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depolarization
(redirected from Depolarizations)

   Also found in: Encyclopedia, Wikipedia 0.03 sec.
depolarization /de·po·lar·iza·tion/ (de-po″lahr-ĭ-za´shun)
1. the process or act of neutralizing polarity.
2. in electrophysiology, reversal of the resting potential in excitable cell membranes when stimulated.

atrial premature depolarization  (APD) see under complex.
ventricular premature depolarization  (VPD) see under complex.

de·po·lar·i·za·tion (d-plr--zshn)
n.
Elimination or neutralization of polarity, as in nerve cells.

depolarization
[dēpō′lərīzā′shən]
the reduction of a membrane potential to a less negative value. It is caused by the influx of cations, such as sodium and calcium, through ion channels in the membrane. In many neurons and muscle cells, depolarization may lead to an electric impulse called an action potential.

depolarization (dēpō´lrizā´shn),
n a neutralization of polarity; the breaking down of polarized semipermeable membranes, as in nerve or muscle cells in the induction of impulses.

depolarization
the process or act of neutralizing polarity as in the decrease of membrane potential.

myocardial depolarization
the conducted cardiac impulse transiently reverses membrane polarity. In this depolarized phase the myocardium is incapable of further contraction.

depolarization
A change in the value of the resting membrane potential towards zero. The inside of the cell becomes less negative compared to the outside. This is due to a change in permeability and migration of sodium ions into the interior of the cell. Depolarization is excitatory because the membrane potential shifts towards the neuron's threshold at which an action potential occurs. See hyperpolarization; synapse.

depolarization
Cardiac pacing 1. The sudden change in electrical potential from negative to slightly positive which occurs during phase O of an action potential in an excitable cell membrane–in nerve and heart muscle 2. A rapid alteration of the resting potential in a large mass of tissue–eg, heart ventricles, which usually results in a contraction. See Action potential, Latency period, Resting potential.


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Patches were held at -100 m V and single-channel currents were recorded during either 100-ms slep depolarizations between -70 and 0 mV or 80-ms steps to potentials between -50 and - 120 mV immediately after a 3-ms depolarization to 0 mV.
Experimental evidence has been provided that phase 2 early after depolarizations (EAD) can be generated from hypertrophied left ventricular wall in the absence of action potential duration (APD) prolonging agents.
Aside from correcting any of these predisposing conditions, treatment of LQTS is directed at regulating the heart rate, normalizing the QT length, and preventing early ventricular depolarizations.
 
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