A Study In Vitro of the Sodium Pump in Fulminant Hepatic Failure

Alam, A. N.; Poston, Lucilla; Wilkinson, Stephen; Golindano, C; Williams, Roger

doi:10.1042/cs0550355

Cited by 13 publications

(6 citation statements)

References 23 publications

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“…None of the sera tested caused leakage of 3H-labelled metabolites from prelabelled human leucocytes; addition of Sendai virus resulted in leakage. It is likely that the ion changes caused by hepatitis serum are due to a faulty Na++K+-stimulated ATPase (Alam et al, 1978), and these results therefore demonstrate that, just as Sendai-virus-mediated permeability changes do not affect the Na+ + K+-stimulated ATPase (Poste & Pasternak, 1978), so a faulty Na++K+stimulated ATPase does not necessarily result in a permeability change.…”

Section: Survey Ofviruses and Cell Typesmentioning

confidence: 69%

Survey of virally mediated permeability changes

Foster¹,

Gill²,

Micklem³

et al. 1980

Biochemical Journal

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1. Sendai virus causes permeability changes when added to freshly isolated brain cells (cerebellum or ependymal cells) or to a culture of forebrain cells. 2. Sendai virus causes permeability changes when added to organ cultures of ferret lung or nasal turbinate. Influenza virus causes no permeability changes under these conditions. 3. Rabies virus and vesicular-stomatitis virus, in contrast with Sendai virus, do not cause permeability changes in BHK cells or Lettrée cells. 4. Serum from patients suffering from viral hepatitis does not cause permeability changes in human leucocytes; addition to Sendai virus causes permeability changes. 5. It is concluded that permeability changes accompanying viral entry occur only with certain types of paramyxovirus, but that there is little restriction on cell type. 6. MDBK cells infected with Sendai virus show permeability changes during viral release, similar to those that occur during viral entry. Because these changes do not appear to be restricted to paramyxoviruses, they may have considerable clinical significance.

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Section: Survey Ofviruses and Cell Typesmentioning

confidence: 69%

Survey of virally mediated permeability changes

Foster¹,

Gill²,

Micklem³

et al. 1980

Biochemical Journal

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“…The inter-assay coefficients of variation for sodium and potassium were 10% and 5%, respectively. This method yields lower values for intracellular Na+ content (mean f SD in normals, 27.8 f 9.5, range 15.9 to 47.8, mmol/kg dry weight) than methods using cells immediately after dextran sedimentation and without reincubation in TC199 for 30 min at 37°C (e.g., Alam et al, 1978;Sewell et al, 1981) for the following reasons. Sedimentation at room temperature decreases Na+ efflux while leaving passive influx unreduced, so that intracellular Na+ content is falsely raised.…”

Section: Intracellular Electrolytesmentioning

confidence: 99%

The Human Leucocyte Sodium Pump in Cushing's Syndrome

Evans

Burke

1988

Clinical Endocrinology

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Because corticosteroids have important effects on sodium homeostasis, we studied leucocyte 22Na efflux in patients with Cushing's syndrome. The ouabain-sensitive 22Na+ efflux rate constant was raised in Cushing's syndrome (mean +/- SD 2.84 +/- 0.32 vs 2.35 +/- 0.53/h, P less than 0.001, n = 15). This efflux rate constant correlated with the urinary free cortisol (rs = 0.61, P less than 0.02), but less significantly with the 0900 h plasma cortisol (rs = 0.46, P less than 0.08). There was no correlation with the supine plasma aldosterone. Intracellular sodium content was significantly lower in Cushing's syndrome (21.1 +/- 4.6 vs 27.8 +/- 9.5 mmol/kg dry weight, P less than 0.01), with a raised intracellular potassium to sodium content ratio (16.1 +/- 3.3 vs 12.9 +/- 3.6, P less than 0.01). After treatment of the Cushing's syndrome by trans-sphenoidal adenomectomy or adrenalectomy, these defects in cellular sodium balance were corrected. Thus, the distribution of sodium between intra- and extracellular fluid may be affected by adrenal corticosteroids via an action on the sodium pump.

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“…Among the toxins accumulating in the circulation of patients with fulminant hepatic failure (FHF) are substances which inhibit leucocyte ouabain-sensitive sodium transport (1). This leads to a high intracellular sodium content (2), and similar impairment of the cell membrane sodium pump in brain cells, as a result of inhibition of Na+,K+-ATPase activity, could be an important factor in the development of cerebral edema.…”

mentioning

confidence: 99%

Inhibition of Rat Brain Na+,K+−ATPase Activity by Serum from Patients with Fulminant Hepatic Failure†

Seda¹,

Hughes²,

Gove³

et al. 1984

Hepatology

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Among the toxins accumulating in the circulation of patients with fulminant hepatic failure (FHF) are substances which inhibit leucocyte ouabain-sensitive sodium transport. A similar inhibition of brain Na+,K+-ATPase could lead to both coma and cerebral edema found in these patients which are associated with high mortality. In this study, we have investigated the effect of sera from FHF on normal rat brain Na+,K+-ATPase activity in vitro. Serum from patients with FHF significantly decreased the ouabain-sensitive Na+,K+-ATPase activity (13.58 +/- S.D. 2.60 mumoles Pi mg protein-1 hr-1) in the rat brain membrane preparation in vitro as compared to normal serum (20.33 +/- 3.24 mumoles Pi mg protein-1 hr-1, p less than 0.001). A final serum dilution of 1 in 40 was required to abolish the inhibition of Na+,K+-ATPase activity. Cerebrospinal fluid obtained at postmortem from FHF patients also contained the inhibitory substances. Serum from patients in coma due to decompensated chronic liver disease inhibited the Na+,K+-ATPase activity (17.25 +/- 1.37 mumoles Pi mg protein-1 hr-1), but this was less marked than with FHF serum. Hence, the inhibition of brain Na+,K+-ATPase by substances accumulating in the serum in FHF may be important in the pathogenesis of hepatic coma.

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A Study In Vitro of the Sodium Pump in Fulminant Hepatic Failure

Cited by 13 publications

References 23 publications

Survey of virally mediated permeability changes

Survey of virally mediated permeability changes

The Human Leucocyte Sodium Pump in Cushing's Syndrome

Inhibition of Rat Brain Na+,K+−ATPase Activity by Serum from Patients with Fulminant Hepatic Failure†

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