Some Aspects of Cell Permeability to Weak Electrolytes

Jacobs, M. H.

doi:10.1101/sqb.1940.008.01.005

Cited by 209 publications

(68 citation statements)

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“…However, a weakness of this proposed acid-base model for ischemic brain is that it did not specifically deal with the behavior of nonionized acid molecules (Boris-Moller et aI., 1988). Since such acid molecules rapidly diffuse through cell membranes (Jacobs, 1940), one might expect astrocytic acidosis to dissipate rapidly as un charged lactic acid molecules diffuse out of cells. That acid remains elevated within astrocytes 46 min after the onset of ischemia (Fig.…”

Section: Astrocytic Phi Behavior During Ischemiamentioning

confidence: 99%

Astrocytic Acidosis in Hyperglycemic and Complete Ischemia

Kraig

Chesler

1990

J Cereb Blood Flow Metab

161

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Summary: Nearly complete brain ischemia under normo glycemic conditions results in death of only selectively vulnerable neurons. With prior elevation of brain glucose, such injury is enhanced to include pancel1ular necrosis (i.e., infarction), perhaps because an associated, severe lactic acidosis preferentially injures astrocytes. However, no direct physiologic measurements exist to support this hypothesis. Therefore, we used microelectrodes to mea sure intracellular pH and passive electrical properties of cortical astrocytes as a first approach to characterizing the physiologic behavior of these cel1s during hypergly cemic and complete ischemia, conditions that produce infarction in reperfused brain. Anesthesized rats (n = 26) were made extremely hyperglycemic (blood glucose, 51.4 ± 2.8 mM) so as to create potentially the most extreme acidic conditions possible; then ischemia was induced by cardiac arrest. Two loci more acidic than the interstitial space (6.17-6.20 pH) were found. The more acidic locus [4.30 ± 0.19 (n = 5); range: 3.82-4.89] was occasional1y seen at the onset of anoxic depolarization, 3-7 min after Excessive brain acidosis is thought to be required for infarction from nearly complete ischemia under hyperglycemic conditions (Myers and Yamaguchi, 1fJ77; Ginsberg et aI., 1980; Welsh et aI., 1980; Ka limo et aI., 1981; Rehncrona et aI., 1981; Pulsinelli et aI., 1982). However, the cellular and physiological bases for such injury remain incompletely defined. Abbreviations used: HA, neutral lactic acid; HRP, horseradish peroxidase; NMR, nuclear magnetic resonance; pHj, intracellu lar pH; pHo' interstitial pH. 104cardiac arrest. The less acidic locus [5.30 ± 0.07 (n = 53); range 4.46-5.93)] was seen 5-46 min after cardiac arrest. A smal1 negative change in DC potential [8 ± 1 m V (n = 5); range -3 to -12 mV and 7 ± 2 mV (n = 53); range + 3 to -31 m V , respectively] was always seen upon im palement of acidic loci, suggesting cellular penetration. In a separate group of five animals, electrical characteristics of these cells were specifically measured (n = 17): mem brane potential was -12 ± 0.2 m V (range -3 to -24 mY), input resistance was 114 ± 16 Mil (range 25-250 Mil), and time constant was 4.4 ± 0.4 ms (range 3.0-7.9 ms). Injection of horseradish peroxidase into cells from either animal group uniformly stained degenerating astro cytes. These findings establish previously unrecognized properties of ischemic astrocytes that may be prerequi sites for infarction from nearly complete ischemia: the capacity to develop profound cellular acidosis and a con comitant reduction in cel1 membrane ion permeability.

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Section: Astrocytic Phi Behavior During Ischemiamentioning

confidence: 99%

Astrocytic Acidosis in Hyperglycemic and Complete Ischemia

Kraig

Chesler

1990

J Cereb Blood Flow Metab

161

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“…The effect of external ammonium ions and ammonia Like C02, ammonia has long been known to penetrate cell membranes relatively easily (Jacobs, 1940). Like C02, it reacts with water, but instead of yielding hydrogen ions it in effect takes them up to produce ammonium ions.…”

Section: W1rimentioning

confidence: 99%

Intracellular pH of snail neurones measured with a new pH‐sensitive glass micro‐electrode

Thomas¹

1974

The Journal of Physiology

341

186

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SUMMARY1. The construction and properties of a new design of pH-sensitive micro-electrode are described. The electrodes are very durable, and have a recessed configuration so that only the extreme tip, which can be as small as 1 ,um in diameter, needs to enter the cell.2. The average intracellular pH in thirty-two snail neurones was 7x4. This was not in accord with a passive distribution of H+ ions across the cell membrane.3. Changing membrane potential or external pH had only slow effects on internal pH.4. Removing external K had no effect, and removing external Na had only slow and variable effects on intracellular pH.5. Anoxia, azide and DNP all caused a slow fall in internal pH. 6. External CO2 caused large and rapid decreases in internal pH, which external bicarbonate appeared to offset slowly. Injected bicarbonate increased internal pH.7. The size of the pH changes caused by CO2 suggested a minimum intracellular buffering power of 25 m-equiv H+/unit pH per 1., equivalent to that of 150 mm Tris maleate, pH 7*4. 8. External ammonia caused a large and rapid increase in internal pH, while the injection of ammonium ions had the opposite effect.

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“…On the other hand, cattle and human erythrocytes are less permeable to erythritol (the times for '75% haemolysis' in isosmotic erythritol solution being about 8 hr and 2 hr, respectively) and are only 'slightly permeable' to adonitol and mannitol (Davson & Danielli, 1952 (Jacobs, 1940;Davson, 1960). This is considered to be the reason why red cells undergo swelling and subsequent lysis in isosmotic ammonium salt solutions of these anions, whereas other cells investigated seem to be no more permeable to the ions of the ammonium salts than they are to the corresponding salts of Na+ and K+ Jacobs, 1940 (Jacobs, 1940) (Hägg, 1964). Thus, in a solution of NH4F at physiological pH there will be a significant concentration of undissociated HF.…”

Section: Sperm Modelsmentioning

confidence: 99%