repolarization


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repolarization

 [re″po-lah-rĭza´shun]
1. the reestablishment of polarity, especially the return of a cell's membrane potential to resting potential after depolarization.
2. in cardiac physiology, the restoration of the cell to its maximal diastolic potential, represented by phase 0 to phase 3 of the action potential.

re·po·lar·i·za·tion

(rē'pō-lăr-i-zā'shŭn),
The process whereby the membrane, cell, or fiber, after depolarization, is polarized again, with positive charges on the outer and negative charges on the inner surface.

repolarization

/re·po·lar·iza·tion/ (re-po″ler-ĭ-za´shun) the reestablishment of polarity, especially the return of cell membrane potential to resting potential after depolarization.

repolarization

(rē-pō′lər-ĭ-zā′shən)
n.
The restoration of a polarized state across a membrane, as in a muscle fiber following contraction.

repolarization

[rēpō′lərīzā′shən]
Etymology: L, re + polus, pole; Gk, izein, to cause
the process by which the membrane potential of a neuron or muscle cell is restored to the cell's resting potential. In a cardiac muscle cell, the repolarization process begins after phase 0 of the action potential and is completed by the end of phase 3. It encompasses the effective and relative refractory periods and correlates with the Q-T interval on the electrocardiogram. See also cardiac action potential.

re·po·lar·i·za·tion

(rē-pō'lăr-ī-zā'shŭn)
The process whereby the membrane, cell, or fiber, after depolarization, is polarized again, with positive charges on the outer and negative charges on the inner surface.

repolarization

Restoration of the resting polarized state in a muscle or nerve fibre. Polarization implies a balanced electrical charge on either side of the fibre membrane, being, in the resting state, negative on the inside and positive on the outside. In depolarization the charges are locally reversed.

repolarization

the re-establishment of polarity, especially the return of cell membrane potential to resting potential after depolarization.
References in periodicals archive ?
2A shows that R(+)-pulegone had a dose-dependent effect on prolonging the time required for action potential repolarization (APR).
We also detected a lengthening in APD90, with a larger relative change in repolarization time than in depolarization time.
5,6,8,10-12,23) The ST segment shows the early phase of ventricular repolarization, and it is normally isoelectric.
Clinical and mechanistic issues in early repolarization of normal variants and lethal arrhythmia syndromes.
It is considered a marker of arrhythmia and sudden cardiac death risk, and a quantitative noninvasive method to determine myocardial repolarization inhomogeneities (12-14), although several trials deny the prognostic value of QT dispersion (15).
Changes in this subunit or Klf15 can affect the potassium current that governs repolarization of the cardiac myocyte.
However, when this effect is confined to a limited area of the heart, segmental delays in myocardial repolarization may produce global cardiac electrical instability.
The QT prolongation results from of delayed myocyte repolarization due to inherited ion channel mutations involving cardiac sodium and potassium currents.
The QT interval is the time required to complete myocardial depolarization and repolarization period.
By preventing repolarization of the nerve ending, the postsynaptic ending becomes refractory and unexcitable, resulting in flaccid muscles.
Repolarization dynamics and variability are of increasing interest as Holter-derived parameters, reflecting changes in myocardial vulnerability, and which contribute to increased risk of arrhythmic events and SD.
Contributors working in cardiology, biomedical sciences and biotechnology, pharmacology, and biology in the US and Europe review basic cardiac electrophysiology, the mechanisms responsible for arrhythmias in the setting of ischemia, and basic pharmacology of antiarrhythmic drugs; repolarization reserve, safety pharmacology and challenges, and regulatory issues for the development of drugs; novel pharmaceutical targets, including both ion channel and non-ion channel targets; and non-pharmacological interventions such as selective cardiac neural disruption or nerve stimulation, aerobic exercise training, and omega-3 fatty acid dietary supplements.