<?xml version="1.0" encoding="ISO-8859-1"?><article xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance">
<front>
<journal-meta>
<journal-id>2696-130X</journal-id>
<journal-title><![CDATA[Revista mexicana de angiología]]></journal-title>
<abbrev-journal-title><![CDATA[Rev. mex. angiol.]]></abbrev-journal-title>
<issn>2696-130X</issn>
<publisher>
<publisher-name><![CDATA[Sociedad Mexicana de Angiología, Cirugía Vascular y Endovascular A.C.]]></publisher-name>
</publisher>
</journal-meta>
<article-meta>
<article-id>S2696-130X2020000100017</article-id>
<article-id pub-id-type="doi">10.24875/rma.m20000009</article-id>
<title-group>
<article-title xml:lang="es"><![CDATA[Modelo experimental biológico y molecular de fuerza tensional para el estudio fisiopatológico de la hiperplasia intimal venosa]]></article-title>
<article-title xml:lang="en"><![CDATA[Experimental biological and molecular model of tensile strength for the pathophysiological study of intimal venous hyperplasia]]></article-title>
</title-group>
<contrib-group>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Laparra-Escareño]]></surname>
<given-names><![CDATA[Hugo]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Ortega-Gómez]]></surname>
<given-names><![CDATA[Alette]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Ventura-Gallegos]]></surname>
<given-names><![CDATA[José L.]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Zentella-Dehesa]]></surname>
<given-names><![CDATA[Alejandro]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Santamaría-del Angel]]></surname>
<given-names><![CDATA[Abel]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Hinojosa]]></surname>
<given-names><![CDATA[Carlos A.]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
</contrib-group>
<aff id="Af1">
<institution><![CDATA[,Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán Departamento de Cirugía Vascular ]]></institution>
<addr-line><![CDATA[Ciudad de México ]]></addr-line>
<country>México</country>
</aff>
<aff id="Af2">
<institution><![CDATA[,Instituto Nacional de Cancerología Laboratorio de Medicina Traslacional ]]></institution>
<addr-line><![CDATA[Ciudad de México ]]></addr-line>
<country>México</country>
</aff>
<aff id="Af3">
<institution><![CDATA[,Universidad Nacional Autónoma de México Instituto de Investigaciones Biomédicas ]]></institution>
<addr-line><![CDATA[Ciudad de México ]]></addr-line>
<country>México</country>
</aff>
<aff id="Af4">
<institution><![CDATA[,Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán Unidad de Bioquímica ]]></institution>
<addr-line><![CDATA[Ciudad de México ]]></addr-line>
<country>México</country>
</aff>
<aff id="Af5">
<institution><![CDATA[,Instituto Nacional de Neurología y Neurocirugía Laboratorio de Aminoácidos ]]></institution>
<addr-line><![CDATA[Ciudad de México ]]></addr-line>
<country>México</country>
</aff>
<pub-date pub-type="pub">
<day>00</day>
<month>03</month>
<year>2020</year>
</pub-date>
<pub-date pub-type="epub">
<day>00</day>
<month>03</month>
<year>2020</year>
</pub-date>
<volume>48</volume>
<numero>1</numero>
<fpage>17</fpage>
<lpage>23</lpage>
<copyright-statement/>
<copyright-year/>
<self-uri xlink:href="http://www.scielo.org.mx/scielo.php?script=sci_arttext&amp;pid=S2696-130X2020000100017&amp;lng=en&amp;nrm=iso"></self-uri><self-uri xlink:href="http://www.scielo.org.mx/scielo.php?script=sci_abstract&amp;pid=S2696-130X2020000100017&amp;lng=en&amp;nrm=iso"></self-uri><self-uri xlink:href="http://www.scielo.org.mx/scielo.php?script=sci_pdf&amp;pid=S2696-130X2020000100017&amp;lng=en&amp;nrm=iso"></self-uri><abstract abstract-type="short" xml:lang="es"><p><![CDATA[Resumen  Objetivo: La hiperplasia intimal del endotelio venoso es una de las principales causas de trombosis en reconstrucciones vasculares. Este proceso patológico se define