Really does temperature reduction and norepinephrine have similar effects on the energy metabolism in rat brown adipose tissue?

CONTEXT: Heat generation by brown adipose tissue (BAT) in response to temperature reduction seems to be entirely related to sympathetic nervous stimulation. OBJECTIVE: To analyse if temperature reduction and norepinephrine may differently affect the expression of proteins related to energy metabolism in BAT. MATERIALS AND METHODS: Isolated rats BAT was incubated with/without norepinephrine (10-6 mol/L, 24 h at 32 °C and 37 °C). RESULTS: In BAT, 32 °C increased the protein expression levels of carnitine palmitoyltransferase-I and -II, mitochondrial uncoupling protein-1 (UCP-1) and the expression and activity of lactate dehydrogenase. Mitochondrial F1-ATP synthase α-chain expression was decreased at 32 °C compared to 37 °C. Norepinephrine and at 32 °C exposure, UCP-1 expression was increased but cytochrome-c oxidase and F1-ATP synthase α-chain expression was reduced with respect to 37 °C. DISCUSSION: Sympathetic stimulation seems not to be the only factor associated with heat generation. CONCLUSIONS: Temperature reduction by itself exerts some different effects on the expression of proteins related to the energy metabolism than norepinephrine.

Endothelial damage in major depression patients is modulated by SSRI treatment, as demonstrated by circulating biomarkers and an in vitro cell model.

There is a link between depression, cardiovascular events and inflammation. We have explored this connection through endothelial dysfunction, using in vivo and in vitro approaches. We evaluated circulating biomarkers of endothelial dysfunction in patients with major depression at their diagnosis (MD-0) and during antidepressant treatment with the selective serotonin reuptake inhibitor escitalopram, for 8 and 24 weeks (MD-8 and MD-24). Results were always compared with matched healthy controls (CON). We measured in vivo circulating endothelial cells (CECs) and endothelial progenitor cells (EPCs) in blood samples, and assessed plasma levels of soluble von Willebrand factor (VWF) and vascular cell adhesion molecule-1 (VCAM-1). CEC counts, soluble VWF and VCAM-1 were statistically elevated in MD-0 (P<0.01 versus CON) and gradually decreased during treatment. Conversely, EPC levels were lower in MD-0, tending to increase throughout treatment. In vitro studies were performed in human endothelial cells cultured in the presence of sera from each study group. Elevated expression of the inflammation marker intercellular adhesion molecule-1 and oxidative stress, with lower presence of endothelial nitric oxide synthase and higher reactive oxygen species production, were found in cells exposed to MD-0 sera (P<0.05 versus CON). These results were normalized in cells exposed to MD-24 sera. Thrombogenicity of extracellular matrices generated by these cells, measured as expression of VWF, tissue factor and platelet reactivity, showed non-significant differences. We provide a model of cultured endothelial cells reproducing endothelial dysfunction in naive patients with major depression, demonstrating endothelial damage and inflammation at diagnosis, and recovering with selective serotonin reuptake inhibitor treatment for 24 weeks.

Metabolic differences between white and brown fat from fasting rabbits at physiological temperature.

It has been suggested that activated brown adipose tissue (BAT) shows increased glucose metabolic activity. However, less is known about metabolic activity of BAT under conditions of fasting and normal temperature. The aim of this study was to compare the possible differences in energetic metabolism between BAT and white adipose tissue (WAT) obtained from rabbits under the conditions of physiological temperature and 24 h after fasting conditions. The study was carried out on New Zealand rabbits (n=10) maintained for a period of 8 weeks at 23±2 °C. Food was removed 24 h before BAT and WAT were obtained. Protein expression levels of the glycolytic-related protein, glyceraldehyde-3-phosphate dehydrogenase, and pyruvate dehydrogenase were higher in WAT than that in BAT. The expression level of carnitine palmitoyltransferase 1 (CPT1) and CPT2, two fatty acid mitochondrial transporters, and the fatty acid ß-oxidation-related enzyme, acyl CoA dehydrogenase, was higher in BAT than in WAT. Cytosolic malate dehydrogenase expression and malate dehydrogenase activity were higher in WAT than in BAT. However, lactate dehydrogenase expression and lactate content were significantly higher in BAT than in WAT. In summary, this study for the first time, to our knowledge, has described how under fasting and normal temperature conditions rabbit BAT seems to use anaerobic metabolism to provide energetic fuel, as opposed to WAT, where the malate-aspartate shuttle and, therefore, the gluconeogenic pathway seem to be potentiated.

