The Application of Fibrin/Hyaluronic Acid–Poly(L-Lactic-co-Glycolic Acid) Construct in Augmentation Rhinoplasty

Althoughmany graftmaterials have been used for augmentation rhinoplasty, an ideal graft has not yet been developed.As the field of tissue engineering has been developing, it has been applied to the reconstruction of many organs, but its application in the rhinoplasty field is still limited. This study evaluated the utility of allogenic chondrocytes with fibrin/hyaluronic acid (HA)–poly(L-lactic-co-glycolic acid) (PLGA) constructs in augmentation rhinoplasty. Chondrocytes from rabbit auricular cartilage were isolated and cultured with fibrin/HA hydrogels and implanted into PLGA scaffolds. After 8 weeks of in vitro culture, the scaffolds were implanted in the nasal dorsum of six rabbits. Eight weeks postoperatively, the implanted siteswere evaluated with gross, radiologic, and histologic analysis. In vitro, more than 90% of the seeded chondrocytes in the PLGA scaffolds survived for 2 weeks, and they produced a large amount of extracellular matrix and were well differentiated. The grafts maintained their initial shape for 8 weeks after implantation. Radiological and histological evaluations showed that the structure was well maintained with minimal inflammatory response and appropriate elevation levels. However, the formation of neo-chondrocytes was not observed. PLGA scaffolds seeded with fibrin/HA and allogenic chondrocytes can be a biocompatible augmentation material in rhinoplasty in the future.

Elevated Contractile Responses to Acetylcholine in Organ Cultured Rabbit Carotid Artery

The aim of the present study was to examine the functional changes that occur when a rabbit carotid artery is cultured in serum-free medium. In endothelium (EC)-intact arteries cultured under serum-free conditions, acetylcholine (ACh)-induced relaxation responses were partially, yet significantly, reduced when compared with freshly isolated arteries. After pretreatment with N(G)-nitro-L-arginine methyl ester (L-NAME), a nitric oxide synthase inhibitor, application of ACh resulted in a significant contraction in organ cultured arteries. The amplitude of the ACh-induced contractions increased with the duration of culture. In EC-denuded arteries cultured under serum-free conditions, ACh induced responses similar to those in EC-intact arteries pretreated with L-NAME. Furthermore, ACh caused a significant increase in intracellular Ca2+ concentration ([Ca2+]i) in EC-denuded arteries cultured under serum-free condition for 7 days. There was little change in either [Ca2+]i or tension in freshly isolated carotid rings. There was no difference in sodium nitroprusside-induced relaxation responses between fresh and cultured arteries. These results suggest that prolonged culture of carotid arteries under serum-free conditions changes the functional properties of vascular reactivity in rabbit carotid arteries.

Testosterone Causes Simultaneous Decrease of Ca2+i and Tension in Rabbit Coronary Arteries: by Opening Voltage Dependent Potassium Channels

The relationship between the level of testosterone and the incidence of coronary heart disease is still controversial in the view of the results of clinical and epidemiologic studies. This uncertainty might be partly due to relatively small number of experimental studies undertaken to investigate the cellular mechanism underlying the vascular responses to testosterone. To further investigate the cellular mechanisms of testosterone with respect to vascular response, we investigated the effect of testosterone on contractility and intracellular Ca2+ regulation in a rabbit coronary artery and evaluated the underlying mechanism of testosterone-induced changes of coronary vascular tone by using various pharmacological blockers. Testosterone was found to relax rabbit coronary arteries in a dose-dependent manner, and no significant difference was found in the relaxation response to testosterone with or without endothelium. Similar results were obtained in male and non-pregnant female rabbit coronary arteries. The relaxation response of rabbit coronary arteries to testosterone was greater for PGF2alpha-contracted rings than for KCl contracted rings, which suggest the involvement of K+ channels. Furthermore, the relaxation response to testosterone was significantly reduced by 4-aminopyridine, a sensitive blocker of voltage dependent K+ channels, but not by low doses of tetraethylammonium or iberiotoxin, a Ca2+ activated K+ channel blocker. Testosterone simultaneously reduced the intracellular Ca2+ concentration ([Ca2+]i) and tension, and 4-AP effectively antagonized the testosterone-induced change of [Ca2+]i and tension. Therefore, it may be concluded that the stimulation of voltage dependent K channels is responsible, at least in part, for the testosterone-induced relaxation of rabbit coronary arteries.