Appearance of heparin antithrombin-active chains in vivo after injection of commercial heparin and in anaphylaxis

Levy, S. W.; Jaques, L. B.

doi:10.1016/0049-3848(78)90129-9

Cited by 23 publications

(8 citation statements)

References 21 publications

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“…It might also mean that a particular biologically active form of heparin, perhaps that bound to antithrombin III, is not determined by the azure A assay. Or it may be, as suggested by Levy and Jaques (16), that heparin is converted in vivo to a more active form. Heparin molecules may be in a particularly inactive configuration in vitro as determined by the manufacturer, and are then converted in vivo to an active configuration.…”

Section: Discussionmentioning

confidence: 94%

A colorimetric assay for chemical heparin in plasma

Klein

Drongowski

Linhardt

et al. 1982

Analytical Biochemistry

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A simple, rapid calorimetric assay for plasma heparin is presented. The assay employs the metachromasia of azure A when heparin is added. It is useful for 0 to 10 units/ml and does not depend on heparin's anticoagulant activity. Heparin concentrations determined with this assay are not exactly the same as those determined with coagulation assays. This is probably because azure A determines chemical heparin, not anticoagulant active heparin.

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Section: Discussionmentioning

confidence: 94%

A colorimetric assay for chemical heparin in plasma

Klein

Drongowski

Linhardt

et al. 1982

Analytical Biochemistry

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“…Since both the chemical assay and the bioassays are based on in vitro reference curves, we have proposed that these observed in vivo differences in heparin activity may be due to an apparent in vivo enhancement of the anticoagulant properties of heparin . Similar heparin assay differences have been observed both in man and animals when heparin activity has been determined by metachromatic assays using toluidine blue or azure A as the chemical assay and by a bioassay based on thrombin time; these studies also demonstrated that heparin can be activated in vivo (Levy & Jaques, 1978).…”

Section: Introductionmentioning

confidence: 53%

“…In vivo activation of heparin has been demonstrated in rabbits following s.c. injection of inactivated heparin; anticoagulant activity rose rapidly and Heparin activity (unit/ml) Heparin activity (unit/ml) reached a maximum in 3 h (Levy & Jaques, 1978). These studies also showed heparin assay differences in man, dogs and rabbits; heparin determined chemically using a metachromatic assay showed lower heparin activity in plasma than did a bioassay based on thrombin time.…”

Section: Discussionmentioning

confidence: 81%

Assay‐dependent kinetics of heparin: evidence for rapid in vivo activation of heparin.

McGowan¹,

Nash²,

Bjornsson³

1983

Brit J Clinical Pharma

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1 Multiple blood samples were collected over the first 15 min after an i.v. injection of 25 units/kg of heparin in four healthy subjects. Plasma heparin activity in each sample was determined by a chemical neutralization assay using polybrene and a bioassay based on activated partial thromboplastin time. 2 Chemically assayed heparin declined much more rapidly than bioassayed heparin over the first 5-7 min after the dose. Subsequently, both heparin activity vs time curves declined with a similar terminal half-life. 3 Slopes of the in vivo ln APTT vs plasma heparin activity (determined by chemical neutralization) relationships were significantly greater than those of the corresponding in vitro relationships between ln APTT vs heparin activity added to plasma. 4 A possible explanation for these heparin assay differences is a rapid in vivo enhancement of the anticoagulant effect of heparin. How such enhancement may occur, however, is presently unclear.

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“…From there heparin is gradually released in a changed form which closely resembles native heparin. 17 The observation in several patients of a reduction in their migraine index and a norrealization of T-cell parameters lasting several weeks after treatment had been suspended, suggests an extended release from the cells or a sustained reactivation of some enzyme systems or other physiological alterations. Since tissue distribution of heparin and PNP are similar, and the biological half life of PNP in the liver is nine days, 6 comparable mechanisms may exist for the release of both drugs.…”

Section: Discussionmentioning

confidence: 99%

Prophylaxis of Migraine with Anionic Polyelectrolytes

Thonnard-Neumann

Bigelow

1988

Headache

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SYNOPSIS In previous studies on patients with migraine headaches we found that 50% had reduced concentrations of basophils and lymphocytes. Treatment with inhalations of heparin often restored these blood indices to normal and was accompanied by a reduction in migraine headache, We report here data on the long term treatment of 37 migraine patients with inhalations of heparin and with an oral semi‐synthetic heparinoid, Pentosan Polysulfate (PNP). 27 patients responded with a mean improvement in migraine index of 79% and as a group showed significant increases in basophil, total lymphocyte, and in particular T‐cell concentrations. Ten patients whose migraine headaches were related to their menstrual cycles were relatively unresponsive to heparin or PNP. They had a general leukopenia, but basophils were within normal range.

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Appearance of heparin antithrombin-active chains in vivo after injection of commercial heparin and in anaphylaxis

Cited by 23 publications

References 21 publications

A colorimetric assay for chemical heparin in plasma

A colorimetric assay for chemical heparin in plasma

Assay‐dependent kinetics of heparin: evidence for rapid in vivo activation of heparin.

Prophylaxis of Migraine with Anionic Polyelectrolytes

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