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La resolvina-D1 previene el remodelamiento cardíaco e hipertensión inducidos por angiotensina II y atenúa la inflamación cardíaca
(Universidad de Chile, 2021)
Introducción: A pesar del arsenal farmacológico disponible para tratar la hipertensión (HTA), los pacientes crónicos pueden desarrollar remodelado cardíaco irreversible y fibrosis. Dentro de los gatillantes de HTA se encuentran las enfermedades...
Introduction: Despite the pharmacological arsenal available to treat hypertension (HBP), chronic patients may develop irreversible cardiac remodeling and fibrosis. Among the triggers of HBP are metabolic diseases, cellular aging and hormonal dysregulation. In the latter context, Angiotensin II (Ang II) regulates the hemodynamics of the circulatory system, maintaining the volume and homeostasis of the cardiovascular system. However, chronic and exacerbated Ang II activity results in inflammation in blood vessels and heart tissue, increased preload, blood pressure, and cardiac remodeling, leading to irreversible heart failure. Resolvin-D1 (RvD1) belongs to the family of autacoid lipids with potent anti-inflammatory and pro-resolution effects in diverse in vitro and in vivo cardiovascular pathological models, such as myocardial infarction, ischemia/reperfusion and aortic stenosis, preventing the recruitment of leukocytes, expression of inflammation markers and cardiac fibrosis. However, to date no studies have yet been conducted evaluating the protective effects of RvD1 against chronic damage caused by HBP. Hence, we set out to evaluate such effects in an Ang II infusion HBP model. Methods: Ang-II (Ang II, 1.5 mg/kg/day) was infused into male C57BL/6 mice via Alzet® mini osmotic pumps for 7 or 14 days, along with the administration of Resolvin-D1 (RvD1, 3 μg/kg/day, ip) one day after surgery and during the infusion period. Blood pressure and functional parameters were evaluated by echocardiography. At the end of the experimental periods, tissues were harvested and histological parameters were studied by immunohistochemistry and plasma cytokines using LUMINEX. Results: RvD1 decreased the cardiac infiltration of neutrophils and granulation tissue formation induced by Ang II at 7 and 14 days; the expression of cardiac ICAM-1 and VCAM-1; the increase in plasmatic levels of IL-1β, TNF-α, IL-6, KC, MCP-1 while IL-10 was increased at both times of infusion. In addition, RvD1 was able to prevent left ventricular and cardiomyocyte hypertrophy, interstitial and perivascular fibrosis, and systolic and diastolic hypertension. In summary, this study reveals new cardioprotective effects of RvD1 on Ang II-induced hypertension and cardiac remodeling, providing novel information on a possible therapeutic application...
Introduction: Despite the pharmacological arsenal available to treat hypertension (HBP), chronic patients may develop irreversible cardiac remodeling and fibrosis. Among the triggers of HBP are metabolic diseases, cellular aging and hormonal dysregulation. In the latter context, Angiotensin II (Ang II) regulates the hemodynamics of the circulatory system, maintaining the volume and homeostasis of the cardiovascular system. However, chronic and exacerbated Ang II activity results in inflammation in blood vessels and heart tissue, increased preload, blood pressure, and cardiac remodeling, leading to irreversible heart failure. Resolvin-D1 (RvD1) belongs to the family of autacoid lipids with potent anti-inflammatory and pro-resolution effects in diverse in vitro and in vivo cardiovascular pathological models, such as myocardial infarction, ischemia/reperfusion and aortic stenosis, preventing the recruitment of leukocytes, expression of inflammation markers and cardiac fibrosis. However, to date no studies have yet been conducted evaluating the protective effects of RvD1 against chronic damage caused by HBP. Hence, we set out to evaluate such effects in an Ang II infusion HBP model. Methods: Ang-II (Ang II, 1.5 mg/kg/day) was infused into male C57BL/6 mice via Alzet® mini osmotic pumps for 7 or 14 days, along with the administration of Resolvin-D1 (RvD1, 3 μg/kg/day, ip) one day after surgery and during the infusion period. Blood pressure and functional parameters were evaluated by echocardiography. At the end of the experimental periods, tissues were harvested and histological parameters were studied by immunohistochemistry and plasma cytokines using LUMINEX. Results: RvD1 decreased the cardiac infiltration of neutrophils and granulation tissue formation induced by Ang II at 7 and 14 days; the expression of cardiac ICAM-1 and VCAM-1; the increase in plasmatic levels of IL-1β, TNF-α, IL-6, KC, MCP-1 while IL-10 was increased at both times of infusion. In addition, RvD1 was able to prevent left ventricular and cardiomyocyte hypertrophy, interstitial and perivascular fibrosis, and systolic and diastolic hypertension. In summary, this study reveals new cardioprotective effects of RvD1 on Ang II-induced hypertension and cardiac remodeling, providing novel information on a possible therapeutic application...
