Manuel L Martí
University of Buenos Aires
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Featured researches published by Manuel L Martí.
British Journal of Pharmacology | 2003
G DiGirolamo; Mariana Farina; M L Riberio; D Ogando; J Aisemberg; A. R. De Los Santos; Manuel L Martí; A.M. Franchi
The therapeutic effect of nonsteroidal anti‐inflammatory drugs (NSAIDs) is thought to be due mainly to its inhibition of cyclooxygenase (COX) enzymes, but there is a growing body of research that now demonstrates a variety of NSAIDs effects on cellular signal transduction pathways other than those involving prostaglandins. Nitric oxide (NO) as a free radical and an agent that gives rise to highly toxic oxidants (peroxynitrile, nitric dioxide, nitron ion), becomes a cause of neuronal damage and death in some brain lesions such as Parkinson and Alzheimer disease, and Huntingtons chorea. In the present study, the in vivo effect of three NSAIDs (lysine clonixinate (LC), indomethacine (INDO) and meloxicam (MELO)) on NO production and nitric oxide synthase expression in rat cerebellar slices was analysed. Rats were treated with (a) saline, (b) lipopolysaccharide (LPS) (5 mg kg−1, i.p.), (c) saline in combination with different doses of NSAIDs and (d) LPS in combination with different doses of NSAIDs and then killed 6 h after treatment. NO synthesis, evaluated by Bred and Snyder technique, was increased by LPS. This augmentation was inhibited by coadministration of the three NSAIDs assayed. None of the NSAIDs tested was able to modify control NO synthesis. Expression of iNOS and neural NOS (nNOS) was detected by Western blotting in control and LPS‐treated rats. LC and INDO, but not MELO, were able to inhibit the expression of these enzymes. Therefore, reduction of iNOS and nNOS levels in cerebellum may explain, in part, the anti‐inflammatory effect of these NSAIDs and may also have importance in the prevention of NO‐mediated neuronal injury.
Current Therapeutic Research-clinical and Experimental | 1995
Luis María Cayetti; Antonio R. de los Santos; Manuel L Martí; Guillermo Di Girolamo; Viviana Niselman
Abstract Lysine clonixinate (2-[3-chloro-o-toluidine] piridin-3 lysine carboxylate) is a nonsteroidal anti-inflammator drug acting mainly at the peripheral level. Preclinical and clinical pharmacologic studies have established the efficacy and tolerability of lysine clonixinate—good efficacy with a very low incidence of side effects. The efficacy of lysine clonixinate was assessed in patients on days 0, 2, 7, and 15 by rating swelling, warmth, redness, and pain on active and passive movement and pressure. Tolerability was assessed by anamnesis at each control day and by fecal occult blood determination at baseline and at the end of the study. The anti-inflammatory and analgesic efficacy of lysine clonixinate was statistically higher than that of aspirin as assessed on almost all clinical parameters. The greater efficacy of lysine clonixinate was associated with excellent tolerability—none of the 53 lysine clonixinate-treated patients showed occult blood in the feces whereas 19 to the 55 aspirin-treated patients showed positive fecal occult blood at the end of the study.
Inflammopharmacology | 1999
A.M. Franchi; G. Di Girolamo; A. R. De LosSantos; Manuel L Martí; Martha A. F. Gimeno
Abstract—Lysine clonixinate (LC) is an anti-inflammatory, anti-pyretic and analgesic drug with minor digestive side effects, which might suggest a weak COX-1 inhibitor. The aim of this study focused on ex vivo effects of LC 40 mg/kg ip and indomethacin (INDO) 10 mg/kg ip in lung and stomach preparations of control rats and LPS-treated rats (5 mg/kg ip). The non-steroidal antiinflammatory drugs were administered concomitantly, following three hours and before one, two or three hours of LPS treatment. Tissues were weighed and incubated in 2 ml of Kress Ringer Bicarbonate buffer containing glucose (11 mM) under an atmosphere of 95% oxygen and 5% CO2. Approximately 200 mg of tissue were used for each determination; 0.25 μCi of 14C-arachidonic acid was added to each tube and the tissues were incubated for 60 min. Prostanoids were extracted from the incubation medium and separated by TLC. Results were expressed as a percentage of the total radioactivity of the plates (% of cpm on plate/100 mg ww). It was found that LC animals that were not given LPS did not modify the synthesis of PGE2; in lung and stomach tissues showing that did not inhibit COX-1 activity. However, LC inhibited clearly the synthesis of PGE2 in both preparations obtained from LPS-treated animals. The inhibition was shown when the rats were treated concomitantly, 3 h after or 1 or 2 h before the injection of LPS.
Current Therapeutic Research-clinical and Experimental | 1995
Daniel Rull; Guillermo Di Girolamo; Antonio R. de los Santos; Manuel L Martí
Abstract Diltiazem is a benzothiazepine calcium channel blocker with depressive activity on sinus and atrioventricular node fibers that is useful in the control of several types of arrhythmias. In an open-label uncontrolled trial, 34 patients with supraventricular tachyarrhythmias (15 with paroxysmal supraventricular tachycardia [PSVT], 17 with atrial fibrillation, and 2 with atrial flutter) were treated with diltiazem 150 μg/kg intravenous bolus once or repeated at the same dose within 20 and 40 minutes if the arrhythmia had not disappeared. Conversion to sinus rhythm was observed in 13 (86.7%) of 15 patients with PSVT, 4 (23.5%) of 17 patients with atrial fibrillation, and 1 (50.0%) of 2 patients with atrial flutter. Improvement or partial treatment success (ie, persistence of arrhythmia but with a ventricular rate lower than 100 beats/min) was observed in 8 patients with atrial fibrillation and 1 with atrial flutter. Five patients with atrial fibrillation and two with PSVT were considered to be treatment failures and received intravenous lanatoside C. No patient developed hypotension. Systolic and diastolic blood pressure increases averaged 10 mm Hg and were associated with hemodynamic improvement. Only four patients complained of transient headache and facial erythema after the first dose of diltiazem.
Prostaglandins Leukotrienes and Essential Fatty Acids | 2002
G. Di Girolamo; E Gonzalez; D. Livio; A. R. De Los Santos; Manuel L Martí; M.A.F. de Gimeno
Medicina-buenos Aires | 2001
Estela H Kramer; Beatriz Sasseti; Alfredo J Kaminker; Antonio R. de los Santos; Manuel L Martí; Guillermo Di Girolamo
Prensa médica argentina | 1998
G. Nasswetter; A. R. De Los Santos; Manuel L Martí; G. Di Girolamo
Nitric Oxide | 2001
A.M. Franchi; G. Di Girolamo; Mariana Farina; A. R. De Los Santos; Manuel L Martí; Martha A. F. Gimeno
Medicina-buenos Aires | 2001
Manuel L Martí
Methods and Findings in Experimental and Clinical Pharmacology | 1999
R. Baistrocchi; A. R. De Los Santos; G. Di Girolamo; Manuel L Martí; J. Pico