Efecto del alprostadil en los cultivos de músculo esquelético isquémico. Estudio proteómico comparativo frente a músculo sano / The effect of alprostadil on ischemic skeletal muscle cultures. Comparative proteomic study with healthy muscle

INTRODUCCIÓN: El alprostadil tiene efecto vasodilatador y antiagregante. Es bien conocido su efecto endotelial, pero se desconocen sus posibles efectos pleiotrópicos sobre el músculo esquelético y si estos difieren en el músculo isquémico. OBJETIVO: Determinar el efecto del alprostadil sobre el metabolismo del músculo esquelético y valorar diferencias en su acción sobre el músculo isquémico frente al sano. MATERIAL Y MÉTODOS: Se obtuvieron muestras de tejido de 10 pacientes con isquemia irreversible intervenidos de amputación supracondílea, tanto de músculo isquémico (extensor corto de los dedos del pie, grupo I) como de músculo sano (músculo cuádriceps del borde de amputación, grupo S). Ambos grupos se cultivaron basalmente y con 5 ng de alprostadil. Se analizó la expresión proteómica de las siguientes enzimas: triosa-fosfato-isomerasa (TPI), malato deshidrogenasa (MDH), lactato deshidrogenasa (LDH) y piruvato carboxilasa (PC). Se determinaron también sus productos, lactato y piruvato. RESULTADOS: La MDH presentó una disminución en el grupo I en las muestras basales (2.196 ± 348 grupo S vs 644 ± 192 grupo I, p < 0,05). La PC estaba aumentada en el grupo I en ambos tipos de muestras (basal: 1,80 ± 1,27 vs 3,16 ± 2,25; alprostadil: 6,72 ± 2,13 vs 8,16 ± 3,63, grupo S vs grupo I, respectivamente, p < 0,05). No hubo diferencias significativas en la concentración de lactato ni en la de piruvato. CONCLUSIONES: La reducción de MDH en el músculo isquémico sugiere una reducción del ciclo de Krebs. El alprostadil estimula la expresión de PC, que induce la formación de oxalacetato; este se introduce en el ciclo de Krebs, permitiéndole funcionar parcialmente en el músculo isquémico y mejorando la obtención de energía

INTRODUCTION: Alprostadil has vasodilator properties and inhibits platelet aggregation. Its effects on endothelial wall have been widely studied, but there is no knowledge about possible skeletal muscle effects, and differences with ischemic muscle. OBJECTIVE: To determine the effects of alprostadil on skeletal muscle metabolism, and to investigate possible differences with ischemic muscle. METHODS: Samples were obtained in 10 patients with leg above-knee amputation due to severe irreversible ischemia, of ischemic muscle (extensor digitorum brevis, group I), and healthy muscle (quadriceps femoris, amputation edge, group S). Muscle segments were incubated with alprostadil 5 ng, or without it (baseline). Proteomic analysis of metabolic enzymes was performed: Triose-phosphate isomerase (TPI), malate dehydrogenase (MDH), lactate dehydrogenase (LDH) and pyruvate carboxylase (PC). Lactate and pyruvate was also determined. RESULTS: A decrease in malate dehydrogenase was observed in group I in the baseline samples (2196 ± 348 group S vs 644 ± 192 group I, P < 0.05). PC was increased in both samples in group I (baseline: 1.80 ± 1.27 vs 3.16 ± 2.25; alprostadil: 6.72 ± 2.13 vs 8.16 ± 3.63, group S vs group I, respectively, P < 0.05). No changes were observed in pyruvate and lactate. DISCUSSION: Decreased MDH in ischemic muscle suggests a Krebs cycle reduction. Alprostadil stimulates the expression of PC, which leads to oxaloacetate production. This product is inserted in Krebs cycle, improving energy obtaining. In this manner, Krebs cycle can work partially in ischemic muscle

