Examinando por Materia "Endothelial dysfunction"
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- PublicaciónAcceso abiertoAppropriate prenatal care system : The best way to prevent preeclampsia in Andean countries(2009-04) Lopez-Jaramillo, Patricio; García, Ronald G.; Reyes, Laura M.; Ruiz, Silvia L.The main cause of maternal mortality in Colombia is preeclampsia; even though it is a major public health problem its etiology and physiopathology remain unknown. However it is believed that endothelial dysfunction plays a central role in the development of this disease. Many clinical trials have been carried out to demonstrate the effect of certain interventions to prevent preeclampsia and improve pregnancy outcomes. Our hypothesis is that the reduction of preeclampsia risk could be achieved through an appropriate health system that would provide an opportune and effective prenatal care to pregnant women allowing early diagnosis and treatment of frequent nutritional and health related problems.
- PublicaciónAcceso abiertoObesity and Preeclampsia. Common Pathophysiological Mechanisms(Frontiers in Physiology, 2018-12-19) Lopez-Jaramillo, Patricio; Barajas, Juan; Rueda-Quijano, Sandra M.; Lopez-Lopez, Cristina; Felix, Camilo; MasiraPreeclampsia is a disorder specific of the human being that appears after 20 weeks of pregnancy, characterized by new onset of hypertension and proteinuria. Abnormal placentation and reduced placental perfusion associated to impaired trophoblast invasion and alteration in the compliance of uterine spiral arteries are the early pathological findings that are present before the clinical manifestations of preeclampsia. Later on, the endothelial and vascular dysfunction responsible of the characteristic vasoconstriction of preeclampsia appear. Different nutritional risk factors such as a maternal deficit in the intake of calcium, protein, vitamins and essential fatty acids, have been shown to play a role in the genesis of preeclampsia, but also an excess of weight gain during pregnancy or a pre-pregnancy state of obesity and overweight, which are associated to hyperinsulinism, insulin resistance and maternal systemic inflammation, are proposed as one of the mechanism that conduce to endothelial dysfunction, hypertension, proteinuria, thrombotic responses, multi-organ damage, and high maternal mortality and morbidity. Moreover, it has been demonstrated that pregnant women that suffer preeclampsia will have an increased risk of future cardiovascular disease and related mortality in their later life. In this article we will discuss the results of studies performed in different populations that have shown an interrelationship between obesity and overweight with the presence of preeclampsia. Moreover, we will review some of the common mechanisms that explain this interrelationship, particularly the alterations in the L-arginine/nitric oxide pathway as a crucial mechanism that is common to obesity, preeclampsia and cardiovascular diseases.
- PublicaciónAcceso abiertoRole of the autonomic nervous system in the endothelial dysfunction of the metabolic syndrome(2011) Lopez-Jaramillo, Patricio; Molina, Dora I.; Aguillon, Alba; Gómez Arbeláez, Diego; Sotomayor Rubio, Aristides; López López, JoseIn the last decade there has been an accelerated growth in the prevalence of metabolic syndrome (MS), especially in Latin American countries, which has led an increased risk of cardiovascular disease (CVD) and type 2 diabetes mellitus (DM2). Recently has been raised the relationship between the autonomic nervous system (ANS), endothelial dysfunction (ED) and the appearance of MS. In the present article we review the evidence that support the proposal that abdominal obesity (AO) produce adypokines that result in insulin resistance and low degree inflammation, which increase the activity of ANS, causing vasoconstriction, hypertension, decreased peripheral glucose uptake, and decreased secretion of insulin, leading to hyperglycemia and increased lipolysis and hypertriglyceridemia. All these factors cause ED, explaining the higher risk of the patients with MS of developing DM2 and CVD.