Heparin coating of the stent graft — effects on platelets, coagulation and complement activation

Christensen, Kjeld; Larsson, Rolf; Emanuelsson, Håkan; Elgue, Graciela; Larsson, Anders

doi:10.1016/s0142-9612(00)00190-3

Cited by 91 publications

(49 citation statements)

References 19 publications

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“…The upregulation of iNOS activity in these cells can be elicited by immunologic and nonimmunologic stimuli [37]. Some observations revealed that induction of iNOS in rats with IC glomerulonephritis was complement-dependent [38, 39, 40]. Chronic blockade of NO synthesis in rats with Heymann nephritis can produce systemic hypertension and glomerular damage [18].…”

Section: Discussionmentioning

confidence: 99%

Inhibitory Effects of Ligustrazine, a Modulator of Thromboxane-Prostacycline-Nitric Oxide Balance, on Renal Injury in Rats with Passive Heyman Nephritis

Wang

Tong²,

Tang³

et al. 2004

Nephron Physiol

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Aims: To explore the effects of ligustrazine on proteinuria, urinary TxB₂ (metabolism of thromboxane A₂, TxA₂) and 6-keto-PGF_1α(metabolism of prostacyclines I₂, PG I₂), glomerular inducible nitric oxide(NO) synthase (iNOS) mRNA, urinary NO^–₃/NO^–₂ (decomposing products of NO) and pathological changes in rats with passive Heymann nephritis (PHN). Methods: A rat PHN model was induced by intravenous injection of rabbit anti-rat renal tubular antigen (Tub-Ag) antiserum, and ligustrazine was given intraperitoneally into PHN rats every 2 days for 1–5 weeks. Then, proteinuria, urinary TxB₂ and 6-keto-PGF_1α, glomerular iNOS mRNA, and urinary NO^–₃/NO^–₂ were measured by sulfosalicylic acid, radioimmunoassay (RIA), Northern blot and nitric acid reductase methods, respectively. Moreover, the damage to the renal tissue of the rats was observed under light and electron microscopy and immunofluorescence (IF). Results: The urinary TxB₂ in PHN rats was significantly higher than that in control rats, but the PHN rats treated with ligustrazine had significantly less proteinuria, urinary TxB₂ and tissue lesions, and more urinary 6-keto-PGF_1α, glomerular iNOS mRNA and urinary NO^–₂/NO^–₃ than the PHN rats without the administration of ligustrazine. Conclusion: These data indicate that ligustrazine has inhibitory roles on the glomerular injury of PHN rats, which may associate with modulating the balance of TxA₂-PGI₂ and elevating synthesis of NO to a certain extent.

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Section: Discussionmentioning

confidence: 99%

Inhibitory Effects of Ligustrazine, a Modulator of Thromboxane-Prostacycline-Nitric Oxide Balance, on Renal Injury in Rats with Passive Heyman Nephritis

Wang

Tong²,

Tang³

et al. 2004

Nephron Physiol

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“…Heparin might have some protecting effect on vIII peptide by suppressing degradation or by blocking blood clotting on the surface. The PAV-heparin surface [11] was used to obtain a covalent binding between the solid phase and the antigen which allows for antibody binding tests to be made also when pH and ion strength vary. The affinity constant of the new antibody was fairly similar when analyzed by surface plasmon resonance (Biacore 2000) and by saturation radioligand studies (45 and 80 nM, respectively).…”

Section: Discussionmentioning

confidence: 99%

“…A so-called PAV-heparin surface [11], in this case a PAV-heparin-SPDP-peptide-vIII surface, was applied. Such surfaces are used when covalent binding between the solid phase and the antigen is needed.…”

Section: Preparation Of Solid Phasementioning

confidence: 99%

“…The peptide vIII was covalently bound to the surface to allow for antibody binding tests not only in cell culture medium but also when pH and ion strength might vary. The covalent coupling method has recently been described in the journal Biomaterials [11] and is only shortly described here. 96-well microtiter plates were prepared stepwise ( fig.…”

