Una nueva etapa, nuevos desafíos para nuestra Revista Médica Universitaria

Fil: Miatello, Roberto M. . Universidad Nacional de Cuyo. Facultad de Ciencias Médica

La investigación en la formación médica

Fil: Renna, Nicolás F.. Universidad Nacional de Cuyo. Facultad de Ciencias MédicasFil: Miatello, Roberto M. . Universidad Nacional de Cuyo. Facultad de Ciencias Médica

XXIV Congreso Argentino de Hipertensión Arterial en Mendoza : abril de 2017

Fil: Renna, Nicolás F..Fil: Miatello, Roberto M.

Effects of Methotrexate on IL-6alphar, VCAM-1 and NF Kappa B Expression in a Rat Model of Metabolic Syndrome

Background: In this study, we used Methotrexate (Mtx) to examine the role of immunomodulation on the activation of IL-6 and VCAM-1, which could generate a microenvironment that supports cardiovascular remodelling.Methods: Male WKY and SHR rats were separated into five groups: Control, FFR: WKY rats receiving a 10% (w/v) fructose solution during all 12 weeks, SHR, FFHR: SHR receiving a 10% (w/v) fructose solution during all 12 weeks and FFHR+Mtx (0,3 mg/kg intraperitoneal one injection per day week for 6 weeks) (n = 8 per group). Metabolic variables and systolic blood pressure were measured. Cardiac and vascular remodelling was also evaluated. To assess this, IL-6R and VCAM-1 immunostaining techniques were used.Results: The FFHR experimental model developed metabolic syndrome, vascular and cardiac remodelling, and vascular inflammation because of increased expression of IL-6 and VCAM-1. Chronic treatment with Mtx completely or partiality reversed the variables studied.Conclusions: The results demonstrated an impact on immunomodulation after mtx treatment, which included a reduction in vascular inflammation and a favourable reduction in metabolic and structural parameters.Fil: Renna, Nicolas Federico. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Mendoza. Instituto de Medicina y Biología Experimental de Cuyo; Argentina. Universidad Nacional de Cuyo. Facultad de Ciencias Médicas; ArgentinaFil: Ramirez, Jésica M.. Universidad Nacional de Cuyo. Instituto de Genética; ArgentinaFil: García, Rodrigo Damián. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Mendoza. Instituto de Medicina y Biología Experimental de Cuyo; Argentina. Universidad Nacional de Cuyo. Facultad de Ciencias Médicas; ArgentinaFil: Diez, Emiliano Raúl. Universidad Nacional de Cuyo. Instituto de Genética; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Mendoza. Instituto de Medicina y Biología Experimental de Cuyo; ArgentinaFil: Miatello, Roberto Miguel. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Mendoza. Instituto de Medicina y Biología Experimental de Cuyo; Argentina. Universidad Nacional de Cuyo. Instituto de Genética; Argentin

La Revista Médica Universitaria crece…

Fil: Salomón, Susana Elsa. Universidad Nacional de Cuyo. Facultad de Ciencias MédicasFil: Miatello, Roberto M. . Universidad Nacional de Cuyo. Facultad de Ciencias Médica

Vascular smooth muscle cell NAD(P)H oxidase activity during the development of hypertension: Effect of angiotensin II and role of insulinlike growth factor-1 receptor transactivation