La plaqueta como célula inflamatoria: modificación de la expresión proteica del citoesqueleto y sistema contráctil de la pared vascular / The platelet as a inflammatory cell: modification of cytoskeletal and contractile protein expression of the vascular wall

A pesar de su sencillez estructural, las plaquetas son células funcionalmente muy complejas debido a su capacidad para producir y liberar biomoléculas. De aquí su importancia en el desarrollo de la arteriosclerosis. Se realizó un experimento in vitro para estudiar la actividad de las plaquetas sobre la pared vascular observando los cambios en la expresión proteica del citoesqueleto en segmentos de aorta bovina incubados con plasma rico en plaquetas. Para intentar simular un estado inflamatorio (arteriosclerosis), se realizaron estas mismas determinaciones en segmentos preestimulados con factor de necrosis tumoral. Se observó una modulación de la expresión de la mayoría de las proteínas del citoesqueleto en los segmentos de aorta sana. Sin embargo, en los segmentos preestimulados el número de proteínas fue menor, pudiendo reflejar una capacidad dual de las plaquetas para alterar la contractilidad vascular en función del estado inflamatorio de la pared vascular (AU)

Despite its structural simplicity, platelets are functionally complex cells due to their ability to produce and release biomolecules. Hence its importance in the development of atherosclerosis. An in vitro experiment was conducted to study the effect of the platelets on the vascular wall by observing changes in the cytoskeletal protein expression in bovine aortic segments incubated with platelet rich plasma. With the aim of simulating an inflammatory state (atherosclerosis), these same measurements were performed on aortic segments pre-stimulated with tumour necrosis factor. We observed a modulation of the expression of most of the cytoskeletal proteins in healthy aorta segments. However, the number of modified proteins was less in pre-stimulated segments. These results may reflect a dual platelet capacity to alter vascular contractility in relation to the inflammatory condition of the vascular wall (AU)

Genética, epigenética y proteómica de los aneurismas de aorta abdominal / Genetics, epigenetics and proteomics of abdominal aortic aneurysms

El aneurisma de aorta abdominal supone una importante causa de mortalidad en nuestra sociedad. Sin embargo, poco conocemos sobre su etiopatogenia. El importante papel de las metaloproteasas y alteraciones genéticas han centrado la mayor parte de los esfuerzos investigadores hasta hoy, pero poco se ha estudiado sobre el origen de esta enfermedad. Para llegar al conocimiento completo de esta, hay que avanzar con nuevas tecnologías que nos muestren el problema desde diferentes prismas. En este sentido, la proteómica como estudio de las proteínas expresadas por el tejido patológico o la epigenética como estudio de la influencia de los factores ambientales sobre los propios genes son técnicas que no han proliferado aún en esta patología, y que sin duda nos van a ayudar a profundizar en ella. Mediante esta revisión se repasan estas nuevas herramientas que invitan a la aventura de la investigación en esta y otras patologías de nuestro ámbito(AU)

Abdominal aortic aneurysm is a major cause of death in our society. However, little is known about its pathogenesis. The important role of metalloproteinases and genetic disorders has been the focus of most research efforts to date, but little has been studied on the origin of this disease. To get the complete knowledge of this, we must move forward with new technologies that show us the problem from different perspectives. In this regard, proteomics as the study of proteins expressed by the diseased tissue, or epigenetics as the study of the influence of environmental factors on the genes themselves, are techniques that are still not widely used in this condition, and would definitely help in increasing our knowledge of it. These new tools that invite adventure of research into this and other diseases in our area are reviewed(AU)

Dronedarone.

