Examinando por Materia "Nitric oxide"

Mostrando 1 - 6 de 6
  • Publicación
    Acceso abierto
    Asociación entre niveles de proteína C-reactiva y oxido nítrico con el pronostico de pacientes con enfermedad cerebro vascular isquémica
    (2015-04) García, Ronald G.; Rosso, Pedro; García, Zaira M.; Álvarez Camacho, Julie; Suárez, Uriel; Gómez Arbeláez, Diego; Lopez-Jaramillo, Patricio; Silva Sieger, Federico Arturo
    Introduction: Inflammation and alterations in the bioavailability of nitric oxide (NO) have been involved in the pathophysiology of cerebrovascular disease. Objective: The aim of the study was to determine the prognostic value of measuring NO metabolites and inflammatory markers in patients with acute ischemic stroke. Materials and methods: A total of 158 patients with acute ischemic stroke were included in an observational cohort study. Between 48 and 72 hours post admission, a fasting blood sample was taken to determine the biochemical profile, inflammatory markers (CRP, IL1-β, IL6, TNF-α) and nitrites/nitrates plasma levels. The cohort’s follow-up was conducted for two years to determine the occurrence of a new event (stroke, myocardial infarction, heart failure) or death of vascular origin. Comparisons between groups were made using the log-rank test. A Cox multivariate regression analysis permitted to determine factors independently associated with the outcome. Results: The mean age was 70.5 ± 12.8 years. 39.2% of the subjects presented the outcome during the first 24 months of follow-up. CRP levels > 12 mg/L (HR 2.22, 95% CI 1.07-4.59) and a score > 13 on the NIHSS scale at admission (HR 2.81 95% CI 1.46-5.41) were significantly associated with an increased risk of a new event. The combination of CRP levels < 12 mg/L and nitrites/nitrates levels < 35.5 mmol/L was identified as a protective factor (HR 0.21, 95% CI 0.06-0.71). Conclusion: This study demonstrates that the determination of CRP and NOx levels could be beneficial in clinical practice to stratify the risk of future events or death of vascular origin in acute ischemic stroke patients.
  • Publicación
    Restringido
    Nitric oxide synthase inhibitor improves de novo and long-term l-DOPA-induced dyskinesia in hemiparkinsonian rats
    (2011-06) Padovan-Neto, Fernando Eduardo; Bermúdez Echeverry, Marcela; Chiavegatto, Silvana; Del-Bel, Elaine
    Inhibitors of neuronal and endothelial nitric oxide synthase decrease l-3,4-dihidroxifenilalanine (l-DOPA)-induced dyskinesias in rodents. The mechanism of nitric oxide inhibitor action is unknown. The aims of the present study were to investigate the decrease of l-DOPA-induced abnormal involuntary movements (AIMs) in 6-hydroxydopamine (6-OHDA)-lesioned rats by nitric oxide inhibitors following either acute or chronic treatment. The primary findings of this study were that NG-nitro-l-Arginine, an inhibitor of endothelial and neuronal nitric oxide synthase, attenuated AIMs induced by chronic and acute l-DOPA. In contrast, rotational behavior was attenuated only after chronic l-DOPA. The 6-OHDA lesion and the l-DOPA treatment induced a bilateral increase (1.5 times) in the neuronal nitric oxide synthase (nNOS) protein and nNOS mRNA in the striatum and in the frontal cortex. There was a parallel increase, bilaterally, of the FosB/ΔFosB, primarily in the ipsilateral striatum. The exception was in the contralateral striatum and the ipsilateral frontal cortex, where chronic l-DOPA treatment induced an increase of approximately 10 times the nNOS mRNA. Our results provided further evidence of an anti-dyskinetic effect of NOS inhibitor. The effect appeared under l-DOPA acute and chronic treatment. The l-DOPA treatment also revealed an over-expression of the neuronal NOS in the frontal cortex and striatum. Our results corroborated findings that l-DOPA-induced rotation differs between acute and chronic treatment. The effect of the NOS inhibitor conceivably relied on the l-DOPA structural modifications in the Parkinsonian brain. Taken together, these data provided a rationale for further evaluation of NOS inhibitors in the treatment of l-DOPA-induced dyskinesia.
  • Publicación
    Acceso abierto
    Obesity 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; Masira
    Preeclampsia 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.
