repolarization


Also found in: Dictionary, Wikipedia.

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 ?
The disarray leads to electrotonic uncoupling of the myocytes resulting in alternation in repolarization and T wave alternans.
In conclusion, the result of this present study suggests that increased glycemic variability associated with prolonged QTc duration and QTc dispersion, which means ventricular depolarization and repolarization are affected by glycemic variability in type 2 diabetic patients.
QT interval, one of the most important duration, is defined as the time lapse between the beginning of the depolarization and the end of the repolarization in heart ventricles.
These include stretching of the papillary muscles with ballooning prolapse of mitral leaflets (27), mechanical stimulation of the endocardium by thickened chordate (28), coronary emboly caused by accumulation of platalets and fibrin as a result of endocardial friction (29), autonomic dysfunction (30,31) and repolarization changes characterized by prolongation in QT interval and increase in QT dispersion (7-9).
Therefore, in this study, we aimed to investigate ventricular repolarization using Tp-e intervals and
Recent evidences suggest that asymmetric brain activity during acute emotional stress causes asymmetric activation of heart leading to production of inhomogeneous areas of repolarization and production of electrical instability of heart.
EADs often occur during bradycardia under the condition of reduced repolarization reserve.
It is an inherited form of ions channelopathy resulting in prolonged cardiac repolarization and abnormal prolongation of QT interval on electrocardiogram (ECG).
A prolonged QTc interval is fundamentally due to a delayed repolarization phase, which is responsible for an increased risk of ventricular arrhythmias and sudden death.
We will quantify the contribution of the regional strain on the spatiotemporal organization of repolarization alternans, and determine the effect of changes in the cardiac strain on the ECG-based indices of alternans.
It describes the normal electrocardiogram, including how the ECG records the path of cardiac activation through the heart, devices and recording techniques, and interpreting normal and pathologic recordings; morphological abnormalities from different pathologies, such as atrial and ventricular enlargement and block, ventricular pre-excitation, atrial repolarization, and ischemia and necrosis; ECG patterns of arrhythmias, as well as patterns of pacemakers; and the use of ECG in clinical practice in the evaluation of symptoms, in other heart diseases and diverse situations, patterns that indicate poor prognosis, and abnormal ECG in patients with normal history and examination and normal ECG in serious heart disease.