Low Molecular Weight Heparin Prevents the Pulmonary Hemodynamic and Pathomorphologic Effects of Endotoxin in a Porcine Acute Lung Injury Model

Darien, B. J.; Jawed, Fareed; Centgraf, Kim S.; Hart, Arlene P.; MacWilliams, Peter S.; Clayton, Murray K.; Wolf, Helmut; Kruse-Elliott, Kris T.

doi:10.1097/00024382-199804000-00007

Cited by 55 publications

(36 citation statements)

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“…For cytokine and chemokine measurements in lungs, supernatants were used from lung homogenates which were diluted 1:1 in lysis buffer (150 Assays Thrombin-antithrombin complexes (TATc; Behring, Marburg, Germany) and fibrin degradation products (FDP; Asserachrom D-Di; Diagnostica Stago, Asnières-sur-Seine, France) were measured using ELISA. AT, plasminogen activator activity (PAA) and plasminogen activator inhibitor (PAI)-1 activity were measured by automated amidolytic assays [15][16][17]. Levels of TNF-a, IL-6 and CINC-3 were measured using ELISA (R&D Systems, Abingdon, UK).…”

Section: Methodsmentioning

confidence: 99%

“…Heparin had been shown to exert lung protective effects during endotoxaemia in sheep [16], while low molecular weight heparin had been able to limit lung injury in endotoxaemic pigs [17] and mice [18]. In the present experiment, heparin had a mild anticoagulant effect and a modest antifibrinolytic effect: pulmonary TATc and systemic PAA were decreased at 4 h after LPS injection, while pulmonary PAI-1 activity was increased after 16 h. This is in contrast with in vitro data suggesting that heparins have pro-fibrinolytic effects [22].…”

Section: Natural Anticoagulants In Endotoxaemiamentioning

confidence: 99%

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Natural anticoagulants limit lipopolysaccharide-induced pulmonary coagulation but not inflammation

Choi

Vlaar²,

Schouten

et al. 2007

Eur Respir J

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Pulmonary coagulopathy and hyperinflammation may contribute to an adverse outcome in sepsis. The present study determines the effects of natural inhibitors of coagulation on bronchoalveolar haemostasis and inflammation in a rat model of endotoxaemia.Male Sprague-Dawley rats were randomised to treatment with normal saline, recombinant human activated protein C (APC), plasma-derived antithrombin (AT), recombinant human tissue factor pathway inhibitor (TFPI), heparin or recombinant tissue plasminogen activator (tPA). Rats were intravenously injected with lipopolysaccharide (LPS), which induced a systemic inflammatory response and pulmonary inflammation. Blood and bronchoalveolar lavage were obtained at 4 and 16 h after LPS injection, and markers of coagulation and inflammation were measured.LPS injection caused an increase in the levels of thrombin-AT complexes, whereas plasminogen activator activity was attenuated, both systemically and within the bronchoalveolar compartment. Administration of APC, AT and TFPI significantly limited LPS-induced generation of thrombin-AT complexes in the lungs, and tPA stimulated pulmonary fibrinolytic activity. However, none of the agents had significant effects on the production of pulmonary cytokines, chemokines, neutrophil influx and myeloperoxidase activity.Natural inhibitors of coagulation prevent bronchoalveolar activation of coagulation, but do not induce major alterations of the pulmonary inflammatory response in rat endotoxaemia.

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Section: Methodsmentioning

confidence: 99%

Section: Natural Anticoagulants In Endotoxaemiamentioning

confidence: 99%

Natural anticoagulants limit lipopolysaccharide-induced pulmonary coagulation but not inflammation

Choi

Vlaar²,

Schouten

et al. 2007

Eur Respir J

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show abstract

“…The inhibition of endothelial MPO binding thus represents an additional mechanism by which heparin analogs exert anti-inflammatory properties (50)(51)(52). Interestingly, there was no competition between MPO and the chondroitin sulfate-dependent binding of XO to endothelium (Figure 2e) (23).…”

Section: Figurementioning

confidence: 99%

Endothelial transcytosis of myeloperoxidase confers specificity to vascular ECM proteins as targets of tyrosine nitration

Baldus¹,

Eiserich²,

Mani³

et al. 2001

J. Clin. Invest.

280

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“…(23)(24)(25) A study in pediatric patients with inhalation injuries revealed that combined heparin nebulization significantly reduced mortality. (12) However, in this study, patients were also treated with N-acetylcysteine, which may have contributed to the favorable outcome.…”

mentioning

confidence: 99%

Nebulized Anticoagulants Limit Pulmonary Coagulopathy, But Not Inflammation, in a Model of Experimental Lung Injury

Hofstra

Vlaar²,

Cornet³

et al. 2010

Journal of Aerosol Medicine and Pulmonary Drug Delivery

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Low Molecular Weight Heparin Prevents the Pulmonary Hemodynamic and Pathomorphologic Effects of Endotoxin in a Porcine Acute Lung Injury Model

Cited by 55 publications

References 0 publications

Natural anticoagulants limit lipopolysaccharide-induced pulmonary coagulation but not inflammation

Natural anticoagulants limit lipopolysaccharide-induced pulmonary coagulation but not inflammation

Endothelial transcytosis of myeloperoxidase confers specificity to vascular ECM proteins as targets of tyrosine nitration

Nebulized Anticoagulants Limit Pulmonary Coagulopathy, But Not Inflammation, in a Model of Experimental Lung Injury

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