Biomer/poly(N-isopropylacrylamide)/[poly(NiPAAm)] thermosensitive polymer blends were prepared and their application as heparin-releasing polymer coatings for the prevention of surface-induced thrombosis was examined. The advantage of using poly(NiPAAm)-based coatings as heparin-releasing polymers is based on the unique temperature-dependent swelling of these materials. At room temperature, i.e., below the lower critical solution temperature (LCST) of poly(NiPAAm), the Biomer/(poly(NiPAAm) coatings are highly swollen. The high swelling enables fast loading of hydrophilic macromolecules (e.g., heparin) into the coating by a solution sorption technique. At a body temperature, i.e., above the LCST of poly(NiPAAm) the coatings are in a deswollen state and the absorbed macromolecules may be slowly released from a dense coating via a diffusion controlled mechanism. Biomer/poly(NiPAAm) coatings were obtained by blending and coprecipitation of the two linear polymers, Biomer and (poly(NiPAAm). The structure and water-swelling properties of the coatings were examined. Significant differences in water swelling at room temperature (RT) and 37°C were observed as a result of the thermosensitivity of poly(NiPAAm). The surface structure of the coatings in dry and swollen states at RT and 37°C was examined by scanning electron microscopy. Heparin was loaded into the coatings via a solution sorption at room temperature. Kinetic studies of heparin loading demonstrated that maximum loading was obtained within 1 h. The in vitro (37°C) release profiles were characterized by a rapid initial release due to the squeezing effect of the collapsing polymer network, followed by a slower release phase controlled by heparin diffusion through the dense coating. The short-term antithrombogenicity of intravenous polyurethane catheters coated with heparin-releasing Biomer/poly(NiPAAm) thermosensitive coating was evaluated in a canine animal model. The results show that the heparin release from Biomer/poly(NiPAAm)-coated surfaces resulted in a significant reduction of thrombus formation on test surfaces in contact with venous blood as compared to control surfaces.
Platelet adhesion to glass, polyethylene, polyvinyl chloride, and Cuprophane has been studied by means of a method specific for quantitation of adhesion. Platelets adhered in larger numbers to polyethylene and polyvinyl chloride than to Cuprophane or glass regardless of the anticoagulant used. In citrated plasma, fewer platelets adhered to glass than to Cuprophane, although adhesion to glass and Cuprophane was nearly the same when EDTA or heparin was used as anticoagulant. The number of adherent platelets decreased appreciably from values obtained with citrated platelet-rich plasma, when EDTA or heparin was used as anticoagulant. Adhesiveness of normal platelets increased with age. A number of different pharmacologic and other agents were found to inhibit platelet adhesion to artificial surfaces. Acetylsalicylic acid and glucosamine were less effective inhibitors than sulfinpyrazone, imipramine, desipramine, amitriptyline, chlorpromazine, or PCMB. Penicillin did not inhibit adhesion. Donors deficient in factors VIII, XI, or XII or donors with von Willebrand’s disease showed normal platelet adhesiveness. Adhesiveness was markedly low in tests with blood from afibrinogenemic or thrombasthenic patients. Decreased adhesiveness of afibrinogenemic platelets could be corrected by addition of fibrinogen.
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. Through this work, the LSMD evolved as a sensitive and an economical research tool for the study of thromboembolic phenomena.
respiratory, cutaneous/ limb and urinary tract (41.7%, 26.4% and 20.8% respectively). Positivity of blood cultures were 43.1%. A total of 66 subjects (91.7%) were mechanically ventilated (median duration 5 days), while 59 (81.9%) required inotropic support (median duration 3 days). Modalities for RRT were haemodialysis (HD) in 84.7% of cohort (n ¼ 61), peritoneal dialysis (PD) in 4.2% of cohort (n ¼ 3), or a combined modality of HD and PD in 11.1% of cohort (n ¼ 8). Median HD catheter days and PD catheter days were 4 days (IQR 3 days) and 2 days (IQR 3 days) respectively. Percentages of subjects receiving 1, 2, 3 and > 4 sessions of HD were 44.1%, 26.5%, 8.8% and 20.6% respectively. Median length of hospitalisation was 14 days (IQR 16 days) with in-hospital mortality of 54.2% (n¼ 39). Causes of death attributed directly to index infection, nosocomial infection and noninfectious causes were 74.4%, 10.3% and 15.4% respectively. Among survivors, 11 (34.4%) were functionally dependent at discharge. Predictors of mortality were use of mechanical ventilation, inotrope use, younger patients, and cutaneous/ limb infection. Comorbidities, CKD status, CCI, positivity of blood culture and SOFA score did not predict mortality. Conclusion: Mortality and morbidity remain high for patients with SA-AKI requiring RRT, primarily driven by the index infection.
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