Atrial fibrillation (AF), the most common cardiac arrhythmia, is associated with substantial morbidity and mortality. Dronedarone is an amiodarone-like benzofuran which lacks the iodine moiety and presents a methane sulfonyl group that decreases its lipophilicity, thus shortening the half-life and decreasing tissue accumulation. Like amiodarone, dronedarone blocks multiple cardiac ion channels and ß-adrenoceptors, presenting electrophysiological characteristics of all four Vaughan Williams classes of antiarrhythmic drugs. In clinical trials, dronedarone has been found effective for both rhythm and rate control. Dronedarone was more effective than placebo in maintaining sinus rhythm in patients with paroxysmal and/or persistent AF and was also effective for ventricular rate control during AF recurrences, providing incremental rate control on top of standard drugs in permanent AF. Furthermore, in the ATHENA trial, dronedarone reduced the incidence of hospitalization due to cardiovascular events or death in patients with nonpermanent AF. Even when dronedarone was less effective than amiodarone in decreasing AF recurrence, it had a better safety profile, being devoid of thyroid, pulmonary and neurological toxicity. This review analyzes the electrophysiological and pharmacological properties, as well as the efficacy and safety of dronedarone in patients with atrial fibrillation.

Síncope de esfuerzo y riesgo de muerte súbita en deportistas jóvenes: perspectiva clínica y genética / Exercise-induced syncope in young athletes and risk of sudden death: clinical and genetic perspectives

El síncope puede ser en ocasiones el resultado o aviso de patologías potencialmente graves y en ocasiones mortales. Los servicios de urgencias (SU) son primordiales para estratificar el riesgo de los pacientes con síncope. La historia clínica dirigida la exploración física y el Electrocardiograma de 12 derivaciones (ECG) identifican las causas del síncope en la mitad de los pacientes. Hay una serie de alteraciones, como anormalidades en el ECG, Patología cardiaca previa, Presión arterial sistólica elevada, alteraciones del patrón respiratorio, descenso del hematocrito, edad avanzada, síncope de esfuerzo o la historia familiar de muerte súbita, que nos señalan a los pacientes de riesgo. La cardiopatía estructural y la enfermedad cardiaca congénita o eléctrica primaria son los principales factores de riesgo de muerte súbita cardiaca y de la mortalidad global en los pacientes con síncope. En estos pacientes la sensibilidad diagnóstica de las pruebas convencionales disponibles es aún hoy en día escasa. La Muerte súbita cardiaca (MSC) normalmente se debe a taquicardia/fibrilación ventricular sostenidas. La causa más frecuente es cardiopatía isquémica, pero en el grupo de pacientes menores de 35 años existen una serie de enfermedades que constituyen la causa más prevalente de MSC. En los últimos dos años el desarrollo de los estudios genéticos cardiovasculares puede haber abierto una vía diagnóstica en un grupo de pacientes con enfermedades congénitas cardiacas que les predisponen a MSC. Enfermedades como la Displasia arritmogénica del ventrículo derecho (DAVD), la Miocardiopatía Hipertrófica obstructiva (MHC),el Síndrome del QT Largo congénito (SQTLC), la Taquicardia Ventricular Catecolaminérgica, el Síndrome de Wolf-parkinson-White (WPW) o el Síndrome de Brugada se analizan en esta revisión (AU)

Syncope may be a warning sign of potentially serious and even life-threatening medical conditions. Emergency service expertise is essential for assessing risk in patients with syncope. A focused medical history and a physical examination that includes a 12-lead electrocardiogram (ECG) will identify the causes of syncope in half the patients. Patients at riskare those with certain ECG abnormalities, a history of heart disease, elevated systolic pressure, changes in breathing pattern, a fall in the hematocrit level, older age, exercise-induced syncope, or a family history of sudden death. Structural heart disease (congenital heart disease or primary electrical abnormalities) are the main risk factors of sudden cardiacdeath (SCD) and all mortality in patients with syncope. The diagnostic sensitivity of conventional tests remains low in these patients. SCD is normally due to sustained tachycardia (ventricular fibrillation). The most common cause overall is ischemic heart disease, but in patients under the age of 35 years a series of diseases have been implicated as the most frequent causes. The past 2 years have seen studies of genetic factors involved in cardiovascular disease that have suggested the possibility of diagnosis for certain patients with congenital heart diseases that predispose them to SCD. This review includes discussions of such conditions as arrhythmogenic right ventricular dysplasia, obstructive hypertrophic cardiomyopathy, congenital long QT syndrome, catecholaminergic ventricular tachycardia, Wolf-Parkinson-White syndrome, or Brugada syndrome (AU)

Increased cyclic guanosine monophosphate production and endothelial nitric oxide synthase level in mononuclear cells from sildenafil citrate-treated patients with erectile dysfunction.

