Regulation of Cellular Volume

Macknight, Anthony D. C.; Leaf, Alexander

doi:10.1007/978-1-4613-3958-8_17

Cited by 64 publications

(80 citation statements)

References 116 publications

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“…As far as in vitro studies are concerned, Na + ,K + -ATPase activity in brain slices or synaptosomes is inhibited by lipid peroxidation (Sun, 1972;Kovachichi andMishra, 1980, 1981), and this is in line with the concept that dysfunction of Na + ,K + -ATPase leads to cellular swelling (MacKnight and Leaf, 1977). Chan and Fishman have shown that the addition of PUFAs in incubation medium of rat brain slices enhances edema formation (1978), increases generation of OZ and TBAR (1980), and decreases the activity of Na + ,K + -ATPase, as well as the uptake of GABA and amino acids (Chan et al, 1983a).…”

Section: Disparity Between Results Obtained In Vitro and In Vivosupporting

confidence: 57%

“…The increased hydroperoxides activate Na + ,K + -ATPase of brain microvessels through stimulation of the lipoxygenase pathway. Since the ratio of sodium to potassium exchanged is >1 (Skou, 1965), the sodium influx calls for the influx of its anionic counterpart, namely C1 -, which also results in the increased influx of water (MacKnight and Leaf, 1977;Siesjo, 1985). It should be emphasized that our paradigm is not in opposition to recently demonstrated ion exchange systems in neuronal and glial cell membranes.…”

Section: Proposed Hypothesis Regarding the Pathogenetic Mechanism Of mentioning

confidence: 86%

“…From a morphological point of view, brain edema owing to focal ischemia begins as a cytotoxic type and is followed by vasogenic edema (Katzman et al, 1977). Since glial swelling occurs vis -avis the alterations of extra-and intracellular ion concentrations, especially of potassium and sodium, its occurrence has been attributed to altered functions of ion exchange mechanisms such as Na', K+-ATPase and Na+/H+ antiporter (MacKnight and Leaf, 1977;Hertz, 1981;Kimelberg and Bourke, 1984;Siesjo, 1985). Recently, it has been suggested that acidosis disrupts volume regulation in glial cells by leading to grossly enhanced Na+/H+ exchange accompanied by Cl -/HCO3 -exchange (Siesjo, 1985;Kempski et al, 1988).…”

Section: The Role Of Sodium In Edema Formationmentioning

confidence: 99%

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The role of free radicals and eicosanoids in the pathogenetic mechanism underlying ischemic brain edema

Asano

Koide

Gotoh

et al. 1989

Molecular and Chemical Neuropathology

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Results of our consecutive study on the pathogenic mechanism underlying ischemic brain edema are summarized in this paper. Pertinent findings are as follows: (1) there is a close correlation between the influxes of water and sodium following ischemia; (2) the edema fluid can be regarded as the ultrafiltrate of serum; (3) there is a significant increase in the brain content of HETEs following ischemia; (4) the lipoxygenase activity of brain microvessels is increased following ischemia; (5) the lipoxygenase activity as well as the Na+, K+-ATPase activity of brain microvessels are enhanced by a hydroperoxide, 15-HPETE; (6) inhibition of Na+, K+-ATPase of brain microvessels by intraarterial infusion of ouabain resulted in a significant decrease in edema formation; and (7) not the cyclooxygenase, but the lipoxygenase pathway seems to be involved in the enhancement of microvessel Na+, K+-ATPase. Lipoxygenase(s) and Na+-K+-ATPase of brain microvessels, the activities of which are enhanced by an increased level of free radicals and/or hydroperoxides, may play a significant role in the occurrence of ischemic brain edema.

