Dextran and its Use as a Plasmasubstitute.

Ingelman, Björn; Laakso, Perttu V.; Oxaal, F.R.; Linnasalmi, Annikki; Laukkanen, Pentti

doi:10.3891/acta.chem.scand.01-0731

Cited by 24 publications

(5 citation statements)

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“…Dextrans were introduced as plasma volume expanders in 1947 (Granwall & Ingelman 1945;Bohmansson et a/. 1946;Ingelman 1947). They have later been widely used for the improvement of microcirculation and in the prophylaxis of thrombosis (Gruber 1969; Ingelman e t a / .…”

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confidence: 99%

Dextran‐Induced Anaphylactoid Reaction in Man: Altered Reactivity of High Molecular Weight Kininogen

Briseid

1980

Acta Pharmacologica et Toxicologica

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Normal levels of factor XI1 and of high and low molecular weight kininogens (HMWK and LMWK) were registered in plasma specimens from 5 individuals who had developed anaphylactoid reactions upon injection of dextran during surgery (dextran reactors, DR). Factor XI1 was assayed as prekallikrein activator (PKA) activated with kaolin at 0 ' . and kininogen fractions were estimated through the release of kinin caused by plasma kallikrein or hog pancreas kallikrein (HPK). Subnormal levels of factor XI1 apparently present in plasma from one DR, and after affinity chromatography on a lysine-Sepharose column also in plasma from another DR, were normalized by addition of plasma deficient in factor XI1 or by addition of purified HMWK.Treatment of plasma from DR with acetone ( 2 5 % v/v) induced a conversion of HMWK into a state which was non-functional as a cofactor in the surface-dependent activation of factor XII, and the passage of plasma from DR through a lysine-Sepharose column altered the HMWK present to a substance that released kinin only very slowly by incubation with HPK. It is concluded that the treatments mentioned will favour the activation in plasma from DR of a factor that will cause the conversion of HMWK. Previous experiments with rat plasma demonstrated that plasmin and also a plasmin-like factor without affinity for lysine-Sepharose were able to destroy the capacity of HMWK to function as a cofactor in the surface-dependent activation of factor XII, without a corresponding release of kinin.

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confidence: 99%

Dextran‐Induced Anaphylactoid Reaction in Man: Altered Reactivity of High Molecular Weight Kininogen

Briseid

1980

Acta Pharmacologica et Toxicologica

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“…Dextran is a hydrophilic, nonionic molecule with adjustable molecular mass distribution (Figure 2) and viscosity/density in solutions. Dextran’s lack (or near lack) of toxic effects, pyrogenic or allergic reactions and accumulation in the body; its thermal and chemical stability allowing sterilization and obtaining the derivatives; its applicability in mass production at comparably low costs (82, 192): all make dextran an appealing biopolymer for multiple applications.…”

Section: Discussionmentioning

confidence: 99%

Targeting the C-type Lectins-Mediated Host-Pathogen Interactions with Dextran

2014

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Dextran, the α-1,6-linked glucose polymer widely used in biology and medicine, promises new applications. Linear dextran applied as a blood plasma substitute demonstrates a high rate of biocompatibility. Dextran is present in foods, drugs, and vaccines and in most cases is applied as a biologically inert substance. In this review we analyze dextran’s cellular uptake principles, receptor specificity and, therefore, its ability to interfere with pathogen–lectin interactions: a promising basis for new antimicrobial strategies. Dextran-binding receptors in humans include the DC-SIGN (dendritic cell–specific intercellular adhesion molecule 3-grabbing nonintegrin) family receptors: DC-SIGN (CD209) and L-SIGN (the liver and lymphatic endothelium homologue of DC-SIGN), the mannose receptor (CD206), and langerin. These receptors take part in the uptake of pathogens by dendritic cells and macrophages and may also participate in the modulation of immune responses, mostly shown to be beneficial for pathogens per se rather than host(s). It is logical to predict that owing to receptor-specific interactions, dextran or its derivatives can interfere with these immune responses and improve infection outcome. Recent data support this hypothesis. We consider dextran a promising molecule for the development of lectin–glycan interaction-blocking molecules (such as DC-SIGN inhibitors) that could be applied in the treatment of diseases including tuberculosis, influenza, hepatitis B and C, human immunodeficiency virus infection and AIDS, etc. Dextran derivatives indeed change the pathology of infections dependent on DC-SIGN and mannose receptors. Complete knowledge of specific dextran–lectin interactions may also be important for development of future dextran applications in biological research and medicine.

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“…The use of purified and fractionated dex tran B 512 preparations of an average mo lecular weight of 70,000 (Macrodex ) and 40.000 (Rheomacrodex ) is well estab lished clinically for therapy of hemorrhagic shock, thromboprophylaxis and improvc-ment of microcirculation [13,23]. Accounts of rare anaphylactoid reactions in connec tion with dextran infusions have been pub lished.…”

Section: Introductionmentioning

confidence: 99%

Dextran-induced Anaphylactoid Reactions in Man

Hedin¹,

Richter²,

Ring³

1976

Int Arch Allergy Immunol

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Dextran reactive antibodies (DRA) were studied in 123 patients having experienced dextran-induced anaphylactoid reactions (DIAR) during 1970–1975. No evidence for reaginic DRA was obtained by radioallergosorbent technique and passive cutaneous anaphylaxis in Cynomolgus monkeys; total IgE levels were within normal range. It is concluded that DIAR are not mediated by dextran-specific reagins. Further, no reaginic antibodies against potential contaminants from the dextran manufacturing process were demonstrable. In two population samples of normal human sera from Sweden and Germany hemagglutinating DRA (IgG, IgA, and IgM classes) were found in 63 and 74%, high titres (16–256) comprising 14 and 25%. In dextran reactors a direct positive correlation between titres of hemagglutinating DRA and increasing severity of DIAR was observed. The accumulation of high DRA titres in severe reactions may be taken as circumstantial evidence for the causal role of hemagglutinating DRA in these cases. However, if high titres of DRA alone were responsible for triggering DIAR, the expected frequency would be more than thousand times higher than the reported global incidence of DIAR. To explain this discrepancy, involvement of certain Ig classes or subgroups, possibly in combination with other predisposing factors is suggested. In mild reactions DRA appear to play a negligible role. Positive dextran wheal and flare reactions, often correlated with high titres of hemagglutinating DRA, were seen in 32% of dextran reactors, indicating that skin tests are of limited predictive value. No significant difference between sexes, age groups, or pre- and intraoperatively started dextran infusions was observed; association with certain diseases was not apparent.

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Dextran and its Use as a Plasmasubstitute.

Cited by 24 publications

References 0 publications

Dextran‐Induced Anaphylactoid Reaction in Man: Altered Reactivity of High Molecular Weight Kininogen

Dextran‐Induced Anaphylactoid Reaction in Man: Altered Reactivity of High Molecular Weight Kininogen

Targeting the C-type Lectins-Mediated Host-Pathogen Interactions with Dextran

Dextran-induced Anaphylactoid Reactions in Man

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