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BACKGROUND: It is known that epinephrine/norepinephrine inhibit acute pain transmission. However, the role of ß-adrenoceptors is not clear. Thus, we analyzed if beta-1 and/or beta-2 adrenoceptors can modulate acute pain transmission by performing in vivo single unit recordings during painful and non-painful peripheral stimulation in rats. METHODS: Longitudinal study in which we analyzed seven groups of male rats Wistar: control group (n = 11): saline (0.9 %); EPI group (n = 8): epinephrine 100 mcg; beta-1 agonist group (n = 8): dobutamine 125 mcg; beta-1-antagonist group (n = 9): metoprolol 100 mcg; beta-2-agonist group (n = 7): clenbuterol 100 mcg; beta-2-antagonist group (n = 8): butoxamine 100 mcg; beta-1-antagonist + EPI group (n = 10): metoprolol 100 mcg + epinephrine 100 mcg. For the statistical analysis we used ANOVA. RESULTS: Epinephrine significantly reduced the basal firing rate (BFR) in 34.1 % (p < 0.05) and also the evoked response by painful stimulation in 56 % (p < 0.05). No change was observed in the evoked response by non-painful stimulation. ANTß1 was the only beta-adrenoceptor acting drug that significantly reduced the evoked response by painful stimulation in 41 % (p < 0.05). None of the other drugs alone affected either the BFR or the evoked response to non-painful or painful stimulation. CONCLUSIONS: It is the first time that a beta-1-adrenoceptor antagonist (metoprolol) probes to be effective in reducing the response to painful stimulation in WDR neurons.

Introducción: la epinefrina/norepinefrina inhibe la transmisión del dolor agudo; empero, no es claro el papel de los receptores beta-adrenérgicos. Por tanto, analizamos si los fármacos de estos receptores modulan la transmisión del dolor agudo mediante registro electrofisiológico unitario extracelular in vivo durante estimulación periférica dolorosa y no dolorosa en ratas. Métodos: estudio longitudinal en el que se cotejaron siete grupos de ratas: control (n = 11): solución salina (0,9 %); EPI (n = 8): 100 mcg epinefrina; agonista beta-1 (n = 8): 125 mcg dobutamina; antagonista beta-1 (n = 9): 100 mcg metoprolol; agonista beta-2 (n = 7): 100 mcg clembuterol; antagonista beta-2 (n = 8): butoxamina 100 mcg; antagonista beta-1 + EPI (n = 10): 100 mcg metoprolol + 100 mcg epinefrina. Se hizo análisis estadístico por medio de ANOVA. Resultados: La epinefrina redujo significativamente la tasa de disparo basal (RDB) en 34.1 % (p < 0.05) y la respuesta evocada por la estimulación dolorosa en 56 % (p < 0.05). No hubo cambios en la respuesta provocada por la falta de estimulación dolorosa. El antagonista beta-1 fue el único fármaco con acción beta-adrenérgica que redujo significativamente la respuesta evocada por la estimulación dolorosa en 41 % (p < 0.05). Conclusión: por primera vez un antagonista de los receptores beta-1-adrenérgicos (metoprolol) prueba ser eficaz en la reducción de la respuesta a la estimulación dolorosa en las neuronas ARD.

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The endothelium plays an important role in the regulation of the intracellular fluid, vascular permeability, and modulation of vascular focal tone and angiogenesis. Endothelial dysfunction is manifested by the loss of the endothelium ability to modulate physiology changes in its vascular bed, and actually it is considered a prognostic marker of coronary artery disease. The relevance of assessing endothelial dysfunction relies in that it has been observed in different pathologies like DM, dyslipidemia, hypertension, tabaquism and in immunologic diseases like antiphospholipid syndrome and systemic lupus. PET is a non invasive method that allows the absolute quantification of myocardial blood flow during rest, stress and adrenergic stimulation, which allows to asses endothelial function. Therefore PET is a useful diagnostic technique to identify patients with endothelial dysfunction, and in the assessment of its response to administered therapy, allowing an optimal control and prevention of secondary adverse events of these diseases.

