Nugent, Michael

In this study, we present a simple and effective process that integrates hydrogels with drugs + ceramics via physical crosslinks resulting in improved mechanical properties. These cryogels have the potential for controlled drug release and stimulus responsive behavior. The hydrogels were produced from polyvinyl alcohol (PVA) and polyacrylic acid by varying the molecular weight of the polymers, via freeze‐thawing technique. The cryogels were combined with two ceramics: (1) a combination of beta‐tricalcium phosphate, wollastonite, magnesium silicate and (2) titanium dioxide nanopowder. Theophylline, a model drug, was incorporated into the structure to analyze the drug release behavior. A layered structure was produced by adding both hydrogels + ceramics into a mold where a PVA dried film acted as a barrier and reinforcing structure. The results showed that the barrier integrated between both hydrogels by a physically crosslinking mechanism. This adhesion was demonstrated using Fourier‐transform infrared spectroscopy and scanning electron microscopy. Swelling of this composite showed the profile of drug release from both hydrogels + ceramics while simultaneously releasing the drug independently without diffusing via the opposite layer. Finally, mechanical properties were improved with the addition of the ceramics, which demonstrates the potential approach in terms of modification of weak hydrogel systems. POLYM. COMPOS., 39:E210–E220, 2018. © 2017 Society of Plastics Engineers

Innovations on the field of smart hydrogels are now being held with loads of advantages. With recent progress, smart polymers can now be used on the market for specific target/objectives desired on medicine. However, the field of smart hydrogels has not been fully overviewed on the ground for drug delivery. In this study, a novel pH‐sensitive smart hydrogel for drug delivery was investigated. Polyvinyl‐alcohol (PVA) with polyacrylic acid (PAA) was blended adding synthetic hydroxyapatite (Hap) with freeze‐thawed cycles and its effects were studied in terms of mechanical strength, bioactivity, and drug release profile. Mechanical strength towards compression tests was decreased after addition of Hap and storage modulus (G') increased. Bioactivity was confirmed after 14 days on simulated body fluid (SBF). Improvement of swelling and gel fraction with the addition of Hap throughout the polymer matrix. Moreover, a study was performed with theophylline‐loaded samples for drug‐delivery studies. Copyright © 2015 John Wiley & Sons, Ltd.

BackgroundInotropic drugs are often used to treat acute, severe heart failure resulting from acute myocardial infarction and other unstable coronary artery syndromes. However, catecholamine inotropic agents may potentiate coronary thrombosis via a platelet α2-adrenergic mechanism, thus exacerbating the original problem. The present studies were designed to determine whether the nonadrenergic inotropic and vasodilator drug amrinone, which elevates platelet cAMP levels, would both inhibit human platelet Ca2+mobilization and adhesion molecule expression ex vivo and protect against experimental coronary thrombosis in vivo in dogs.Methods and ResultsHuman platelets in suspension were preincubated with amrinone 2.5 to 15 μg/mL; stimulated with the agonists thrombin 0.1 U/mL, ADP 10−6mol/L, or arginine vasopressin 10−7mol/L; and studied for Ca2+mobilization, glycoprotein IIb/IIIa activation, and P-selectin expression by fluorescent flow cytometry methods. Experimental coronary thrombosis in vivo was studied in an open-chest dog model with critical coronary artery stenosis and deep vessel wall injury. Results showed that at the cellular level, amrinone inhibited agonist-induced Ca2+mobilization and had modest inhibitory effects on adhesion molecule expression. In vivo in dogs, intravenous amrinone 2 mg/kg plus infusion at 20 μg·kg−1·min−1completely abolished coronary thrombosis.ConclusionsThe fact that amrinone inhibited human platelet activation at the cellular level and protected against experimental coronary thrombosis in vivo in dogs suggests a potentially advantageous antithrombotic action for this inotropic and vasodilator drug.