Modelo de negocio para un emprendimiento de apoyo al automanejo de pacientes con hipertensión arterial y/o diabetes mellitus
(Universidad de Chile, 2022)
El presente trabajo de título tiene como objetivo diseñar un modelo de negocios para un emprendimiento que busca apoyar el automanejo de pacientes con hipertensión arterial y/o diabetes mellitus en Chile mediante una plataforma tecnológica. Validado...
How far should blood pressure be lowered in essential hypertension to optimize the results? A qué niveles bajar la presión arterial en la hipertensión esencial para optimizar el resultado?
(1995)
How far should blood pressure be lowered in essential hypertension to optimize
the results? A qué niveles bajar la presión arterial en la hipertensión esencial
para optimizar el resultado?
Román,
Early studies...
Etiopathogenic factors of arterial hypertension Factores en la etiopatogenia de la hipertensión arterial.
(1992)
Etiopathogenic factors of arterial hypertension Factores en la etiopatogenia de
la hipertensión arterial.
Pérez-Olea,
High blood pressure of unknown etiology has been related to many pathogenetic factors, mainly
dietary...
Regression of left ventricular hypertrophy in essential arterial hypertension Reversión de la hipertrofia ventricular izquierda en la hipertensión arterial esencial.
(1994)
Regression of left ventricular hypertrophy in essential arterial hypertension
Reversión de la hipertrofia ventricular izquierda en la hipertensión arterial
esencial.
Román,
The classic concept of a direct pathogenic...
Nuevas perspectivas en el manejo de la hipertensión
(Sociedad Médica de Santiago, Chile, 2021)
Estudio preliminar sobre neuralgia esencial del trigémino en relación a hipertensión arterial.
(Universidad de Chile, 2005)
Sobrevida en hipertensión pulmonar
(Soc. Médica Santiago, 2016)
827
EDITORIAL
Rev Med Chile 2016; 144: 827-828
Sobrevida en hipertensión pulmonar
Mónica Zagolín Blancaire
Pulmonary hypertension survival
Departamento de Medicina Oriente,
Facultad de Medicina, Universidad de
Chile...
promedio de 2,8 años para los pacientes con hipertensión pulmonar idiopática (HAPI), en aquel entonces llamada HP primaria (PPH), se ha recorrido un extenso camino hasta la década actual en que registros como el francés con 354 pacientes, diferenciando...
promedio de 2,8 años para los pacientes con hipertensión pulmonar idiopática (HAPI), en aquel entonces llamada HP primaria (PPH), se ha recorrido un extenso camino hasta la década actual en que registros como el francés con 354 pacientes, diferenciando...
Acceso a medicamentos en chile: impacto de las GES y el FOFAR sobre el acceso a los medicamentos asociados a diabetes, dislipidemia e hipertensión
(Universidad de Chile, 2022)
Objetivo: evaluar el impacto de las GES sobre el acceso, por parte de los beneficiarios del
FONASA y las ISAPRE, a medicamentos asociados al tratamiento de la hipertensión y la
diabetes en Chile, y del FOFAR, por parte de los beneficiarios del...