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Section: Disparity Between Results Obtained In Vitro and In Vivosupporting

confidence: 57%

Section: Proposed Hypothesis Regarding the Pathogenetic Mechanism Of mentioning

confidence: 86%

Section: The Role Of Sodium In Edema Formationmentioning

confidence: 99%

See 1 more Smart Citation

The role of free radicals and eicosanoids in the pathogenetic mechanism underlying ischemic brain edema

Asano

Koide

Gotoh

et al. 1989

Molecular and Chemical Neuropathology

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“…Net ion movement is, however, dependent upon the net cation gradient; therefore, under certain circumstances, diuretic-sensitive net salt loss, and thus cell shrinkage, may be observed [24,38]. This behavior of the "cotransport" system may explain earlier observations of cell volume regulation via cardiac-glycoside insensitive "Na pumps" [34]. Direct measurement of the volume sensitivity of outward furosemide-sensitive Na + + K + "cotransport" into Na +-and K+-free media in human red cells, however, has failed to show a volume dependence, other than an uncoupling of Na + from furosemide-sensitive K + efflux [1].…”

Section: Introductionmentioning

confidence: 53%

Role of passive potassium fluxes in cell volume regulation in cultured HeLa cells

1985

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Cultured HeLa cells behave as ideal osmometers when subjected to hyperosmolar media, and show no volume regulatory behavior. In hypoosmolar solutions, cell swelling is not as great as predicted, and this is due largely to a loss of intracellular KCl. In hyperosmolar solutions there is a stimulation of the ouabain-insensitive but loop diuretic-sensitive 86Rb+ (K+) pathway. Analysis of the K+, Na+ and Cl- dependency of this K+ flux pathway demonstrates that the increase is principally due to an increase in its maximal velocity (Vmax). The sensitivity of this pathway to diuretic inhibition is unchanged in hyperosmolar media. Diuretic-sensitive 86Rb+ (K+) efflux stimulated by hypertonicity shows no marked dependence on external K+. The K+ loss observed in hypoosmolar media is distinct from the K+ transport pathway stimulated by hyperosmolar media on the basis of its sensitivity to furosemide and anion dependence.

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“…1). Dies erklärt, warum jedes Energiedefizit -sei es durch Sauerstoff (O 2 ) oder Substratmangel be dingt -über eine gedrosselte Pumpaktivi tät letztlich ein Zellödem hervorruft [26]. Eine Abkühlung vermag, indem sie den Energiebedarf reduziert und damit die Diskrepanz zu einem verminderten An gebot minimiert, eine hypoxischischä mische Zellschädigung zu verzögern oder zu verhindern.…”

Section: Metabolische Grundbedingungen Des Zellulären Lebensunclassified

Warum 37°C?

Singer

2007

Anaesthesist

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Homeothermy is the result of an evolutionary process during which every increase in oxygen supply led to a consecutive increase in metabolic rate and, thus, to a new dependence on favorable ambient conditions. In response to the food scarcity of winter months, some inhabitants of temperate zones developed an ability to hibernate which is characterized by a fully thermocontrolled reduction in body temperature down to near zero values. Hibernation thus illustrates that in homeotherms, not only the body shell is poikilothermic, but also the core temperature is more variable than often assumed. However, in contrast to clinical hypothermia, natural torpidity does not consist of a cold-induced reduction in metabolic rate, but of an endogenous metabolic reduction with subsequent lowering of body temperature. As a factor of metabolic suppression, the pH has been suspected which, in hibernators, is kept constant at 7.4 by relative hypoventilation (pH-stat) which differs from its passive shift in the poikilothermic body shell (alpha-stat). In clinical hypothermia, temperature governs the metabolic rate in that, depending on the state of thermoregulation, either a cold defense reaction with an increased metabolic rate (accidental hypothermia) or a cold-induced reduction in metabolic rate (induced hypothermia) occurs. However, as can be learned from hibernators, the lower limit of hypothermia tolerance seems to be due to a uniform minimal metabolic rate rather than to the species-specific body temperature at which this metabolic limit is reached, depending on body size and basal metabolic rate. Accordingly, in judging the sequelae of hypothermia, the degree of cooling should be given less emphasis than the resulting effects on metabolic rate.

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Regulation of Cellular Volume

Cited by 64 publications

References 116 publications

The role of free radicals and eicosanoids in the pathogenetic mechanism underlying ischemic brain edema

The role of free radicals and eicosanoids in the pathogenetic mechanism underlying ischemic brain edema

Role of passive potassium fluxes in cell volume regulation in cultured HeLa cells

Warum 37°C?

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