Prevention of Platelet Adhesion and Aggregation by a Glutardialdehyde-Stabilized Heparin Surface

Olsson, Per; Lagergren, H; Larsson, Rolf; Rådegran, Kjell

doi:10.1055/s-0038-1649228

Cited by 45 publications

(16 citation statements)

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“…Tracheostomy was performed but respiration was not assisted. Blood pressure was measured through a heparin coated' (Olsson et al 1977) PE-catheter in the right, common carotid artery, connected to a Statham 23 AC pressure transducer recording on a Grass polygraph. An identical catheter was put into a central vein through the right external jugular vein for sampling and injections.…”

mentioning

confidence: 99%

Correlative analysis of microcirculatory and cellular metabolic events in skeletal muscle during hemorrhagic shock

Amundson¹,

Jennische²,

Haljamäe

1980

Acta Physiologica Scandinavica

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Skeletal muscle reactions to hemorrhagic shock were investigated in anesthetized cats (n = 23). The tenuissimus muscle was exposed for vital microscopy and shock was induced by single-withdrawal of 45% of the blood volume. Muscle microcirculation, energy metabolism and cell membrane potentials were followed over a 2 h period along with blood pressure, hematocrit and blood leukocyte, platelet, glucose, pyruvate and lactate contents. Bleeding usually caused complete cessation of muscle blood flow for 5--20 min, while the animal compensated the blood pressure. Reflex constriction occurred in medium-sized but not in terminal arterioles. When flow reappeared a marked maldistribution was evident in the capillary bed. Flow remained in 30--50% of the capillaries, permanently or intermittedly. Leukocytes could be found lodged in many arrested capillaries and also adhering to venules in large numbers. Erythrocyte or platelet plugs were not seen in the muscle microvasculature. Glucose and G6-P contents doubled and lactate increased 5-fold in muscle tissue during shock. CP was reduced by about 25% while the ATP-level remained unchanged. Membrane potentials declined 12% in shock and the spread in potentials from adjacent fibers increased.

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mentioning

confidence: 99%

Correlative analysis of microcirculatory and cellular metabolic events in skeletal muscle during hemorrhagic shock

Amundson¹,

Jennische²,

Haljamäe

1980

Acta Physiologica Scandinavica

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“…This extends observations from previous reports describing the anti-adhesive properties of the HS chains of perlecan, although the underlying mechanism was not known (Klein, Conzelmann, Beck, Timpl, & Muller, 1995; Lord et al, 2009). Moreover, heparinized polymers showed less platelet adhesion than their non-heparinized counterparts (Han, Jeong, & Kim, 1989; Lindhout et al, 1995; Olsson, Lagergren, Larsson, & Radegran, 1977). Our results with platelets from G6b-B-deficient mice demonstrate that heparin or HS engagement by G6b-B on these surfaces induce an inhibitory signal, blocking platelet activation and adhesion.…”

Section: Discussionmentioning

confidence: 99%

Heparan sulfates are critical regulators of the inhibitory megakaryocyte-platelet receptor G6b-B

Vögtle

Sharma

Mori

et al. 2019

Preprint

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The immunoreceptor tyrosine-based inhibition motif (ITIM)-containing receptor G6b-B is critical for platelet production and activation, loss of which results in severe macrothrombocytopenia and aberrant platelet function in mice and humans. Using a combination of immunohistochemistry, affinity chromatography and proteomics, we identified the extracellular matrix heparan sulfate (HS) proteoglycan perlecan as a G6b-B binding partner. Subsequent in vitro biochemical studies and a cell-based genetic screen demonstrated that the interaction is specifically mediated by the HS chains of perlecan. Biophysical analysis revealed that heparin forms a high-affinity complex with G6b-B and mediates dimerization. Using platelets from humans and genetically-modified mice, we demonstrate that binding of G6b-B to HS and multivalent heparin inhibits platelet and megakaryocyte function by inducing downstream signaling via the tyrosine phosphatases Shp1 and Shp2. Our findings provide novel insights into how G6b-B is regulated and contribute to our understanding of the interaction of megakaryocytes and platelets with glycans.

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“…On in vitro contact with fresh heparinized or citrated human whole blood there was no measurable adhesion of radioactive-labeled platelets and no detectable platelet aggregation in the blood samples after their contact with the surface. 6 In animal experiments, when native blood was circulated in arteriovenous shunts for several hours, platelet adhesion was actually detectable but was still reduced by 90% as compared to the untreated polyethylene surfaces.…”

Section: Platelet Interactionmentioning

confidence: 99%

REQUIREMENTS FOR THROMBORESISTANCE OF SURFACE‐HEPARINIZED MATERIALSa

Olsson¹,

Larm²,

Larsson³

et al. 1983

Annals of the New York Academy of Sciences

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Any surface except the endothelial lining of the vascular wall will initiate a sequence of deleterious reactions when it is brought in contact with blood. The most well known are those associated with the activation of the platelets and the plasma coagulation system leading to the formation of a thrombus. The lack of suitable artificial thromboresistant surfaces is still a major obstacle for the further development of devices such as equipment for hemodialysis, heart-lung machines, artificial heart valves, vascular grafts, and sensors for intravascular monitoring of blood parameters, the use of which mostly require systemic anticoagulant treatment of the patient.Bonding of heparin to artificial materials has attracted a great deal of attention as a possible approach for achieving a thromboresistant surface.' The present communication will review our studies on the mechanism for action of the surface-bound heparin immobilized by either stabilizing an ionic heparin complex with glutaraldehyde or covalent bonding. The advantages of applying a heparin coating on an intravascular PO, sensor and a hollow-fiber dialyzer will also be demonstrated. STUDIES ON THE GLUTARALDEHYDE-STABILIZED IONIC HEPARIN COMPLEX SURFACE AND SURFACES WITH OTHER SULFATED POLYSACCHARIDES Method of PreparationAs a rule, low density polyethylene has been used as the substrate material for the studies on the function of the heparin-glutar surface, although the method of preparation can also be applied to a variety of materials, provided that they can be furnished with a net negative surface charge. The coating procedure relies on surface adsorption of colloidal particles composed of heparin and hexadecyla-

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Prevention of Platelet Adhesion and Aggregation by a Glutardialdehyde-Stabilized Heparin Surface

Cited by 45 publications

References 0 publications

Correlative analysis of microcirculatory and cellular metabolic events in skeletal muscle during hemorrhagic shock

Correlative analysis of microcirculatory and cellular metabolic events in skeletal muscle during hemorrhagic shock

Heparan sulfates are critical regulators of the inhibitory megakaryocyte-platelet receptor G6b-B

REQUIREMENTS FOR THROMBORESISTANCE OF SURFACE‐HEPARINIZED MATERIALSa

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