The Quantitative Estiniation of Mechanical Haeniolysis for Clinical Application

Schubothe, H.; Fok, Ferdinand Po‐Tun

doi:10.1111/j.1365-2141.1960.tb06252.x

Cited by 30 publications

(7 citation statements)

References 9 publications

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“…We have shown that irrespective of red cell type, an increased exposure to mechanical stress leads to enhanced lysis, as observed previously (63). As expected, normal cell lysis occurred similarly in the presence or absence of oxygen, confirming that AA cells remain unchanged when alterations in oxygen tension take place.…”

Section: Discussionsupporting

confidence: 89%

“…DC is a numerical representation of red cell deformability, defined by: DC = L/W; where the DC increases as the red cell deformablity increases (61, 62). The flow rates were correlated to the amount of shear stress and plotted with respect to the deformability constant [63]. The data are an average of several trials taken from three different blood samples from three separate donors.…”

Section: Methodsmentioning

confidence: 99%

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Effects of a Single Sickling Event on the Mechanical Fragility of Sickle Cell Trait Erythrocytes

et al. 2010

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Hemolysis contributes to the pathology associated with sickle cell disease. However, the mechanism of hemolysis or relative contribution of sickling due to hemoglobin polymerization vs. oxidative damage remains unknown. Earlier studies aimed at deciphering the relative importance of these two mechanisms have been complicated by the fact that sickle red cells (SS) have already been affected by multiple rounds of sickling and oxidative damage before they are collected. In our study, we examine the mechanical fragility of sickle cell trait cells, which do not sickle in vivo, but can be made to do so in vitro. Thus, our novel approach explores the effects of sickle hemoglobin polymerization on cells that have never been sickled before. We find that the mechanical fragility of these cells increases dramatically after a single sickling event, suggesting that a substantial amount of hemolysis in vivo probably occurs in polymer-containing cells.

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Section: Discussionsupporting

confidence: 89%

Section: Methodsmentioning

confidence: 99%

Effects of a Single Sickling Event on the Mechanical Fragility of Sickle Cell Trait Erythrocytes

et al. 2010

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“…Although the MF test bears the closest physiological resemblance of all currently available in vitro models to red cell fragmentation in vivo [17,19,26], MF has been neglected as a tool for investigating the mechanisms responsible for breakage of normal and G-6-PD deficient erythrocytes. The more popular osmotic fragility test was also employed in our previous studies [8,9] but failed to reveal effects of the model drug metabolites.…”

Section: Discussionmentioning

confidence: 99%

“…Since erythrocytes are nearly always under isosmotic conditions in the circulation, osmotic fragility does not seem to represent a good in vitro model for hemolytic phenomena in vivo. MF appears to be a much better in vitro model of the physical stresses to which the erythro cyte is subject in vivo and offers a more relevant index of membrane damage [7,19].…”

Section: Discussionmentioning

confidence: 99%

Alterations in Normal and G-6-PD Deficient Human Erythrocytes of Various Ages after Exposure to Metabolites of Hemolytic Drugs

Fraser¹,

Tilton²,

Vesell³

1971

Pharmacology

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Since in vivo studies indicate that older erythro cytes hemolyze preferentially in drug-induced hemolysis, differential centrifugation was used to separate young and old normal and G-6-PD deficient erythrocytes. Older cells were identified by their lower level of G-6-PD activity; in corporation of ⁵⁹Fe into erythrocytes confirmed this division of cells by age. Mechanical fragility (MF) of old cells was greater than that of young cells. Effects of 8-amino-5,6-quino linediol (AQD) (a possible primaquine metabolite) and of 2-hydroxyphenetidine (HP) (a phenacetin metabolite) on hemolysis, MF and reduced glutathione (GSH) and methemoglobin content were examined in vitro. AQD (2.5 × 10^–4 m) did not produce hemolysis but selectively increased MF of old G-6-PD deficient cells. HP (5 × 10^–4 m) produced considerable hemolysis of both normal and G-6-PD deficient cells with a selective effect in old G-6-PD deficient cells. HP also selectively increased the MF of old G-6-PD deficient cells. Incubation with AQDor HP depleted GSH content more in old than in young G-6-PD deficient cells. This depletion of GSH was followed by increased MF of old G-6-PD deficient cells. Hemolysis of normal cells occurred without GSH depletion but was accompanied by GSH depletion in G-6-PD deficient cells. Smaller differences in methemoglobin formation occurred but were not well correlated with hemolysis or increased MF. Although not applicable as a routine diagnostic test in the clinical laboratory, increased MF in vitro of old G-6-PD deficient erythrocytes is suggested as a useful research tool in assessing the potential of drugs or drug metabolites to cause hemolysis in vivo, particularly in combination with parallel studies of glutathione depletion.

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“…Resistenzprüfungen, a) Mechanische Resistenz nach Schubothe [14]; b) osmotische Resistenz gegen 0,10-0,85 g% Kochsalzlösungen, gemessen 30 min nach Inkubation bei Z im m ertem peratur; c) Spontanhäm olysc im Serum der P roben (Extinktionsm essung bei X -546 nm, D = 10 mm, gegen mitinkubiertes Leerserum).…”

Section: F G Räm Lich Und F K Ir C H H O Ffunclassified

Der Einfluß dysproteinämischer Seren auf die Resistenz normaler Erythrozyten

Gramlich¹,

Kirchhoff²

1969

Acta Haematol

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The Quantitative Estiniation of Mechanical Haeniolysis for Clinical Application

Cited by 30 publications

References 9 publications

Effects of a Single Sickling Event on the Mechanical Fragility of Sickle Cell Trait Erythrocytes

Effects of a Single Sickling Event on the Mechanical Fragility of Sickle Cell Trait Erythrocytes

Alterations in Normal and G-6-PD Deficient Human Erythrocytes of Various Ages after Exposure to Metabolites of Hemolytic Drugs

Der Einfluß dysproteinämischer Seren auf die Resistenz normaler Erythrozyten

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