Efecto del tratamiento antipurinérgico específico para el receptor p2y14 en la función cardiorrespiratoria y sobrevida en un modelo de ratas con hipertensión arterial pulmonar
(Universidad de Chile, 2021)
rata con Hipertensión Arterial Pulmonar. Se utilizaron tres
grupos de animales, un grupo de ratas sanas, un grupo de ratas HAP y un grupo de ratas HAP
tratadas con PPTN (un inhibidor específico del receptor P2Y14). Comparamos la masa del VD,
las...
Pulmonary arterial hypertension (PAH) is a chronic cardiopulmonary, progressive and mortal disease. PAH is presented with unspecific symptoms which leads to a delay in diagnosis and optimal therapy. Idiopathic PAH is characterized by an inflammatory process that generates obstruction and obliteration of the pulmonary vascular lumen, generating an increase in pulmonary vascular resistance, as consequence, right ventricle (RV) hypertrophy and dilation is generated, producing loss of cardiorespiratory capacity and low survival rates. The activation of the P2Y14 purinergic receptor is an important factor to induce expression of inflammatory genes, recruitment of neutrophils and vascular remodeling. Current PAH treatments are not specifically target to the cause of the PAH, such as vascular remodeling and inflammation. For that reason, the objective of this study was to evaluate the effect of specific antipurinergic treatment for the P2Y14 receptor on cardiorespiratory function in a PAH rat model. Three groups of animals was used, a group of healthy rats, a group of PAH rats and a group of PAH rats treated with PPTN (an specific P2Y14 receptor inhibitor), to evaluate the cardiorespiratory function. We compared RV mass, echocardiographic variables, cardiorespiratory capacity and survival. Our results indicate that the echocardiographic variable pulmonary artery aceleration time (PAAT) diminished significantly at the fourth week in PAH animals, but not in PAH+PPTN group. On the other hand, the cardiorespiratory capacity decreased we at the fourth week in the PAH and PAH+PPTN animals test. The survival in PAH and PAH+PPTN rats was lower than control rats and also a significant increase in RV mass in PAH and PAH+PPTN rats was observed We concluded that the PPTN treatment achieved a delay in the PAH progression in rats. However, PPTN did not improve cardiorespiratory function or survival in a PAH rat model. We suggest to explore another way of administration and also other dosis of the PPTN to determine the inflammatory parameters impact of the rats....
Pulmonary arterial hypertension (PAH) is a chronic cardiopulmonary, progressive and mortal disease. PAH is presented with unspecific symptoms which leads to a delay in diagnosis and optimal therapy. Idiopathic PAH is characterized by an inflammatory process that generates obstruction and obliteration of the pulmonary vascular lumen, generating an increase in pulmonary vascular resistance, as consequence, right ventricle (RV) hypertrophy and dilation is generated, producing loss of cardiorespiratory capacity and low survival rates. The activation of the P2Y14 purinergic receptor is an important factor to induce expression of inflammatory genes, recruitment of neutrophils and vascular remodeling. Current PAH treatments are not specifically target to the cause of the PAH, such as vascular remodeling and inflammation. For that reason, the objective of this study was to evaluate the effect of specific antipurinergic treatment for the P2Y14 receptor on cardiorespiratory function in a PAH rat model. Three groups of animals was used, a group of healthy rats, a group of PAH rats and a group of PAH rats treated with PPTN (an specific P2Y14 receptor inhibitor), to evaluate the cardiorespiratory function. We compared RV mass, echocardiographic variables, cardiorespiratory capacity and survival. Our results indicate that the echocardiographic variable pulmonary artery aceleration time (PAAT) diminished significantly at the fourth week in PAH animals, but not in PAH+PPTN group. On the other hand, the cardiorespiratory capacity decreased we at the fourth week in the PAH and PAH+PPTN animals test. The survival in PAH and PAH+PPTN rats was lower than control rats and also a significant increase in RV mass in PAH and PAH+PPTN rats was observed We concluded that the PPTN treatment achieved a delay in the PAH progression in rats. However, PPTN did not improve cardiorespiratory function or survival in a PAH rat model. We suggest to explore another way of administration and also other dosis of the PPTN to determine the inflammatory parameters impact of the rats....