The role of extracellular potassium transport in computer models of the ischemic zone

2007 ◽  
Vol 45 (12) ◽  
pp. 1187-1199 ◽  
Author(s):  
Mark Potse ◽  
Ruben Coronel ◽  
A.-Robert LeBlanc ◽  
Alain Vinet
Author(s):  
Maxwell Deutscher

Memory is central to every way in which we deal with things. One might subsume memory under the category of intellect, since it is our capacity to retain what we sense, enjoy and suffer, and thus to become knowing in our perception and other activities. As intelligent retention, memory cannot be distinguished from our acquisition of skills, habits and customs – our capabilities both for prudence and for deliberate risk. As retention, memory is a vital condition of the formation of language. Amnesia illustrates dramatically the difference between memory as retention of language and skills, and memory as the power to recollect and to recognize specific events and situations. In amnesia we lose, not our general power of retention, but rather our recall of facts – the prior events of our life, and our power to recognize people and places. Amnesiacs recognize kinds of things. They may know it is a wristwatch they are wearing, while unable to recognize it as their own. This recall of events and facts that enables us to recognize things as our own, is more than just the ability to give correctly an account of them. One might accurately describe some part of one’s past inadvertently, or after hypnosis, or by relying on incidental information. Thus, present research on memory both as retention and as recall of specific episodes, attempts to describe the connection which persists between experience and recall. Neurological or computer models of such a connection owe something to traditional notions of a memory trace, but emphasize also the re-tracing of original memories by later experience and episodes of recall. Historically, recollection has often been thought of as a mode of perceiving the past. Such an idea lends an exaggerated status to the role of imagery, which is but one member of a family of recollective activities that includes reliving, remembering, reminiscing and mulling over what has happened. It may be not in having imagery but in miming someone’s behaviour that one relives an event. Also, like imagery, what we feel about the past may seem integral to recollection. A sense of being brought close to the past arises particularly when events that involve our feelings are concerned. Yet we may also recollect an event, vividly and accurately, while feeling clinically detached from it, devoid of imagery. How a past event or situation remains connected with subsequent recollection has become a principal theoretical question about memory. It is argued that it is because of what we did or experienced that we recollect it. Otherwise, we are only imagining it or relying upon ancillary information. Neurological or computer models of such a connection owe something to traditional notions of a memory trace, but emphasize also the re-tracing of original memories by later experience and episodes of recall. Some argue that our very idea of memory is that of the retention of a structural analogue of what we do recall of them. Such an idea is not of some perfect harmony between what we remember and our recollection of it. Rather, it is suggested, only to the extent that we retain a structural analogue of some aspect of an event or situation do we remember, rather than imagine or infer it.


1986 ◽  
Vol 251 (2) ◽  
pp. F199-F207
Author(s):  
S. K. Mujais ◽  
M. A. Chekal ◽  
J. P. Hayslett ◽  
A. I. Katz

The purpose of this study was to characterize the alterations in collecting tubule Na+-K+-ATPase activity produced by sustained increments in dietary potassium in the rat and to evaluate the role of aldosterone in their generation. In adrenal-intact animals, feeding a high-potassium diet (10-fold that of control) or administration of a high physiological dose of aldosterone (5 micrograms X 100 g-1 X day-1), which simulates the delivery rate of this hormone during potassium loading (both for 7 days), caused marked increments in Na+-K+-ATPase activity in the cortical collecting tubule (CCT) but had no effect on the enzyme in the inner stripe of the medullary collecting tubule (MCT). A significant increase in enzyme activity was also observed after smaller dietary potassium increments (2.5 and 5 times the control) and after 4 (but not 2) days of dietary potassium load. In adrenalectomized rats provided with physiological replacement doses of corticosterone and aldosterone (0.8 micrograms X 100 g-1 X day-1), Na+-K+-ATPase activity in both CCT and MCT was similar to that of adrenal-intact controls but remained unchanged after 7 days on the potassium-enriched (10-fold) diet. In contrast, adrenalectomized animals receiving the high physiological dose of aldosterone displayed an increase in Na+-K+-ATPase activity of CCT comparable with that of adrenal-intact animals, whereas the enzyme activity in the MCT was unaffected. In conclusion, 1) following chronic potassium loading Na+-K+-ATPase activity increases significantly in the CCT with no change in its activity in the inner stripe of the MCT.(ABSTRACT TRUNCATED AT 250 WORDS)


1989 ◽  
Vol 23 (11) ◽  
pp. 1402-1408 ◽  
Author(s):  
Marnie L. Ceazan ◽  
E. Michael Thurman ◽  
Richard L. Smith

1989 ◽  
Vol 257 (1) ◽  
pp. H226-H237 ◽  
Author(s):  
H. Satoh ◽  
M. Vassalle

Caffeine-norepinephrine interactions were studied in canine cardiac Purkinje fibers perfused in vitro. Caffeine (0.5-1 mM) or theophylline (0.5-1 mM) increased and then decreased contractile force in the absence and presence of 0.5-10 microM norepinephrine (NE) [in high extracellular calcium concentration ([Ca]o) caffeine only decreases force]. Occasionally, caffeine only decreased force in the presence of NE. In the presence of NE and 12 mM (sometimes even 4 mM) extracellular potassium concentration, caffeine did not decrease force below the precaffeine level. Reciprocally, in 0.5-2 mM caffeine NE increased force, although less than in the absence of caffeine. Even in 9 mM caffeine, NE increased force but slowed the final phase three repolarization of the action potential. Both NE and 8.1 mM [Ca]o increased force, but NE decreased force in the presence of high [Ca]o. In NE and propranolol (or propranolol alone), caffeine only increased force, whereas it had the usual effects in the presence of methoxamine or phenotolamine. In the presence of iodoacetic acid and 2-deoxy-D-glucose, NE caused contracture and caffeine exaggerated it. In contrast, in NE and 2 mM Mn, caffeine only increased force. It is concluded that initially NE diminishes the cytoplasmic calcium overload induced by caffeine (by promoting Ca uptake into the sarcoplasmic reticulum) and subsequently enhances it (by increasing the slow inward current).


1979 ◽  
Vol 1 (1) ◽  
pp. 39-49 ◽  
Author(s):  
Isao Hashimoto ◽  
Shinya Manaka ◽  
Keiji Sano

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