como la respuesta celular y molecular caracterizada por una proliferación anormal de células musculares lisas. Se ha descrito una asociación importante de la hiperplasia intimal con señales tróficas, algunas asociadas a factores de crecimiento como el factor de crecimiento derivado de plaquetas. Dichos mecanismos iniciadores aún no han sido bien caracterizados a nivel molecular. La hiperplasia intimal generalmente incluye la presencia de células de músculo liso alfa-actina positivas, matriz extracelular, componentes celulares inflamatorios como macrófagos, leucocitos y una amplia variedad de mediadores y citocinas. El objetivo de este estudio fue desarrollar un modelo experimental para el estudio de la fisiopatología de la hiperplasia intimal venosa en los primeros 7 días.  Métodos: Nuestro estudio incluyó 12 conejos. A 6 de estos se les realizó una lesión inducida mediante angioplastia con balón en la vena femoral (fuerza tensional por barotrauma), los restantes fueron controles.  Resultados: Utilizando un modelo de lesión tensional venosa por medio de barotrauma pudimos reproducir los eventos detonantes de las primeras fases en el desarrollo de la hiperplasia intimal venosa. Estos cambios se reflejaron a nivel sistémico e histopatológico.  Conclusiones: La experiencia del manejo del conejo como modelo experimental cumplió las expectativas técnicas para la evaluación de la fisiopatología de la hiperplasia intimal venosa y esto aunado a la ausencia de complicaciones (0% de mortalidad, 0% de morbilidad).]]></p></abstract>
<abstract abstract-type="short" xml:lang="en"><p><![CDATA[Abstract  Objective: Intimal venous endothelial hyperplasia is one of the main causes of thrombosis in vascular reconstructions. This pathological process is defined as the cellular and molecular response characterized by an abnormal proliferation of smooth muscle cells. An important association of intimal hyperplasia with trophic signals has been described, some associated with growth factors such as growth factor derived from platelet-derived growth factor platelets. Such initiating mechanisms have not yet been well characterized. Intimal hyperplasia generally includes the presence of alpha-actin positive smooth muscle cells, extracellular matrix, inflammatory cellular components such as macrophages, leukocytes and a wide variety of mediators and cytokines. The objective of this study was to develop an experimental model for the study of the pathophysiology of venous intimal hyperplasia in the first 7 days.  Methods: Our study included 12 rabbits. 6 of these patients underwent an injury by balloon angioplasty in the femoral vein (tension force by barotrauma), the remaining were controls.  Results: Using a model of endothelial lesion through barotrauma, we were able to reproduce the detonating events of the early stages in the development of venous intimal hyperplasia. These changes were reflected at the systemic and histopathological level.  Conclusions: The experience of rabbit management as an experimental model met the technical expectations for the evaluation of the pathophysiology of venous intimal hyperplasia and this coupled with the absence of complications (0% mortality, 0% morbidity).]]></p></abstract>
<kwd-group>
<kwd lng="es"><![CDATA[Hiperplasia intimal]]></kwd>
<kwd lng="es"><![CDATA[PDGF]]></kwd>
<kwd lng="es"><![CDATA[Modelo de lesión tensional]]></kwd>
<kwd lng="es"><![CDATA[Vascular]]></kwd>
<kwd lng="es"><![CDATA[Endotelio venoso]]></kwd>
<kwd lng="en"><![CDATA[Intimal hyperplasia]]></kwd>
<kwd lng="en"><![CDATA[Platelet-derived growth factor]]></kwd>
<kwd lng="en"><![CDATA[Tension force]]></kwd>
<kwd lng="en"><![CDATA[Barotrauma]]></kwd>
<kwd lng="en"><![CDATA[Venous endothelium]]></kwd>
</kwd-group>
</article-meta>
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