Mononuclear cells express enzymes involved in the NO/cyclic guanosine monophosphate (cGMP) generating system, as well as PDE5. The objective of the study was to determine the effect of sildenafil citrate administration on the level of proteins involved in the NO/cGMP generating system in mononuclear cells from patients with ED. Twenty-one patients with ED (International Index of Erectile Function-Erectile Function Domain (IIEF-EFD) 17.9+/-0.8) were enrolled and 100 mg sildenafil citrate on-demand was administered during 12 weeks. All patients showed cardiovascular risk factors. After sildenafil citrate administration, IIEF-EFD score was improved (26+/-1.2 P<0.05). In the mononuclear cells, the protein level of endothelial NO synthase (eNOS) was higher after sildenafil citrate treatment. It was accompanied by reduction in the circulating plasma levels of both high-sensitive C-reactive protein and soluble intercellular adhesive molecule-1. The protein level of soluble guanylate cyclase and PDE5 did not change in the mononuclear cells after sildenafil citrate treatment. However, in the mononuclear cells exogenous NO induced a higher cGMP production after 12-weeks sildenafil citrate administration. In conclusion, in mononuclear cells from patients with ED sildenafil citrate administration increased the level of eNOS protein and increased cGMP production in response to NO. Moreover, sildenafil citrate administration reduced the plasma circulating levels of two biomarkers associated with inflammation.

[Testosterone, endothelial function, cardiovascular health and androgen deficiency in the old man]. / Testosterona, función endotelial, salud cardiovascular y androgenodeficiencia del varón añoso.

Testosterone determination in an old men population has demonstrated its about the as general health marker, not only sexual, prompting a greater in to arrest for this analytic determination and the potential relations of testosterone with other markers of cardiovascular health, obesity, hypertension, erectile dysfunction, sarcopenia, metabolic syndrome, ageing, and other conditions. We specifically review the relationship between cardiovascular health, erectile dysfunction, and androgen deficiency, processes easily recognizable, prevented and treated. Current information gives such a prominence to testosterone as a health reference that its determination seems to be inexcusable in the ageing male consult.

Testosterona, función endotelial, salud cardiovascular y androgenodeficiencia del varón añoso / Testosterone, endothelial function, cardiovascular health and androgen deficiency in the old man

La determinación de testosterona en la población de varones añosos, ha demostrado su valor como marcador de salud general, no sólo sexual, motivando un mayor interés por esta determinación analítica y las potenciales interrelaciones de la testosterona con otros marcadores de salud cardiovascular, obesidad, hipertensión, disfunción eréctil, sarcopenia, síndrome metabólico, envejecimiento y otras condiciones. Se revisa de manera específica la interrelación entre salud cardiovascular, disfunción eréctil y androgenodeficiencia, procesos de fácil reconocimiento, prevención y tratamiento. La información actual concede tal protagonismo a la testosterona como referente de salud que su determinación parece inexcusable en la consulta del varón añoso(AU)

Testosterone determination in an old men population has demonstrated its about the as general health marker, not only sexual, prompting a greater in to arrest for this analytic determination and the potential relations of testosterone with other markers of cardiovascular health, obesity, hypertension, erectile dysfunction, sarcopenia, metabolic syndrome, ageing, and other conditions. We specifically review the relationship between cardiovascular health, erectile dysfunction, and androgen deficiency, processes easily recognizable, prevented and treated. Current information gives such a prominence to testosterone as a health reference that its determination seems to be inexcusable in the ageing male consult(AU)

Aspectos proteómicos y genéticos de la resistencia a la aspirina / Proteomics and genetics aspects of aspirin resistance

