Extracellular potassium

This technique has been used to investigate the effect of the photoactivation of rose bengal on /wa/K in isolated rabbit ventricular myocytes (Shattock and Matsuura, 1993). Using this procedure, 5 min exposure to illuminated rose bengal reduced 7Na/K to 60% of control at 0 mV and to 75% of control at -75 mV. In the absence of extracellular potassium, no active ionic currents remain... 

Webb, S.C., Fleetwcxjd, G. and Montgomery, R. (1983). Absence of a relationship between extracellular potassium accumulation and contractile failure in the ischaemic or hypoxic rabbit heart. J. Mol. Cell. Cardiol. 15, 27. 

The ventricular action potential is depicted in Fig. 6-2.2 Myocyte resting membrane potential is usually -70 to -90 mV, due to the action of the sodium-potassium adenosine triphosphatase (ATPase) pump, which maintains relatively high extracellular sodium concentrations and relatively low extracellular potassium concentrations. During each action potential cycle, the potential of the membrane increases to a threshold potential, usually -60 to -80 mV. When the membrane potential reaches this threshold, the fast sodium channels open, allowing sodium ions to rapidly enter the cell. This rapid influx of positive ions... 

The distal tubules secrete 90% to 95% of the daily dietary intake of potassium. The fractional excretion of potassium (FEk) is approximately 25% with normal kidney function.29 The GI tract excretes the remaining 5% to 10% of dietary potassium intake. Following a large potassium load, extracellular potassium is shifted intracellularly to maintain stable extracellular levels. 

Patients with acute hyperkalemia usually require other therapies to manage hyperkalemia until dialysis can be initiated. Patients who present with cardiac abnormalities caused by hyperkalemia should receive calcium gluconate or chloride (1 g intravenously) to reverse the cardiac effects. Temporary measures can be employed to shift extracellular potassium into the intracellular compartment to stabilize cellular membrane effects of excessive serum potassium levels. Such measures include the use of regular insulin (5 to 10 units intravenously) and dextrose (5% to 50% intravenously), or nebulized albuterol (10 to 20 mg). Sodium bicarbonate should not be used to shift extracellular potassium intracellularly in patients with CKD unless severe metabolic acidosis (pH less than 7.2) is present. These measures will decrease serum potassium levels within 30 to 60 minutes after treatment, but potassium must still be removed from the body. Shifting potassium to the intracellular compartment, however, decreases potassium removal by dialysis. Often, multiple dialysis sessions are required to remove potassium that is redistributed from the intracellular space back into the serum. 

In contrast to the metabotropic effects described for presynaptic kainate receptors in CA1 (90,94), the effects of kainate in CA3 appear to be mediated by direct depolarization of the presynaptic terminals. The kainate-induced facilitation is not sensitive to antagonists of other receptors (e.g., GABAb), and can be mimicked by elevating the extracellular potassium concentration (77,100). It has been proposed that the facilitation is owing to increased calcium influx that is induced by modest depolarization of the terminals by kainate receptors, whereas a strong depolarization, in response to activation of a larger receptor population, causes the sodium channels to inactivate and thereby depresses transmission (77,84,88,100-102). 

Fujikawa DG, Kim JS, Daniels AH, Alcaraz AF, Sohn TB. 1996. In vivo elevation of extracellular potassium in the rat amygdala increases extracellular glutamate and aspartate and damages neurons. Neuroscience 74(3) 695-706. 

Dofetilide blocks IKr in all myocardial tissues. It blocks open channels, and its binding and release from the channels is voltage dependent. The effects of dofetilide are exaggerated when the extracellular potassium concentration is reduced, which is important, as many patients may be receiving diuretics concurrently. Conversely, hyperkalemia decreases the effects of dofetilide, which may limit its efficacy when local hyperkalemia occurs, such as during myocardial ischemia. Dofetilide demonstrates reverse use dependence, that is, less influence on the action potential at faster heart... 

In pacemaker cells (whether normal or ectopic), spontaneous depolarization (the pacemaker potential) occurs during diastole (phase 4, Figure 14-1). This depolarization results from a gradual increase of depolarizing current through special hyperpolarization-activated ion channels (If, also called If,) in pacemaker cells. The effect of changing extracellular potassium is more complex in a pacemaker cell than it is in a nonpacemaker cell because the effect on permeability to potassium is much more important in a pacemaker (see Effects of Potassium). In a pacemaker—especially an ectopic one—the end result of an increase in extracellular potassium is usually to slow or stop the pacemaker. Conversely, hypokalemia often facilitates ectopic pacemakers. 

