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Biomedical subjects

J M Rico

Publications and source records attributed to J M Rico.

13 recordsLinked to original sources

The influence of vacuum mixing on methylmethacrylate liberation from acrylic cement powder.

Polymethylmethacrylate (PMMA) bone cement is a biomaterial used to anchor prostheses during joint replacement surgery. Residual methylmethacrylate monomer (MMA) may be related with the cytotoxic effect of PMMA. The aim of the present paper was to investigate the effect of two different cement mixing methods: hand stirring at atmospheric pressure and under partial vacuum (0.330 and 0.154 bar) on residual monomer liberation in phosphate buffer saline solution from acrylic cement powder. Residual MMA content was determined by high-performance liquid chromatography. Mathematical models were applied to experimental dissolution data revealing that monomer release was significantly reduced in bone cement powder obtained at 0.154 bar vacuum pressure compared to the other mixing conditions. The kinetic models applied are consistent with a simple diffusion mechanism of the monomer from the polymer matrix.

Acrylates↗

In vitro release studies of methylmethacrylate liberation from acrylic cement powder.

Bone cement or polymethylmethacrylate (PMMA) is commonly used for anchoring cemented prosthesis to the bone. Cytotoxic effect of culture media exposed to PMMA powder may be related with long term problems associated with acrylic cement application, being the monomer (methylmethacrylate) one of the cement's component partly responsible for the cytotoxic effect. The present work reports the studies of monomer release from acrylic bone cement powder under different experimental conditions: setting time of PMMA (in solution and air) and different culture media composition. High-performance liquid chromatography was used for the determination of residual monomer. Mathematical models were applied to experimental dissolution data revealing that monomer release is lightly affected by the studied variables. The monomer release seems to be a surface phenomena, suggesting that the possible actions of monomer will mainly be due to the initial loss of non polymerized monomer rather than to further depolymerization of the already polymerized cement.

Bone Cements↗

Dietary beta-adrenoceptor agonists have a persistent effect on nitric oxide synthesis in rat cultured smooth muscle cells.

Several compounds including lipopolysaccharide and sympathomimetics stimulate the expression of the inducible nitric oxide synthase in vascular smooth muscle cells. We evaluated the effect of clenbuterol on nitric oxide (NO) production by vascular smooth muscle cells of the rat aorta in culture. Wistar rats were divided into three diet groups (control, clenbuterol and washout). Aortic vascular smooth muscle cells from rats from these 3 diet groups were cultured in the presence and absence of lipopolysaccharide and/or beta-adrenoceptor agonists. NO release was measured by Griess reagent. Clenbuterol or salbutamol added to cells from control rats potentiated lipopolysaccharide-induced NO release. Cells from rats fed on clenbuterol, in a medium without beta-adrenoceptor agonists, showed a similar potentiation, even after a 10-day washout period. The addition of beta-adrenoceptor agonists to the latter cells did not increase NO production. NG-Nitro-L-arginine decreased nitrite production in lipopolysaccharide-stimulated cells. Our results demonstrate that dietary clenbuterol has a persistent 'ex vivo' effect on lipopolysaccharide-induced NO production by cultured vascular smooth muscle cells.

Adrenergic beta-Agonists↗

DL-propranolol augments production of NO induced by cytokines in cultured aortic smooth muscle of the rat.

The effect of DL-propranolol on the production of nitric oxide (NO.) by cultured arterial smooth muscle cells from normotensive (WKY) and spontaneously hypertensive rats (SHR) was studied before and after stimulation by lipopolysaccharide or interleukin-1 beta. The influence of L-arginine and NG-nitro-L-arginine on these events was also studied. Lipopolysaccharide-stimulated SHR-derived smooth muscle cells produced less NO. than WKY cells. However the amounts produced in response to interleukin-1 beta were similar for the two cell types. DL-propranolol increased the NO. production in both types of cells exposed to lipopolysaccharide, but had no significant effect on this parameter in WKY-derived cells exposed to interleukin-1 beta. Inclusion of L-arginine during incubations with propranolol had no effect on the levels of NO. produced by either cell type exposed to lipopolysaccharide. The basal production of NO. was enhanced in smooth muscle cells from both normotensive and hypertensive rats when the cells were treated with L-arginine after exposure to interleukin-1 beta. L-Arginine increased the response to DL-propranolol only in the WKY cells. NO. production was depressed by inclusion of NG-nitro-L-arginine during incubations in both cell types regardless of the treatment regime used to induce NO. synthase activity. The results suggest that DL-propranolol may induce the production of NO. by cultured smooth muscle cells exposed to cytokines.

