705 research outputs found
Treatment of the cardiovascular remodeling in hypertensive patients
El corazón del hipertenso se adapta al aumento de sobrecarga que la elevación de
las resistencias vasculares sistémicas conlleva aumentando del grosor de la pared ventricular.
Los miocitos cardÃacos adultos no proliferan, por lo que la hipertrofia cardÃaca conlleva
un aumento del volumen de las células musculares. Además, aparece hipertrofia e
hiperplasia de los componentes non-miocitarios cardÃacos. El resultado es una fibrosis
perivascular e intersticial que dÃsminuye la dÃstensibilidad ventricular y ocluye los vasos
coronarios, dÃsminuye la reserva coronaria y facilita la isquemia miocárdÃca. La estructura
vascular también se modifica en respuesta al aumento del estrés de la pared arterial,
aumentando el cociente pared/luz vascular consecuencia de un aumento del grosor de la
pared vascular o del remodelado de los componentes celulares y no celulares de la
misma. Estos cambios aumentan la reactividad vascular y potencien el aumento de las
resistencias vasculares periféricas caracteristico del hipertenso.
La pobre correlación existente entre reducción de la presión arterial y la magnitud
del remodelado cardÃovascular confirma el importante papel de factores no-hemodÃnámicos
en su patogenia (estimulación de los receptores ATI y al- adrenérgicos, edad, sexo, raza,
factores genéticos, etc.). EstudÃos experimentales y clÃnicos han demostrado que todos
los antihipertensivos previenen o revierten la hipertrofia cardÃaca. Sin embargo, no sólo
existen dÃferencias entre los dÃstintas familias de fármacos, sino también entre los
miembros de cada una de ellas. Los fármacos que inhiben el tono simpático y el sistema
renina-angiotensina-aldosterona o reducen la [Ca]i son lo que mayor regresión producen,
aunque el efecto parece ser más marcado con los inhibidores de la enzima de conversión.
La activación refleja neurohumoral reducida por diuréticos o vasodilatadores arteriales
podria explicar su incapacidad para revertir el remodelado cardiovascular a pesar de que
normalizan la presión arterial.
Es lógico, por tanto, sugerir que el futuro desarrollo de fármacos antihipertensivos
debe ir dirigido no sólo a obtener fármacos capaces de revertir el proceso de remodelado
cardÃovascular del hipertenso, es decir, conseguir restaurar la estructura y función de los
órganos dÃana. Sólo de esta forma podremos reducir la morbiortalidad del hipertenso.The heart adapts to increasing afterload, such as that which occurs in arterial
hypertension with an increase in wall thickness (left ventricular hipertrophy) in order to
bring wall stress back to normal. Adult cardiac myocytes are unable to proliferate, so that
myocyte hypertrophy is the hallmark of left ventricular hipertrophy. Cardiac remodelling,
however, involves not only myocyte growth but also hypertrophy/hyperplasia of nonmyocyte
cells within the myocardium. The result is a perivascular and intersticial fibrosis that
impair myocardial stiffuess. In response to increased arterial pressure, the vessel structure
is altered such that the ratio of the width of the wall to the width of the lumen is
increased by either an increase in mass or rearrangements of vascular smooth muscle
cells and other cellular and noncellular elements of the vascular wall. These changes
increased vascular reactivity, potentiated the increase in peripheral vascular resistance
characteristic of hypertension and attenuated the coronary reserve to ischemic provocation.
The poor correlation between blood pressure and the magnitude of cardiovascular remodelling
strongly suggests a role for nonhemodynarnic factors in its pathogenesis (i.e. neurohumoral
activation, neurogenic stimuli, genetic predisposition, gender, age and race). An increase
in sympathetic (cd-adrenoceptors) and renin-angiotensin-aldosterone systerns (ATl receptors)
piay an important role in both cardiac myocyte and nonmyocyte growth and remodelling.