Objetivo: Analizar si existe alguna asociación entre la resistencia a aspirina (RA) y la presencia de polimorfismos genéticos de un único nucleótido (SNPs) en el gen de la COX-1, así como su relación con modificaciones en la expresión de proteínas plasmáticas en pacientes con enfermedad isquémica estable y tratamiento continuado de aspirina. Materiales y métodos: Analizamos el proteoma plasmático de 19 pacientes sensibles, 19 resistentes. RA se definió mediante el sistema PFA-100. Se realizó electroforesis bidimensional (IPG 17cm, pH(4-7), geles SDS-PAGE 10%) y tinción con plata. Se analizaron cambios en tres SNPs (A-842G, C22T y C50T) en 50 pacientes sensibles, 33 resistentes y 83 controles mediante PCR a tiempo real. Resultados: La expresión de cuatro isoformas de alfa1-antitripsina estaba aumentada en los pacientes resistentes. No encontramos diferencias en la expresión de ceruloplasmina, precursor de haptoglobina, apolipoproteína AI y precursor de albúmina entre ambos tipos de pacientes. Ningún paciente presentó cambios en el SNP A-842G. La frecuencia de cambio en C22T y C50T fue relativamente baja con respecto a la población total. Conclusiones: No encontramos asociación entre la presencia de polimorfismos en el gen de la COX-1 y la peor respuesta a la aspirina. Los cambios en observados alfa1-antitripsina podrían estar relacionados con un diferente estado inflamatorio entre ambos tipos de pacientes (AU)

Aim: To evaluate the existence of a possible association between Aspirin resistance (AR), COX-1 single-nucleotide polymorphisms (SNPs) and the modifications in the plasma proteome of clinically stable coronary patients. Materials and methods: AR was defined according to the PFA-100 assay. AR-sensitive and AR-resistant patients had been taken aspirin for the last 9 months. The proteomic study (19 AR-sensitive, 19 AR-resistant) was performed using IPG strips (17cm, pH 4-7), SDS-PAGE gels (10%) and silver staining. We study three SNPs (A- 842G, C22T y C50T) in 50 AR-sensitive patients, 33 AR-resistant and 83 controls using a real-time PCR. Results: The expression of four alpha1-antitripsin isoforms was increased in the aspirin-resistant patients. No differences were found in the expression of ceruloplasmin, haptoglobin-precursor, apolipoprotein-AI and albumin- precursor between both groups of patients. The A-842G SNP was undetectable in all subjects. The remaining two SNPs (C22T y C50T) showed a low frequency with respect the global population. Conclusions: The low SNPs frequencies were unlikely to explain the difference in aspirin responsiveness between both groups of patients. The changes in alpha1-antitripsin could be linked with a different inflammatory state in these patients (AU)

El facultativo, un elemento necesario en el triaje de un Servicio de Urgencias en un hospital terciario / The physician is necessary in triage at Tertiary Hospital Emergency Department

Objetivo: Evaluar la necesidad de intervención de un facultativo en el triaje, para identificar al paciente potencialmente de alta complejidad en un servicio de urgencias que tiene implantado el sistema de triaje de Manchester (MTS). Método: Estudio observacional prospectivo, que seleccionó a los pacientes clasificados como muy urgentes (nivel 2 o naranja) y urgentes (nivel 3 o amarillo), según el MTS, en la Unidad de Primera Asistencia (UPA) del Servicio de Urgencias (SU) durante un periodo de 12 horas, para ser valorados por un médico adjunto con experiencia que decidió la ubicación inmediata según criterios médicos en una sala de agudos o en consultas de la UPA. La validez de la decisión fue establecida por el destino de los pacientes una vez visitados y medida por su índice de ingreso. Resultados: Se incluyeron un total de 100 pacientes, de los que 45 se seleccionaron para el estudio: 10 (22,22%) ubicables por el MTS en la sala de agudos como muy urgentes o naranjas y 35 (77,78%) ubicables por el MTS en la consulta de la UPA como urgentes o amarillos. El índice de ingreso de los pacientes ubicables en sala de agudos según el MTS, fue del 40% (N = 4) y el de los ubicables en consulta de la UPA del 20% (N = 7) (p = 0,23). El facultativo de triaje ubicó 12 pacientes (26,67%) en sala de agudos, 4 (8,89%) por requerir procedimientos técnicos y 8 (17,78%) por su complejidad y 33 pacientes (73,33%) en consulta de la UPA. El índice de ingreso de los pacientes ubicados, según criterio del facultativo, en sala de agudos por su complejidad fue del 87,5% (N = 7) y el de los ubicados en consulta de la UPA del 12,1% (N = 4) (p < 0,001). Conclusiones: La escasa capacidad del MTS para detectar los pacientes potencialmente complejos hace necesaria la intervención de un facultativo que asegure la ubicación inmediata de los pacientes, adecuando los servicios disponibles a la medida de las necesidades individuales y, por tanto, optimizando los recursos (AU)

