L-arginine pathway in the sepsis syndrome

Ja, Lorente; Landín, Luis; R, de Pablo; Renes, Emilio; Liste, D.

doi:10.1097/00003246-199309000-00010

Cited by 226 publications

(82 citation statements)

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“…The antivasodilatory effect of methylene blue was not followed by the decrease in cardiac output that often occurs with various specific competitive L-arginine antagonists (17,18,31). The different effects of inhibitors of nitric oxide production and methylene blue on cardiac output may be due to a more intense vasoconstriction induced by the former than by the latter, but the cause is not known (32).…”

Section: Discussionmentioning

confidence: 97%

“…In experimental studies, the decreased response to vasopressors is associated with an increased nitric oxide production (14)(15)(16). The hemodynamic changes seen in septic shock patients may also be related to overproduction of nitric oxide (17,18). Blood concentrations of nitrites/nitrates, the stable byproducts of nitric oxide, are increased in severely septic patients (19,20).…”

Section: Introductionmentioning

confidence: 99%

“…Blood concentrations of nitrites/nitrates, the stable byproducts of nitric oxide, are increased in severely septic patients (19,20). The serum concentration of L-arginine, a precursor of nitric oxide, is reduced and its administration provokes vasodilation in these patients (17).…”

Section: Introductionmentioning

confidence: 99%

“…However, a blockade of such magnitude may be deleterious. The cardiac output decreased in several studies due to an excessive systemic vasoconstriction (17,22) and the worsening in hemodynamic status increased the mortality in animal studies (5,6). In addition, pulmonary vascular resistance is often increased during sepsis and a further increase in pulmonary arterial pressure by nitric oxide synthesis inhibitors could precipitate right heart failure.…”

Section: Introductionmentioning

confidence: 99%

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Blockade of the action of nitric oxide in human septic shock increases systemic vascular resistance and has detrimental effects on pulmonary function after a short infusion of methylene blue

Weingartner

Oliveira

Sant'Anna

et al. 1999

Braz J Med Biol Res

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To investigate the role of nitric oxide in human sepsis, ten patients with severe septic shock requiring vasoactive drug therapy and mechanical ventilation were enrolled in a prospective, open, non-randomized clinical trial to study the acute effects of methylene blue, an inhibitor of guanylate cyclase. Hemodynamic and metabolic variables were measured before and 20, 40, 60, and 120 min after the start of a 1-h intravenous infusion of 4 mg/kg of methylene blue. Methylene blue administration caused a progressive increase in mean arterial pressure (60 [55-70] Arterial lactate concentration decreased from 5.1 ± 2.9 to 4.5 ± 2.1 mmol/ l, mean ± SD (P<0.05) after 60 min. Heart rate, cardiac filling pressures, cardiac output, oxygen delivery and consumption did not change. Methylene blue administration was safe and no adverse effect was observed. In severe human septic shock, a short infusion of methylene blue increases systemic vascular resistance and may improve myocardial function. Although there was a reduction in blood lactate concentration, this was not explained by an improvement in tissue oxygenation, since overall oxygen availability did not change. However, there was a significant increase in pulmonary vascular tone and a deterioration in gas exchange. Further studies are needed to demonstrate if nitric oxide blockade with methylene blue can be safe for patients with septic shock and, particularly, if it has an effect on pulmonary function.

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Section: Discussionmentioning

confidence: 97%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Blockade of the action of nitric oxide in human septic shock increases systemic vascular resistance and has detrimental effects on pulmonary function after a short infusion of methylene blue

Weingartner

Oliveira

Sant'Anna

et al. 1999

Braz J Med Biol Res

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“…Ensayos clínicos con humanos en los que se administró dosis reducidas de IL-1 y TNF-alfa advirtieron que éstos experimentaban fiebre, dolores de cabeza y artromialgias, síntomas que se desvanecían con la administración de un antiinflamatorio inhibidor de la ciclooxigenasa (42). Adicionalmente, la IL-1 y el TNFalfa son potentes inductores de la expresión genética que codifica la síntesis de sintasa NO inducible, con el correspondiente aumento en la producción endotelial de NO, máximo responsable de la hipotensión vascular que acontece en la sepsis (43)(44)(45).…”

Section: Mediadores Endógenosunclassified

Sepsis y shock séptico: un torbellino de mediadores inflamatorios de difícil manejo terapéutico

