Publications by authors named "Kenneth Solen"

Background: Fibrin-based sealants are commonly used to arrest bleeding following surgery. A new method has been developed for preparation of autologous fibrin sealant (FS) from protamine-precipitated fibrinogen concentrate. This FS has the potential to be a low-cost, safe, and convenient alternative to commercial sealants or cryoprecipitates usually prepared from patient or banked plasma.

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A subpopulation of patients would benefit from an anticoagulation strategy during extracorporeal circulation (ECC) that does not involve systemic administration of heparin and protamine. Inhibition of coagulation by adsorption of plasma clotting factors using protamine immobilized on a Sepharose matrix (PSM) has been explored. This investigation extends previous in vitro studies and demonstrates the feasibility of heparin-free ECC.

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Heparin is associated with adverse effects in some patients during extracorporeal circulation. A potential alternate anticoagulation strategy explored in this investigation involved mitigation of coagulation by removing clotting factors from blood by adsorption on a protamine-immobilized Sepharose matrix (PSM). Human or porcine plasmas treated with PSM in vitro were tested for clotting factors I (fibrinogen), II (prothrombin), VIII, and X, and proteins C and S, and for prothrombin time (PT), activated partial thromboplastin time (APTT), and total protein concentration.

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Fibrin-based sealants are commonly employed to arrest bleeding after surgery. Usually, fibrinogen obtained from pooled human plasma is used to prepare sealants, with attendant risk of blood-borne infections. Availability of autologous fibrinogen would eliminate this risk.

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Combined anti-platelet-anticoagulant therapy is increasingly being used to reduce the risk of device-induced thrombosis and thromboembolism. However, direct quantitative confirmation of the effectiveness of this combination approach is lacking. This study was undertaken to quantify the effects of various combinations of heparin (anticoagulant) and tirofiban (antiplatelet agent) on device-induced thrombosis and thromboembolism using a coronary stent as a prototype device.

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A numerical model of thrombosis/thromboembolism (T/TE) is presented that predicts the progression of thrombus growth and thromboembolization in low-shear devices (hemodialyzers, oxygenators, etc.). Coupled convection-diffusion-reaction equations were solved to predict velocities, platelet agonist (ADP, thromboxane A2, and thrombin) concentrations, agonist-induced and shear-induced platelet activation, and platelet transport and adhesion to biomaterial surfaces and adherent platelets (hence, thrombus growth).

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Hypothermia-induced platelet aggregation (HIPA) was previously reported in whole blood exposed to synthetic surfaces at 24 degrees-32 degrees C in one-third of normal subjects tested. Cardiopulmonary bypass, conducted with hypothermia, may lead to such aggregation, resulting in microvascular occlusion contributing to cognitive impairment. This pilot study was conducted to explore the relationship between HIPA and cognitive outcome at hospital discharge in patients undergoing coronary artery bypass graft (CABG) surgery as a first step toward a longer-term study.

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The characteristics and capabilities of a light-scattering microemboli detector (LSMD) are delineated by detailing its state-of-the-art configuration, by discussing the theoretical and empirical aspects of instrument calibration, and by summarizing various experimental studies that have benefited from this instrument. In the past, thromboembolism, which often results when blood contacts medical devices, has eluded scientific scrutiny due to the absence of instruments that could detect and quantify thromboemboli in circulating blood. More recently, the ability of the LSMD to provide continuous, noninvasive detection of thromboemboli in whole blood (meaning that the LSMD probe does not contact the blood) was exploited in various in vitro and ex vivo models to explore thromboembolic phenomena.

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Cold-induced platelet aggregation (CIPA) in PRP has previously been documented in connection with platelet preservation (4-15 degrees C). This report describes hypothermia-induced platelet aggregation (HIPA) in whole blood and at temperatures used in open-heart surgery (24-32 degrees C). HIPA (specifically, the formation of occlusive aggregates) was studied in human whole blood.

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Hypothermia-induced platelet aggregation (HIPA) with or without neutrophil involvement may cause neurologic dysfunction during hypothermic surgery. We report the use of a previously developed model to study the contributions of several surfaces, surface area, shear rate, and blood-material exposure time to HIPA. Heparinized (1.

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