  • Publicación
    Acceso abierto
    Plasma nitrate levels and flow-mediated vasodilation in untreated
    (2011-05) García, Ronald G.; Zarruk, Juan G.; Barrera, Carlos; Pinzón, Alexander; Trillos, Elizabeth; Arenas, William D.; Luengas, Carlos; Tomaz, Carlos A.; Lopez-Jaramillo, Patricio
    Objective: Findings from several studies have revealed that major depression is associated with an increased cardiovascular risk. The physiopathologic mechanisms of this association remain unclear, although recently, it has been hypothesized that a decreased production of nitric oxide could be a potential contributor to vascular dysfunction in depressive patients. The objective of this study was to evaluate nitric oxide production and vascular endothelial function in treatment-naive young healthy adults with a first episode of major depression. Methods: A case-control study in 50 treatment-naive young adults with a first episode of major depression and 50 healthy control subjects was conducted. Plasma levels of nitric oxide metabolites (nitrates/nitrites) were determined using a colorimetric assay based on Griess reaction. Endothelial function was assessed by flow-mediated vasodilation measurements after reactive hyperemia. Results: The mean age of the depressed patients was 22.6 (standard deviation [SD], 4.6) years, whereas the controls were 23.4 (SD, 4.8) years. Sixteen men (32%) and 34 women (68%) were included in each group. The plasma nitrite/nitrate concentrations were significantly lower in depressive subjects compared with healthy controls (17.5 [SD, 4.9] Kmol/L versus 21.6 [SD, 7.0] Kmol/L, p G .001); however, flow-mediated vasodilation values were similar in both groups (13.1% [SD, 4.3%] versus 12.1% [SD, 5.0%], p = .10). Conclusions: Decreased plasma concentrations of nitric oxide metabolites are not associated with vascular endothelial dysfunction in young subjects with a first episode of major depression. Reduced nitrate/nitrite levels could reflect a decreased nitric oxide production in the central nervous system of depressed subjects. Further studies are needed to confirm this hypothesis.
  • Publicación
    Acceso abierto
    The role of the L-arginine-nitric oxide pathway in preeclampsia
    (2008-08-01) Lopez-Jaramillo, Patricio; Arenas, William D.; García, Ronald G.; Rincón, Melvin Y.; López Casillas, Marcos
    : Preeclampsia (PE) is a major cause of maternal and perinatal mortality, especially in developing countries. Its etiology involves multiple factors, but no specific cause has been identified. Evidence suggests that clinical manifestations are caused by endothelial dysfunction. Nitric oxide (NO), which is synthesized from L-arginine in endothelial cells by the endothelial nitric oxide synthase (eNOS), provides a tonic dilator tone and regulates the adhesion of white blood cells and platelet aggregation. Alterations in the L-arginine-NO pathway have been associated with the development of PE. Various studies, reporting decreased, elevated or unchanged levels of nitrite (NO2) and nitrate (NO3), two end products of NO metabolism, have been published. Our group contributed to those contradictory reports describing cases of PE with both elevated and decreased levels of NO2 and NO3. Apparently, diminished levels of NO could be related to deficiencies in the ingestion of dietary calcium associated to low levels of plasma ionic calcium, which is crucial to the eNOS’ activity. Also, low levels of NO could be associated with the presence of eNOS polymorphisms or the presence of increased levels of ADMA, the endogenous inhibitor of NO. High levels of NO associated to low levels of cGMP suggest a decreased bioactivity of NO, which is probably related to an increased degradation of NO caused by a high production of superoxide in states of infection and inflammation. The present article analyses and reviews the reported paradoxical roles of the L-arginine-NO pathway in PE and gives a possible explanation for these results.
  • Publicación
    Acceso abierto
    Subclinical infection as a cause of inflammation in preeclampsia
    (2008-07) Lopez-Jaramillo, Patricio; Casas Herrera, Julián Augusto; Arenas Mantilla, Mario; Jáuregui, Isabel E.; Mendoza, Mayaris A.
    Preeclampsia, a pregnancy-exclusive hypertensive disorder, is the major cause of maternal and perinatal mortality, with a greater importance in developing countries. The role of inflammation in the pathogenesis of preeclampsia has been the object of recent studies by our group. We have described elevated levels of inflammatory markers (tumor necrosis factor alpha, interleukin-6, and C-reactive protein) in preeclamptic patients and demonstrated that Latin-American women present a higher degree of inflammation than women from developed countries. We have results that suggest that chronic subclinical infections and insulin resistance are the most probable causes of the increased inflammation in preeclampsia. Moreover, we showed that early treatment of urinary and vaginal infections decreased the incidence of preeclampsia. We also have evidence that suggests that inflammation leads to endothelial dysfunction, predisposing women to develop preeclampsia. Increased levels of inflammation markers and endothelial dysfunction are found in the early stages of pregnancy in women who later on develop preeclampsia. Appropriate prenatal care programs, including screening and treatment of urinary, vaginal, and periodontal infections in early pregnancy and prevention of factors that predispose to insulin resistance, such as excessive weight gain during pregnancy, may reduce the incidence of preeclampsia in Latin-American women.