Giménez-Rico

Reyero

Ruigomez

et al. 2002

An. Med. Interna (Madrid)

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INTRODUCCIÓNEn los últimos años se ha producido un extraordinario aumento en la incidencia de la sepsis y el shock séptico (1) por lo que nos enfrentamos a un capítulo dentro de la medicina de enorme interés y debate, no sólo ya por su creciente aparición, sino también por tratarse, en los albores del sigo XXI, de un auténtico reto terapéutico pendiente de una solución definitiva. No hay que olvidar que su mortalidad oscila entre el 35-80% y que ésta, apenas ha variado en las dos últimas décadas a pesar de los enormes progresos en el conocimiento de su fisiopatología y de las novedades curativas y de soporte vital surgidas en los últimos tiempos (2,3).La sepsis y el shock séptico constituyen, sin duda, una realidad clínica en la que los mediadores químicos de la inflamación propios del organismo desempeñan un papel relevante en su explicación fisiopatológica. Dentro de la biología quirúrgica el estudio de estos mediadores es donde quizás estén siendo más evidentes los avances en biología molecular y celular. El actual interés que ha suscitado este estudio no nos debe sorprender y ello se debe, fundamentalmente, a dos razones. Por un lado, una gran parte de la morbimortalidad asociada con la práctica quirúrgica diaria es debida a anomalías en la respuesta inflamatoria; por el otro, es cada vez más patente en la patogenia de afecciones tan dispares como la artritis reumatoide, el asma bronquial, el infarto cerebral o el síndrome de distrés respiratorio del adulto, todas ellas, pertenecientes a distintas especialidades médico-quirúrgicas, la alteración en la síntesis de tales mediadores (4).47 [0212-7199(2002) RESUMENLa sepsis y el shock séptico continúan siendo un capítulo de enorme interés por su elevada frecuencia, y por no existir una disminución en las cifras de mortalidad a pesar de los nuevos conocimientos adquiridos en su fisiopatología y los avances surgidos en los diversos tratamientos aplicados.El propósito de la presente revisión es actualizar los conceptos presentes en la literatura especializada, tratando de resumir la compleja interacción existente entre diferentes mediadores de doble carácter: exóge-nos y endógenos, y enunciar las posibles causas por las que los tratamientos novedosos aplicados en la sepsis siguen siendo poco prometedores.

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Understanding the Inflammatory Cytokine Response in Pneumonia and Sepsis

Kong²,

et al. 2007

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Background: Severe sepsis is common and frequently fatal, and community-acquired pneumonia (CAP) is the leading cause. Although severe sepsis is often attributed to uncontrolled and unbalanced inflammation, evidence from humans with infection syndromes across the breadth of disease is lacking. In this study we describe the systemic cytokine response to pneumonia and determine if specific patterns, including the balance of proinflammatory and anti-inflammatory markers, are associated with severe sepsis and death.Methods: This is a cohort study of 1886 subjects hospitalized with CAP through the emergency departments in 28 US academic and community hospitals. We defined severe sepsis as CAP complicated by new-onset organ dysfunction, following international consensus conference criteria. We measured plasma tumor necrosis factor, IL-6 (interleukin 6), and IL-10 levels daily for the first week and weekly thereafter. Our main outcome measures were severe sepsis and 90-day mortality.Results: A total of 583 patients developed severe sepsis (31%), of whom 149 died (26%). Systemic cytokine level Conclusions:The circulating cytokine response to pneumonia is heterogeneous and continues for more than a week after presentation, with considerable overlap between those who do and do not develop severe sepsis. Unbalanced activation is uncommon, and mortality is highest when both proinflammatory and antiinflammatory cytokine levels are high.

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L-arginine pathway in the sepsis syndrome

Cited by 226 publications

References 0 publications

Blockade of the action of nitric oxide in human septic shock increases systemic vascular resistance and has detrimental effects on pulmonary function after a short infusion of methylene blue

Blockade of the action of nitric oxide in human septic shock increases systemic vascular resistance and has detrimental effects on pulmonary function after a short infusion of methylene blue

Sepsis y shock séptico: un torbellino de mediadores inflamatorios de difícil manejo terapéutico

Understanding the Inflammatory Cytokine Response in Pneumonia and Sepsis

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