Section: Preparation Of Solid Phasementioning

confidence: 99%

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A New Antibody Recognizing the vIII Mutation of Human Epidermal Growth Factor Receptor

Öhman

Gedda²,

Hesselager

et al. 2002

Tumor Biol

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The epidermal growth factor receptor (EGFR) gene is frequently amplified and the receptor overexpressed in different types of human tumors. Furthermore, genomic rearrangements can cause expression of modified receptors, as one frequently occurring truncated form, EGFRvIII. This mutated receptor has previously been described and is formed by a 267-amino acid in-frame deletion and an insertion of a glycine in the fusion junction of the extracellular domain. EGFRvIII is a tumor-specific marker and therefore of interest for diagnostic and therapeutic applications. In this study we report on a new monoclonal antibody (Ua30:2) directed to the mutation site of EGFRvIII. The antibody was generated by immunization of mice with a synthetic peptide corresponding to the mutated sequence of the receptor. The affinity of Ua30:2 was found to be high [K_d = 45 nM (Biacore) and 80 nM (saturation analysis)]. Immunohistochemistry in tissue sections from human gliomas demonstrated a similar expression pattern for Ua30:2 as for the recently characterized antibodies L8A4 and DH8.3. The antibody binding was EGFRvIII specific with no measurable cross-reactivity to the wild-type receptor, wtEGFR, as analyzed both with displacement analysis, Western blots and immunohistochemistry. The new antibody is a candidate for radioimmunotargeting aiming at diagnostic and therapeutic applications.

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“…Biomaterials, e.g., different kinds of tubing which can be closed into loops, can be tested directly in this setup, and biomedical devices such as stents, catheters, or lenses may be inserted into heparincoated loops (Christensen et al 2001(Christensen et al , 2006Sinn et al 2011 ) . In this model, it is possible to monitor activation of the cascade systems in the fl uid phase (i.e., plasma) and the activation and/or consumption of blood cells.…”

Section: Tubing Loops For Testing Biomaterials and Soluble Inhibitorsmentioning

confidence: 99%

Evaluation of the Blood Compatibility of Materials, Cells, and Tissues: Basic Concepts, Test Models, and Practical Guidelines

Ekdahl

Hong

Hamad

et al. 2012

Complement Therapeutics

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Medicine today uses a wide range of biomaterials, most of which make contact with blood permanently or transiently upon implantation. Contact between blood and nonbiological materials or cells or tissue of nonhematologic origin initiates activation of the cascade systems (complement, contact activation/coagulation) of the blood, which induces platelet and leukocyte activation. Although substantial progress regarding biocompatibility has been made, many materials and medical treatment procedures are still associated with severe side effects. Therefore, there is a great need for adequate models and guidelines for evaluating the blood compatibility of biomaterials. Due to the substantial amount of cross talk between the different cascade systems and cell populations in the blood, it is advisable to use an intact system for evaluation. Here, we describe three such in vitro models for the evaluation of the biocompatibility of materials and therapeutic cells and tissues. The use of different anticoagulants and specific inhibitors in order to be able to dissect interactions between the different cascade systems and cells of the blood is discussed. In addition, we describe two clinically relevant medical treatment modalities, the integration of titanium implants and transplantation of islets of Langerhans to patients with type 1 diabetes, whose mechanisms of action we have addressed using these in vitro models.

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Heparin coating of the stent graft — effects on platelets, coagulation and complement activation

Cited by 91 publications

References 19 publications

Inhibitory Effects of Ligustrazine, a Modulator of Thromboxane-Prostacycline-Nitric Oxide Balance, on Renal Injury in Rats with Passive Heyman Nephritis

Inhibitory Effects of Ligustrazine, a Modulator of Thromboxane-Prostacycline-Nitric Oxide Balance, on Renal Injury in Rats with Passive Heyman Nephritis

A New Antibody Recognizing the vIII Mutation of Human Epidermal Growth Factor Receptor

Evaluation of the Blood Compatibility of Materials, Cells, and Tissues: Basic Concepts, Test Models, and Practical Guidelines

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