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El endotelio juega un papel importante en la regulación del líquido intracelular, la permeabilidad vascular, en la modulación del tono vascular focal y la angiogénesis. La disfunción endotelial se manifiesta por la pérdida de la capacidad del endotelio de modular el comportamiento fisiológico del lecho vascular y actualmente se considera un marcador pronóstico de la enfermedad arterial coronaria. La relevancia de estudiar la disfunción endotelial radica en que ésta se ha observado en diversas patologías como diabetes mellitas (DM), dislipidemia, hipertensión arterial sistémica, tabaquismo o en enfermedades inmunológicas como síndrome antifosfolípido y lupus eritematoso sistémico. La Tomografía por Emisión de Positrones (PET) es un método no invasivo que permite cuantificar en términos absolutos el flujo miocárdico en reposo, esfuerzo y durante la estimulación adrenérgica, siendo considerado en la actualidad el estándar de oro para valorar la función endotelial. Por lo tanto el PET es una herramienta diagnóstica muy útil en identificar a los pacientes con disfunción endotelial y en evaluar la respuesta a la terapia administrada en enfermedades que se acompañen de ésta. Permitiendo un control óptimo y prevención de eventos adversos de estas enfermedades.

The endothelium plays an important role in the regulation of the intracellular fluid, vascular permeability, and modulation of vascular focal tone and angiogenesis. Endothelial dysfunction is manifested by the loss of the endothelium ability to modulate physiology changes in its vascular bed, and actually it is considered a prognostic marker of coronary artery disease. The relevance of assessing endothelial dysfunction relies in that it has been observed in different pathologies like DM, dyslipidemia, hypertension, tabaquism and in immunologic diseases like antiphospholipid syndrome and systemic lupus. PET is a non invasive method that allows the absolute quantification of myocardial blood flow during rest, stress and adrenergic stimulation, which allows to asses endothelial function. Therefore PET is a useful diagnostic technique to identify patients with endothelial dysfunction, and in the assessment of its response to administered therapy, allowing an optimal control and prevention of secondary adverse events of these diseases.

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INTRODUCTION: Clostridium difficile-associated disease (CDAD) has been clearly associated with the use of broad-spectrum antibiotics worldwide. However, information about CDAD is scarce in Mexico and Latin America. MATERIAL AND METHODS: We studied clinical characteristics, associated factors and outcomes of all cases of CDAD diagnosed by toxin A fecal detection in a tertiary care hospital in Mexico City from 2003 to 2007. Cases were paired with controls by date of hospital discharge. RESULTS. A total of 3170 tests were performed; we evaluated 113 cases and 226 controls, with an incidence of 5.04 cases x 1000 hospital discharges during the study period. There was no difference in gender or primary diagnosis. After multivariate analysis, we found as significant risks the following: use of H2 blockers (OR 21.73, 95% CI 7.14-66.67, p < 0.001), age < 65 y (OR 10.21, IC95% 2.74-38.00, p < 0.001), prior hospitalization within 12 weeks of diagnosis (OR 4.39, IC95% 1.81-40.64, p < 0.001), prior use of cephalosporins (OR 3.41, CI 95% 1.56-7.46, p = 0.002), and fluoroquinolones (OR 3.11, IC95% 1.12-8.62, p = 0.029), stay at the intensive care unit (ICU) (OR 2.76, IC95% 1.38-5.49, p = 0.004); and, extended hospital stay (OR 1.10, IC95% 1.05-1.16, p < 0.001) or antimicrobial use before diagnosis (OR 1.05, IC95% 1.01-1.09, p = 0.010). We described an outbreak of 12 cases occurred in August of 2005 (29.5 cases per 1,000 discharges). We also observed a higher seasonal incidence of disease during the summer in the study period. CONCLUSIONS: The use of H2 blockers, age < 65 years, prior hospitalization or earlier use of cephalosporins or fluoroquinolones, as well as stay at the ICU were independent risk factor for CDAD.

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It used to be thought that the consequences of coronary artery disease were final, and that the prognosis of the patient was limited to the extent of the ventricular dysfunction. This paradigm changed radically when the concept of hibernating myocardium was introduced, which states the existence of tissue that can regain contractile function after being re-vascularized. This introduced a new concept in cardiology: myocardial viability. This work presents a clear example of the importance of detecting myocardial viability in selected patients, due to the impact not only in treatment but in prognosis as well. It is also emphasized that positron emission tomography (PET) is the gold standard method to detect myocardial viability.

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It used to be thought that the consequences of coronary artery disease were final, and that the prognosis of the patient was limited to the extent of the ventricular dysfunction. This paradigm changed radically when the concept of hibernating myocardium was introduced, which states the existence of tissue that can regain contractile function after being re-vascularized. This introduced a new concept in cardiology: myocardial viability. This work presents a clear example of the importance of detecting myocardial viability in selected patients, due to the impact not only in treatment but in prognosis as well. It is also emphasized that positron emission tomography (PET) is the gold standard method to detect myocardial viability.

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