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Rich Plasma (rich + plasma)
Selected AbstractsUse of a collagen-platelet rich plasma scaffold to stimulate healing of a central defect in the canine ACLJOURNAL OF ORTHOPAEDIC RESEARCH, Issue 4 2006Martha M. Murray Abstract The anterior cruciate ligament (ACL) of the knee fails to heal after primary repair. Here we hypothesize that a beneficial biologic repair response can be induced by placing a collagen-platelet rich plasma (collagen-PRP) material into a central ACL defect. A collagen-PRP scaffold was used to treat a central ACL defect in vivo. In the first experiment, the histologic response in treated and untreated defects was evaluated at 3 (n,=,5) and 6 weeks (n,=,5). In the second experiment, biomechanical testing of the treated ligaments (n,=,8) was performed at 6 weeks and compared with the results of biomechanical testing of untreated defects at the same time-point (n,=,6). The percentage filling of the defects in the treated ACLs was significantly higher at both the 3- and 6-week time-points when compared with the untreated contralateral control defects (50,±,21% vs. 2,±,2% at 3 weeks, and 43,±,11% vs. 23,±,11 at 6 weeks; all values mean,±,SEM. Biomechanically, the treated ACL defects had a 40% increase in strength at 6 weeks, which was significantly higher than the 14% increase in strength previously reported for untreated defects (p,<,0.02). Placement of a collagen-PRP bridging scaffold in a central ACL defect can stimulate healing of the ACL histologically and biomechanically. © 2006 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 24:820,830, 2006 [source] In Vitro and In Vivo Study of Ion-Implanted Collagen for the Substrate of Small Diameter Artificial GraftsARTIFICIAL ORGANS, Issue 6 2003Kimi Kurotobi Abstract: Ion implantation into the collagen-coated inner surface of the grafts was performed and evaluated in vitro and in vivo to develop small diameter artificial vascular grafts. He+ ion implanted collagen-coated grafts with a fluence of 1 × 1014 ions/cm2 inhibited platelet adhesion and demonstrated patency for 240 days in an animal study. The platelet adhesion test using platelet rich plasma (PRP) showed antithrombogenicity at the fluence of 1 × 1014 ions/cm2. Washed platelet adhesion test showed thrombus formation at the fluence of 1 × 1014 ions/cm2. The results suggested that plasma protein adsorption onto the ion-implanted collagen significantly improved performance of these synthetic grafts. [source] Inhibition of human platelet aggregation by a novel S-nitrosothiol is abolished by haemoglobin and red blood cells in vitro: implications for anti-thrombotic therapyBRITISH JOURNAL OF PHARMACOLOGY, Issue 7 2000Ian L Megson S-Nitrosothiols are nitric oxide (NO) donor drugs that have been shown to inhibit platelet aggregation in platelet rich plasma (PRP) in vitro and to inhibit platelet activation in vivo. The aim of this study was to compare the platelet effects of a novel S-nitrosated glyco-amino acid, RIG200, with an established S-nitrosothiol, S-nitrosoglutathione (GSNO) in PRP, and to investigate the effects of cell-free haemoglobin and red blood cells on S-nitrosothiol-mediated inhibition of platelet aggregation. The effects of GSNO and RIG200 in collagen (2.5 ,g ml,1)-induced platelet aggregation in PRP and whole blood were investigated in vitro. Both compounds were found to be powerful inhibitors of aggregation in PRP, and RIG200 was significantly more potent (IC50=2.0 ,M for GSNO and 0.8 ,M for RIG200; P=0.04). Neither compound inhibited aggregation in whole blood, even at concentrations of 100 ,M. Red blood cell concentrations as low as 1% of the haematocrit, and cell-free haemoglobin (2.5 ,M), significantly reduced their inhibitory effects on platelets. Experiments involving measurement of cyclic GMP levels, electrochemical detection of NO and electron paramagnetic resonance of haemoglobin in red blood cells, indicated that scavenging of NO generated from S-nitrosothiols by haemoglobin was responsible for the lack of effect of S-nitrosothiols on platelets in whole blood. These studies suggest that scavenging of NO by haemoglobin in blood might limit the therapeutic application of S-nitrosothiols as anti-platelet agents. British Journal of Pharmacology (2000) 131, 1391,1398; doi:10.1038/sj.bjp.0703731 [source] Isosorbide dinitrate inhibits platelet adhesion and aggregation in nonthrombolyzed patients with acute myocardial infarctionCLINICAL CARDIOLOGY, Issue 11 2000Jadwiga Gebalska M.D., Ph.D. Abstract Background: Apart from their vasodilatator properties, nitrates have been shown to inhibit platelet aggregation. The effects of nitrates on platelet adhesion have not been studied. Nonselected patients with acute myocardial infarction (AMI) have been suggested to gain no benefit from administration of nitrates. However, the importance of nitrates may be greater in a subgroup of nonthrombolyzed patients with AMI. Hypothesis: Isosorbide dinitrate (ISDN) decreases platelet adhesion and aggregation in nonthrombolyzed patients with AMI. Methods: Consecutive 48 men with AMI, not eligible for thrombolytic therapy because of late presentation (> 12 h), were prospectively randomized 2:1 to double-blind ISDN (mean dose 2.4 ± 0.9 mg/h) (n = 33) or placebo (0.9% sodium chloride) (n = 15) infusion. All patients received aspirin. Blood samples were taken at baseline (no study medication) and 3 h into ISDN or placebo infusion. Platelet adhesion to collagen was measured in the ethylene diamine tetraacetic acid (EDTA)-platelet rich plasma by recording changes in light transmission with an optical aggregometer. Platelet aggregation was measured using the Born's method. Results: Isosorbide dinitrate significantly decreased both platelet adhesion and aggregation. No effect was seen in the placebo group. Conclusions: In patients with AMI who do not receive thrombolytic therapy, ISDN effectively inhibits platelet adhesion and aggregation. These effects of nitrates may be of therapeutic and prognostic significance in this group of patients. [source] | ||||||||||