Aim: To assess the need of a physician on the ED triage, with the aim of identifying high-complexity patients using Manchester Triage System (MTS) at an Emergency Department. Methods: Prospective observational study which enrolled all patients classified as very urgent (level 2 or orange) and urgent (level 3 or yellow) by the MTS in the First Assistance Unit (FAU) of the Emergency Department during a period of 12 hours, to be assessed by an experimented physician who decided the immediate location in an acute care or FAU area based on medical criteria. The validity of the decision was established according to the destiny of the patients once visited and measured by the admission index. Results: The study included 100 patients, 45 of whom were eligible for the study, 10 (22.22%) placed by the MTS in acute care area as very urgent or orange and 35 (77.78%) in FAU area as urgent or yellow. The admission index of patients placed in acute care area by MTS was 40% (N=4) and in those placed in FAU area was 20% (N=7) (p=0.23). The triage physician placed 12 patients (26.67%) in an acute care area, 4 (8.89%) due to technical procedures and 8 (17.78%) due to their complexity and 33 patients (73.33%) in a FAU area. According to the physician criteria, the admission index of the patients placed in an acute care area due to their complexity was 87.5% (N=7) and of those placed in FAU 12.1% (N=4) (p<0,000). Conclusions: The low capacity of the MTS to detect patients with potential high-complexity, makes the assessment of the physician necessary to guarantee the immediate location, adapting available services to individual necessities and therefore, optimising the resources (AU)

Medicación mantenida con inhibidores de la fosfodiesterasa (PDE-5) ¿algo más que tratar la disfunción eréctil? / Chronic treatment with PDE-5 inhibitors is there anything more than treating erectile dysfunction?

No disponible

Soluble guanylate cyclase beta1-subunit expression is increased in mononuclear cells from patients with erectile dysfunction.

The aim was to determine in circulating mononuclear cells from patients with erectile dysfunction (ED), the level of expression of endothelial nitric oxide synthase (eNOS), soluble guanylate cyclase (sGC) beta1-subunit and phosphodiesterase type-V (PDE-V). Peripheral mononuclear cells from nine patients with ED of vascular origin and nine patients with ED of neurological origin were obtained. Fourteen age-matched volunteers with normal erectile function were used as control. Reduction in eNOS protein was observed in the mononuclear cells from patients with ED of vascular origin but not in those from neurological origin. Although sGC beta1-subunit expression was increased in mononuclear cells from patients with ED, the sGC activity was reduced. However, only the patients with ED of vascular origin showed an increased expression of PDE-V. This work shows for the first time that, independently of the aetiology of ED, the expression of sGC beta1-subunit was increased in circulating mononuclear cells; however, the expression of both eNOS and PDE-V was only modified in the circulating mononuclear cells from patients with ED of vascular origin.

Involvement of endothelium and endothelin-1 in lead-induced smooth muscle cell dysfunction in rats.