We investigated whether angiotensin II (Ang II)-induced reactive oxygen species (ROS) generation is altered in vascular smooth muscle cells (VSMCs) from spontaneously hypertensive rats (SHR) during the phases of prehypertension, developing hypertension, and established hypertension and assessed the putative role of insulinlike growth factor-1 receptor (IGF-1R) in Ang II-mediated actions. The VSMCs from SHR and Wistar-Kyoto rats (WKY) aged 4 (prehypertensive), 9 (developing hypertension), and 16 (established hypertension) weeks were studied. The ROS production and NAD(P)H oxidase activation were determined by fluorescence and chemiluminescence, respectively. The role of IGF-1R was assessed with the selective inhibitor AG1024. The ROS bioavailability was manipulated with Tiron (10-5 mol/L) and diphenylene iodonium (DPI) (10-6 mol/L). Angiotensin II dose dependently increased ROS production in WKY and SHR at all ages. The Ang II-induced responses were greater in SHR versus WKY at 9 and 16 weeks (P < .05). The Ang II-stimulated ROS increase was greater in 9- and 16-week-old SHR versus 4-week SHR (P < .05). These effects were reduced by AG 1024. Basal NAD(P)H oxidase activity was higher in VSMCs from 9-week-old SHR versus 4-week-old rats (P < .05). Angiotensin II induced a significant increase in oxidase activity in VSMCs from 9- and 16-week-old SHR (P < .001), without influencing responses in cells from 4-week-old SHR. Pretreatment of 9- and 16-week-old SHR cells with AG1024 reduced Ang II-mediated NAD(P)H oxidase activation (P < .05). Basal and Ang II-induced NAD(P)H-driven ROS generation are enhanced in VSMCs from SHR during development of hypertension, but not in cells from prehypertensive rats. Transactivation of IGF-1R by Ang II may be important in vascular oxidative excess in the development of hypertension in SHR.Fil: Cruzado, Montserrat Cecilia. Universidad Nacional de Cuyo; Argentina. Universidad de Mendoza; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Risler, Norma Raquel. Universidad Nacional de Cuyo; ArgentinaFil: Miatello, Roberto Miguel. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Mendoza. Instituto de Medicina y Biología Experimental de Cuyo; ArgentinaFil: Yao, Guoying. Institut de Recherches Cliniques de Montréal; CanadáFil: Schiffrin, Ernesto L.. Institut de Recherches Cliniques de Montréal; CanadáFil: Touyz, Rhian M.. Institut de Recherches Cliniques de Montréal; Canad

Antiarrhythmic mechanisms of Malbec wine and resveratrol in isolated rat heart

Oxidative stress during myocardial reperfusion contributes to ventricular arrhythmias onset. We aim to evaluate the antiarrhythmic effect of Malbec wine and resveratrol and compare them with the synthetic antioxidant tiron. Since alcohol use is controversial, we also assessed dealcoholized wine.Isolated hearts from male Sprague Dawley rats were perfused with Krebs-Henseleit solution added with: Malbec wine (5 ml/L), resveratrol (10 μM,) compared to controls with alcohol (0.5 ml/L); dealcoholized wine (5 ml/L), tiron (10 mM) were compared with controls without alcohol. Epicardial action potentials were analyzed during basal state, regional ischemia and reperfusion (10 minutes each period). The incidence of arrhythmias was determined. Te antioxidant effect was assessed in left ventricle homogenates and expressed as a percentage of inhibition of the ABTS?+ radical.Malbec wine and resveratrol reduced reperfusion arrhythmias in 56% and 50%, respectively, compared to 100% incidence in the control group with alcohol. Dealcoholized wine reduced arrhythmias to 50% compared to non-alcoholic control (90.5%), but tiron did not protect (69%). Te free radicals inhibitory effect increased with all the compounds (resveratrol 54.2%, tiron 43.2%, Malbec wine 42.9%, dealcoholized wine 40.2%) with respect to the control groups (with alcohol 23.5%, without alcohol 21.2%). Resveratrol shortened action potential duration and prevented ischemic depolarization. Malbec prevented ischemic-induced action potential shortening. We conclude that Malbec wine and resveratrol are antiarrhythmic beyond their antioxidant properties. Alcohol content or was not essential. Protection from ischemic action potential changes could be relevant to the antiarrhythmic effect of both resveratrol and wine.Fil: Prado, Natalia Jorgelina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Mendoza. Instituto de Medicina y Biología Experimental de Cuyo; ArgentinaFil: Perdicaro DJ. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Mendoza. Instituto de Medicina y Biología Experimental de Cuyo; ArgentinaFil: Parra, M. Universidad Nacional de Cuyo Facultad de Ciencias Médicas; ArgentinaFil: Carrión AM. Universidad Nacional de Cuyo Facultad de Ciencias Médicas; ArgentinaFil: Miatello RM. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Mendoza. Instituto de Medicina y Biología Experimental de Cuyo; ArgentinaFil: Renna NF. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Mendoza. Instituto de Medicina y Biología Experimental de Cuyo; ArgentinaFil: Ponce Zumino AZ. Universidad Nacional de Cuyo Facultad de Ciencias Médicas; ArgentinaFil: Vazquez Prieto M. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Mendoza. Instituto de Medicina y Biología Experimental de Cuyo; ArgentinaFil: Diez ER. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Mendoza. Instituto de Medicina y Biología Experimental de Cuyo; Argentin

