Depolarization zone

Figure 2.1. Schematic representation of the dependence of pol3rmer surface tension 72 on the surface tension yi of wetting liquid 1-depolarization zone, 2-unperturbed zone, 3-zone of additional polarization.

Effects of antiarrhythmics. Antiarrhythmics of the Na -channel blocking type reduce the probability that Na+ channeb will open upon membrane depolarization ( membrane stabilization ). The potential consequences are (A, bottom) 1) a reduction in the velocity of depolarization and a decrease in the speed of impulse propagation aberrant impulse propagation is impeded. 2) Depolarization is entirely absent pathological impulse generation, e.g., in the marginal zone of an infarction, is suppressed. 3) The time required until a new depolarization can be elicited, i.e., the refractory period, is increased prolongation of the AP (see below) contributes to the increase in refractory period. Consequently, premature excitation with risk of fibrillation is prevented. 

The dielectric behavior of PMCHI was studied by Diaz Calleja et al. [210] at variable frequency in the audio zone and second, by thermal stimulated depolarization. Because of the high conductivity of the samples, there is a hidden dielectric relaxation that can be detected by using the macroscopic dynamic polarizability a defined in terms of the dielectric complex permittivity e by means of the equation ... 

In experimental stroke, the zone of dense ischemia leads to the rapid exhaustion of substrates, particularly oxygen and glucose. The impaired energy yield cannot maintain the ion pumps so that cells loose their membrane potential (anoxic depolarization of glia and neurons). As a consequence, volt-... 

Leenders AGM, Scholten G, De Lange RPJ, Lopes Da Silva FH, Ghijsen WEJM. 2002. Sequential changes in synaptic vesicle pools and endosome-like organelles during depolarization near the active zone of central nerve terminals. Neuroscience 109 195-206. 

ACh is found to be stored within the terminals of motor neurons. Detailed analysis has demonshated that ACh is stored within small packages called synaptic vesicles that are concenhated around active zones on the presynaptic membrane. These active zones have been identified as specialized sites for neurohansmitter containing vesicle release. The enzyme for synthesizing ACh from choline and acetyl-Co A, choline acetyl transferase, is also found within the presynaptic terminal. Choline acetyl transferase is found in the cytoplasm. When ACh is synthesized it is pumped into synaptic vesicles by means of a specific carrier molecule located in the vesicle membrane. Once released, ACh subsequently diffuses across the synapse and activates nicotinic ACh receptors localized on the plasma membrane of the postsynapdc muscle cell producing depolarization of the muscle (see below). 

Suxamethonium consists of two acetylcholine molecules linked together. Initially, it acts like acetylcholine by depolarizing the motor end-plate. However, unlike acetylcholine, which on dissociation from the receptor is immediately destroyed by acetylcholinesterase present in the neuromuscular junction, suxamethonium is hydrolysed by a (pseudo)cholinesterase present in the plasma but not at the neuromuscular junction. Most of an injected dose of suxamethonium is normally destroyed before it reaches the neuromuscular junction. If the activity of plasma cholinesterase in a particular patient is reduced, more of the suxamethonium reaches the neuromuscular junction and its action is proportionately prolonged. The molecules of suxamethonium that reach the acetylcholine receptor sites interact repeatedly with them, producing prolonged depolarization of the motor end-plate, which becomes surrounded by an electrically inactive zone. The end-result is flaccid paralysis. The action of suxamethonium is terminated by diffusion away from the neuromuscular junction. Hydrolysis results in choline and succinylmonocholine, which has a very weak competitive blocking action and is further slowly hydrolysed by plasma cholinesterase to choline and succinic acid. 

The localization of adducts to the epicardial border zone suggested the possibility that IsoK/LG adducts contribute to cardiac arrhythmias. Ventricular tachycardia/fibrillation following myocardial infarction is a major cause of sudden cardiac death. Arrhythmias in ischemic myocardium arise from sodium channel blockade. Sodium channels are hypothesized to cycle between three conformational states a deactivated closed state, an activated open state, and an inactivated closed state. Upon depolarization, the deactivated state converts to the activated state and sodium current flows for a brief time before the channel enters the inactive state. The channel only converts from the inactive state to the deactivated state when the membrane repolarizes during the falling phase of the action potential. Changes in the ability to convert from the inactive to the deactivated state are critical to the initiation and perpetuation of arrhythmias. 

Also the system polarizes and depolarizes very slowly. However, the potential is also susceptible to changes in the environment (temperature, humidity), as well as the applied current, so reading must be taken within a reasonable time period while the environment around the structure is reasonably stable. This is particularly important for tidal zones of structures in marine exposure conditions where the polarization/depolarization period should either be through a full tidal cycle or while the steel adjacent to the reference electrode is fully exposed. The full tidal cycle (about 12 h 20 min) is preferred at the steel should be in the same condition at the beginning and the end of the period while its condition will be changing (drying out) during an exposure period... 

If suddenly the channels (Figure 5.5) open so that the intracellular potential changes abruptly, the ions must also supply a transient discharge current of the membrane capacitance. At the extracellular side, the current is not with respect to a far-away reference electrode, but concentrated to an interstitial fluid zone near the cell. The current flow can be modeled with local current dipoles and is clearly measurable with unipolar or bipolar pickup electrodes in the interstitial liquid. When the cell is depolarizing, cations... 

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