Lead exposure induces dysfunction of the cyclic guanosine monophosphate-dependent vasodilator system through downregulation of soluble guanylate cyclase (sGC) expression. The endothelium not only releases vasodilators but also vasoconstrictors such as endothelin-1 (ET-1). Our aim was to explore the role of the vascular endothelium and ET-1 as possible mediators of lead-induced downregulation of sGC. Isolated aortic segments from Wistar Kyoto rats were incubated in the presence or absence of lead (1 parts per million) for 24 h. Endothelium was mechanically removed in some of the aorta segments. As reported previously, lead exposure induced downregulation of sGC protein expression in the intact aortic segments. However, lead exposure failed to significantly modify sGC-beta1 subunit expression in the endothelium-denuded aortic segments. Incubation with a selective ETA-type receptor inhibitor, BQ-123 (10(-6) mol/l), restored sGC protein expression in lead-exposed intact aortic segments. As it has also been previously observed, incubation in lead-containing medium resulted in the upregulation of cyclooxygenase-2 (COX-2) in the intact aortic segments. Denudation of endothelium partially abrogated this effect of lead. Incubation with BQ-123 prevented the lead-induced upregulation COX-2 in the intact aortic segments. However, neither ET-1 content nor ETA-type receptor expression were modified by lead exposure of the aortic segments. As conclusion, the endothelium through the activation of ETA-type receptors mediates the downregulation of sGC expression by lead in the vascular wall.

[Erectile dysfunction: the role of laboratory in the diagnostic and pronostic evaluation]. / Disfunción eréctil: papel del laboratorio en la evaluación diagnóstica y pronóstica.

OBJECTIVE: To review and to update the different laboratory tests recommended for etiologic diagnostic of erectile dysfunction and to evaluate the effect these tests could have on the pronostic and therapeutic strategy of this pathology. MATERIAL AND METHODS: We review the last articles related with etiopathogenics and pathophysiologics mechanisms of erectile dysfunction, including our studies on endothelial dysfunction and erectile dysfunction. RESULTS: The depth and extension of the laboratory protocol in erectile dysfunction is not necessaryly the same in all situations. The age, coincidence of comorbilities, set a different limit between patients demanding complementaries investigations that go beyond the basic request. CONCLUSIONS: The etiopathogenic laboratory work up in erectile dysfunction is currently changing incorporating news tests. The traditional search of commorbilities like diabetes, hepatic dysfunction, hypogonadism, hyperglucemia is getting broad with recents analitics evaluations related with potential markers of endothelial disease.

Disfunción eréctil: papel del laboratorio en la evaluación diagnóstica y pronóstica / Erectile dysfunction: the role of laboratory in the diagnostic and pronostic evaluation

Objetivo: Revisar y actualizar las diferentes pruebas de laboratorio recomendadas para el diagnóstico etiológico de la disfunción eréctil y el efecto que pudiera tener sobre el pronóstico y tratamiento de la enfermedad. Material y Métodos: Se han revisado las publicaciones más recientes y las que aportan nuevos conocimientos sobre los mecanismos etiopatogénicos y fisiopatológicos de la disfunción eréctil. Resultados: La profundidad o extensión del protocolo analítico en la disfunción eréctil no ha de ser necesariamente la misma en todas las circunstancias. La edad, la coincidencia real o presumible de comorbilidades, marcan un límite diferencial entre los pacientes, exigiendo investigaciones complementarias que superan las demandas básicas. Conclusión: La investigación etiopatogénica de la disfunción eréctil se ha ampliado considerablemente incluyendo nuevas pruebas de laboratorio. La tradicional búsqueda de comorbilidades como diabetes, disfunción hepática, hipogonadismo, hipercolesterolemia, se ha enriquecido con recientes valoraciones analíticas de potenciales marcadores de enfermedad endotelial (AU)

Objective: To review and to update the different laboratory tests recommended for etiologic diagnostic of erectile dysfunction and to evaluate the effect these tests could have on the pronostic and therapeutic strategy of this pathology. Material and methods: We review the last articles related with etiopathogenics and pathophysiologics mechanisms of erectile dysfunction, including our studies on endothelial dysfunction and erectile dysfunction. Results: The depth and extension of the laboratory protocol in erectile dysfunction is not necessaryly the same in all situations. The age, coincidence of comorbilities, set a different limit between patients demanding complementaries investigations that go beyond the basic request. Conclusions: The etiopathogenic laboratory work up in erectile dysfunction is currently changing ;;incorporating news tests. The traditional search of commorbilities like diabetes, hepatic dysfunction, hypogonadism, hyperglucemia is getting broad with recents analitics evaluations related with potential markers of endothelial disease (AU)