Effects of dipeptidyl-peptidase 4 inhibitor about vascular inflammation in a metabolic syndrome model.

BACKGROUND: In this study, we used vidagliptin(V) to examine the role of the DDP-IV, incretin system component, in the activation of different molecular inflammatory cytokines, NF-kB and VCAM-1 to generate a microenvironment that supports cardiovascular remodeling. METHODS: Male WKY and SHR were separated into five groups: Control, FFR: WKY rats receiving a 10% (w/v) fructose solution during all 12 weeks, SHR, FFHR: SHR receiving a 10% (w/v) fructose solution during all 12 weeks and FFHR+V: (5 mg/kg per day for 6 weeks) (n = 8 each group). Metabolic variables and systolic blood pressure were measured. The TBRAS, eNOS activity, and NAD(P)H oxidase activity were estimated to evaluate oxidative stress. Cardiac and vascular remodeling were evaluated. To assess the cytokine, NF-kB and VCAM-1 immunostaining techniques were used. RESULTS: The FFHR experimental model presents metabolic syndrome criteria, vascular and cardiac remodeling, vascular inflammation due to increased expression of NF-kB, VCAM-1, and pro-atherogenic cytokines. Chronic treatment with V was able to reverse total or partiality of variables studied. CONCLUSIONS: Data demonstrated an important effect of DDP-IV in reducing vascular inflammation, accompanied by a favorable reduction in metabolic and structural parameters

Corrigendum to: Vascular Repair and Remodeling: A Review

Vascular remodeling is alterations in the structure of resistance vessels contributing to elevated systemic vascular resistance in hypertension. In this review, physiopathology of vascular remodeling is discussed, and the impact of antihypertensive drug treatment on remodeling is described, emphasizing on human data, fundamentally as an independent predictor of cardiovascular risk in hypertensive patients. Then we discussed a vascular repair by endothelial progenitor cells (EPCs) that play important roles in the regeneration of the vascular endothelial cells (ECs). The normal arterial vessel wall is mostly composed of ECs, vascular smooth muscle cells (VSMCs), and macrophages. Endothelial impairment is a major contributor to atherosclerosis and restenosis after percutaneous coronary intervention (PCI). Reendothelialization can effectively inhibit VSMC migration and proliferation and decrease neointimal thickening

Pathophysiology of Vascular Remodeling in Hypertension

Vascular remodeling refers to alterations in the structure of resistance vessels contributing to elevated systemic vascular resistance in hypertension. We start with some historical aspects, underscoring the importance of Glagov’s contribution. We then move to some basic concepts on the biomechanics of blood vessels and explain the definitions proposed by Mulvany for specific forms of remodeling, especially inward eutrophic and inward hypertrophic. The available evidence for the existence of remodeled resistance vessels in hypertension comes next, with relatively more weight given to human, in comparison with animal data. Mechanisms are discussed. The impact of antihypertensive drug treatment on remodeling is described, again with emphasis on human data. Some details are given on the three mechanisms to date which point to remodeling resistance arteries as an independent predictor of cardiovascular risk in hypertensive patients. We terminate by considering the potential role of remodeling in the pathogenesis of endorgan damage and in the perpetuation of hypertension