Elevated extracellular calcium partially antagonizes the action of local anesthetics owing to the calcium-induced increase in the surface potential on the membrane (which favors the low-affinity rested state). Conversely, increases in extracellular potassium depolarize the membrane potential and favor the inactivated state, enhancing the effect of local anesthetics. 

If seizures do occur, it is important to prevent hypoxemia and acidosis. Although administration of oxygen does not prevent seizure activity, hyperoxemia may be beneficial after onset of seizures. Hypercapnia and acidosis may lower the seizure threshold, and so hyperventilation is recommended during treatment of seizures. In addition, hyperventilation increases blood pH, which in turn lowers extracellular potassium. This action hyperpolarizes the transmembrane potential of axons, which favors the resting (or low-affinity) state of the sodium channels, resulting in decreased local anesthetic toxicity. 

However, an enhanced extracellular potassium concentration and depolarization of the fibers besides the other factors lead to a reduced sodium channel availability, to a reduced maximum depolarization velocity, shortened action potentials and to a slowing of conduction. These changes result in an alteration in the activation patterns [Dhein et al., 1994] and an increase in dispersion of action potential duration, which is even more pronounced in the presence of neutrophilic leukocytes [Dhein et al., 1995a],... 

Coronel R Distribution of Extracellular Potassium during Acute Myocardial Ischemia thesis, Amsterdam,... 

Longuemare, M. C., and Swanson, R. A. (1997). Net glutamate release from astrocytes is not induced by extracellular potassium concentrations attainable in brain. J. Neurockem. 69, 879-882. 

Of greater therapeutic relevance is the zone lying peripheral to the region of dense ischemia and perfused at somewhat higher CBF levels the ischemic penumbra. In baboons subjected to MCA occlusion, CBF was measured along with the extracellular potassium concentration and sensory evoked poten-... 

Branston NM, Hope DT, Symon L (1979) Barbiturates in focal ischemia of primate cortex effects on blood flow distribution, evoked potential and extracellular potassium. Stroke 10 647-653... 

Branston NM, Strong AJ, Symon L (1977) Extracellular potassium activity, evoked potential and tissue blood flow. Relationships during progressive ischaemia of baboon cerebral cortex. J Neurol Sci 32 305-321... 

Sick T. J., Tang R., and Perez-Pinzon M. A. (1999) Cerebral blood flow does not mediate the effect of brain temperature on recovery of extracellular potassium ion activity after transient focal ischemia in the rat. Brain Res. 821,400-406. 

While there has been considerable interest in the ionic changes that occur during focal ischemia, little attention has been paid to disturbances associate with reperfusion. Most earlier investigations, for example, have shown that extracellular potassium ion activity recovers to or near preischemic levels on reperfusion (29,37), suggesting normalization of potassium ion homeostasis. We have recently shown, however, that focal ischemia is accompanied by early secondary elevation of extracellular potassium ion activity that is dependent on brain temperature but not cerebral blood flow (38). 

Takahashi H., Manaka S., and Sano K. (1981) Changes in extracellular potassium concentration in cortex and brain stem during the acute phase of experimental closed head injury. J. Neurosurg. 55,708-717. 

Katayama Y., Becker D. P., TamuraT., andHovda D. A. (1990) Massive increases in extracellular potassium and the indiscriminate release of glutamate following concussive brain injury. J. Neurosurg. 73, 889-900. 

Astrup J., Skovsted P., Gjerris F., and Sorensen H. R. (1981) Increase in extracellular potassium in the brain during circulatory arrest effects of hypothermia, lidocaine, and thiopental. Anesthesiology 55, 256-262. 

Lantos J., Temes G., andTorokB. (1986) Changes during ischaemia in extracellular potassium ion concentration of the brain under nitrous oxide or hexobarbital-sodium anaesthesia and moderate hypothermia. Acta Physiol. Hung. 67,141-153. 

Gido G., Kristian T., and Siesjo B. K. (1997) Extracellular potassium in a neocor-tical core area after transient focal ischemia. Stroke 28, 206-210. 

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