization increases as the stimulus cycle length is decreased, or after premature stimulation, and as a result can reach threshold to yield nondriven, sustained rhythmic activity which we term triggered activity. This sustained rhythmic activity can be terminated by a single, appropriately timed, premature stimulus. The amplitude of the action potentials of mitral valve fibers is increased by catecholamines; the amplitude and rate of depolarization are depressed by verapamil. The amplitude of the action potentials is little affected by tetrodotoxin (TTX) but the maximum rate of depolarization is reduced by TTX. The delayed after-depolarization induced by catecholamines is abolished by verapamil, as is triggered activity. These observations suggest that mitral valve fibers generate slow response action potentials, that triggerable sustained rhythmic activity may be a property of the slow response and that such activity may cause the types of cardiac arrhythmias that usually are attributed to reentry.

Action Potentials↗
PubMed1976

Two levels of resting potential in canine cardiac Purkinje fibers exposed to sodium-free solutions.

Canine cardiac Purkinje fibers exposed to sodium-free solutions containing 16 mM CaCl2, 20 mM tetraethylammonium chloride, 108 mM tetramethylammonium chloride, and 2.7 mM KCl may be quiescent at a resting potential of either -50 mV or -90 mV. The membrane potential of these fibers can be switched from -50 mV to -90 mV by a hyperpolarizing current pulse and from -90 mV to -50 mV by a depolarizing current pulse. The transition from -50 mV to -90 mV depends on a voltage-dependent increase in potassium conductance, that conductance being low at -50 mV and high at -90 mV. A reduction in potassium conductance causes the fiber to depolarize from -90 mV to -50 mV because of the presence of an inward current which apparently is carried mainly by Ca. Fibers that show a high resting potential cannot be excited except by depolarizing stimuli strong enough to move the membrane from -90 mV to a threshold potential of about -40 mV. Fibers that show a low resting potential are more easily excited and may show rhythmic activity sustained by afterpotentials that appear only if the low membrane potential is accompanied by a low potassium conductance. Slow changes in membrane potential also are seen; these changes may result from movements of chloride.

Action Potentials↗
PubMed1975

Ernest Harms.

Explore the source record for details and available documents.

History, Modern 1601-↗
PubMed1975

The effects of verapamil and paired-pulse stimulation on mammalian ventricle.

Postextrasystolic potentiation induced by paired-pulse stimulation was studied in mammalian ventricle muscle in the presence of verapamil (0.2-4.0 muM). Verapamil exerts a negative inotropic effect on the potentiated contraction, but the force of the potentiated contraction in the presence of verapamil is greater than that of the normal, unpotentiated contraction in the absence of verapamil. The positive inotropic effect of paired stimulation appears to result both from an additional calcium influx appearing as a calcium current during the plateau of the premature action potential and from some additional mechanism, tentatively identified as a Na: Ca exchange. Our results suggest that paired-pulse stimulation could be used clinically to counteract the negative inotropic effects of verapamil; moreover, the antiarrhythmic action of verapamil might counteract any arrhythmias caused by paired pacing.

Animals↗
PubMed1974

Effect on membrane potential and electrical activity of adding sodium to sodium-depleted cardiac purkinje fibers.

Canine cardiac Purkinje fibers exposed to Na-free solutions containing 128 mM TEA and 16 mM Ca show resting potentials in the range -50 to -90 mV; if the concentration of Na in the perfusate is raised from 0 to 4 to 24 mM, hyperpolarization follows. If the initial resting potential is low, the hyperpolarization tends to be greater; the average increase in the presence of 8 mM Na is 14 mV. Such hyperpolarization is not induced by adding Na to K-free solutions, is not seen in cooled fibers, or in fibers exposed to 10(-3) M ouabain, nor is it induced by adding Li and thus may result from electrogenic sodium extrusion. Fibers exposed to Na-free solutions are often spontaneously active; if they are quiescent they often show repetitive activity during depolarizing pulses. Such spontaneous or repetitive activity is suppressed by the addition of Na. This suppression may or may not be related to the hyperpolarization.

Action Potentials↗
PubMed1973

The electrical activity of canine cardiac Purkinje fibers in sodium-free, calcium-rich solutions.

Propagated action potentials can be obtained in canine cardiac Purkinje fibers exposed to Na-free solutions containing no inorganic cation other than Ca and K. Essentially similar action potentials are obtained if Na is replaced by tetraethylammonium (TEA), tetramethylammonium (TMA), or choline. In a solution containing 128 mM TEA and 16.2 mM Ca the characteristics of these electrical responses were: maximum diastolic potential, -59 +/- 3.3 mV; overshoot, 20 +/- 6.8 mV; maximum upstroke velocity, 3.7 +/- 2.3 V/s; conduction velocity, 0.1 m/s; and action potential duration, 360 +/- 45 ms. The magnitude of the overshoot varied with log Ca(o) with a slope of about 30 mV/10-fold concentration change. The upstroke velocity was an approximately linear function of Ca(o). The active response was greatly diminished or abolished by Mn and D-600 but was unaffected by tetrodotoxin. These Ca-dependent responses appeared in a region of transmembrane potential (about -50 mV) at which the rapid Na-dependent upstroke is abolished even when Na is present.

Action Potentials↗