Animals↗

Effect of Ca2+ modulators on acetylcholine-induced phasic and tonic contractions and A23187-induced contractions in ileal longitudinal muscle and IP3 production.

The influence of different sources of Ca2+ on the Emax and ED50 values of acetylcholine (ACh)-induced phasic and tonic contractions and on A23187-induced contractions was studied using different extracellular Ca2+ concentrations ([Ca2+]o) and the Ca2+ modulators TMB-8 and D600. IP3 production induced by both stimulants was also studied. The results are compatible with: (a) the mobilization of Ca2+ from an intracellular source as a primary event in the phasic response. (b) The primary involvement of a D600-sensitive inward Ca2+ current in the ACh-tonic response. (c) An inward D600-sensitive Ca2+ current associated with the ionophore transported ion. (d) The involvement of an IP3 independent, TMB-8 sensitive mechanism of Ca2+ mobilization involved in the A23187-induced responses.

Acetylcholine↗

[Left atrial thrombus. Its evolution with oral anticoagulation].

UNLABELLED: Left ventricular thrombi were found in 25 patients by two-dimensional echocardiography. All patients were in atrial fibrillation, 16 had mitral or mitroaortic valve diseases and nine mitral or mitroaortic bioprosthetic valves. Nine patients (36%) had history of arterial embolism. At diagnostic time, oral anticoagulation with coumadin was instaured in all the patients. Periodic clinic and echocardiography follow-up was performed. Left atrial thrombi either disappeared (18 patients [72%]) or reduced their size (one patient). Six patients with mitral stenosis were considered as candidates to percutaneous mitral valvuloplasty, which was performed in 4 patients whose thrombi disappeared with anticoagulation therapy in 6 months. During the follow-up one patient had cerebral embolism without sequelae. CONCLUSIONS: 1st. Patients with left atrial thrombi have high risk for arterial embolism. 2nd. Left atrial thrombi disappear in a high proportion after prescribing oral anticoagulation, which has some important therapeutic implications.

Administration, Oral↗

The effect of strontium on the drug-receptor interaction on cholinergic drugs.

The effect of replacing calcium with strontium in the perfusion fluid was qualitatively and quantitatively studied in the isolated longitudinal muscle of the guinea-pig ileum. In the presence of strontium hyoscine could be considered a competitive antagonist of acetylcholine for the acetylcholine receptor of the longitudinal muscle of the guinea-pig ileum; dibenamine still blocked this receptor in an irreversible way. The equilibrium constants for acetylcholine (KA) and hyoscine (KI) were obtained in the presence of calcium (KA = 3.16 +/- 0.63 microM; KI = 0.38 +/- 0.07 nM), and strontium (KA = 7.00 +/- 0.89 microM; KI = 0.93 +/- 0.16 nM). The results show a decrease in the affinity of both drugs for the muscarinic receptor in the presence of strontium.

Acetylcholine↗

Modification by indomethacin of the blood pressure lowering effect of pindolol and propranolol in conscious rabbits.

In conscious rabbits, the intravenous administration of pindolol (0.125 mg/kg) and propranolol (1 mg/kg) induced a highly significant (p less than 0.001) decrease of mean arterial blood pressure and with propranolol, a significant (p less than 0.01) bradycardia. In the same model the intravenous administrtion of saline (1 ml/kg) and of indomethacin (1 mg/kg) did not affect mean arterial blood pressure or heart rate (p greater than 0.3). Pretreatment of the animals with indomethacin (1 mg/kg) abolished the effect of both beta-blockers on mean arterial blood pressure (p greater than 0.05) and had no significant effect on heart rate.

Animals↗