Experimental and clinical studies have demonstrated that all antihypertensive agents may
prevent or cause regression of cardiovascular remodelling. However, despite their equipotent
blood-lowering effects, there are not only marked differences in the ability of different
types of antihypertensive drugs to prevent or reverse cardiovascular remodelling but also
whithin the same class of pharmacological drugs. Antihypertensive drugs that modulate
the sympathetic or renin-angiotensin-aldosterone systems or the intracellular free Ca
concentration can reverse cardiovascular remodelling, this effect being more pronounced
with ACE inhibitors. Reflex neurohumoral activation may be responsible for the failure
of sorne antihypertensive drugs to produce regress cardiovascular remodelling (diuretics,
vasodilators, ~-blockers with intrinsic sympathomirnetic activity and dihydropyridines),
even through they reduce arterial blood presure to normotensive levels.
It is therefore, logical to suggest that a more ambitious approach to modem treatrnent
of hypertension would not only be to reduce elevated blood pressure, but also to introduce
an important additional goal, namely to attain regression of structurally remodelled heart
and vasculture to, or toward, normal structure and function. Only this therapeutic approach
might truly reduce the risk of cardiovascular complications in the hipertensive patient
Tratamiento de la insuficiencia cardÃaca
La insuficiencia cardÃaca congestiva (lCC) puede definirse como la incapacidad del
corazón para proveer las necesidades tisulares y/o la necesidad de mantener unas presio nes de llenado ventricular anormalmente elevadas para producir un volumen minuto
adecuado. Los objetivos del tratamiento de la ICC incluyen la mejorÃa de los sÃntomas
y la limitación de la actividad fÃsica, prevenir la progresión del proceso y prolongar la
supervivencia. Clásicamente hay dos formas de tratamiento: aumentar la contractilidad
cardiaca y disminuir la pre y postcarga. Los diuréticos constituyen la primera lÃnea de
tratamiento en la mayorÃa de los pacientes con ICC sintomática ya que producen una
mejorÃa rápida y mantenida de los sÃntomas que, en su mayorÃa, son consecuencia de la
retención hidrosalina que se manifiesta como edemas y congestión pulmonar. La digoxina,
el único fármaco inotrópico positivo utilizado por vÃa oral, no sólo bloquea la ATPas-Na/
K, sino que además restaura la sensibilidad de los barorreceptores e inhibe el tono
simpático. Por el contrario, los inhibidores de la fosfodiesterasa aumentan la indicencia
de arritmias, aceleran la progresión del cuadro y disminuyen la supervivencia del pacien te. La utilización de vasodilatadores se basa en su capacidad para mejorar la función
ventricular actuando sólo sobre el componente vascular, reduciendo la precarga y/o la
postcarga. Los inhibidores de la enzima de conversión interfieren con la activación
neurohumoral que conlleva a la vaso constricción y la retención hidrosalina y reduce la
supervivencia. Asociados a diuréticos y digoxina mejoran la situación clÃnica y hemodinámica
y aumentan la supervivencia
Correlation functions in scalar field theory at large charge
We compute general higher-point functions in the sector of large charge operators ϕn,ϕ¯¯¯n at large charge in O(2) (ϕ¯¯¯ϕ)2 theory. We find that there is a special class of "extremal" correlators having only one insertion of ϕ¯¯¯n that have a remarkably simple form in the double-scaling limit n →∞ at fixed g n2 ≡ λ, where g ~ ϵ is the coupling at the O(2) Wilson-Fisher fixed point in 4 − ϵ dimensions. In this limit, also non-extremal correlators can be computed. As an example, we give the complete formula for ⟨ϕ(x1)nϕ(x2)nϕ¯¯¯(x3)nϕ¯¯¯(x4)n⟩, which reveals an interesting structure
Mise au point d'une méthode d'extraction des lipides solubles totaux, des glucides solubles totaux et des composés phénoliques solubles totaux des organes de la vigne
Il est possible d'obtenir très rapidement et à partir d'une même poudre la totalité des lipides solubles, des glucides solubles et des composés phénoliques solubles. Le nombre d'opération nécessaires dépend des organes et a été déterminé pour les rameaux principaux, les feuilles, les rafles, les baies et les pépins.Adjustment of a method of extraction of total soluble lipids, total soluble carbohydrates and total soluble phenolic compounds from the organs of the vineIt is possible to obtain very quickly from the same powdered plant material total amounts of soluble lipids, soluble carbohydrates and soluble phenolic compounds. The number of operations required depends upon the organ concerned and has been determined for the fruiting shoots, the leaves, the rachises, the berries and the seeds
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Cardiovascular Pharmacotherapy in Older People - Challenges Posed by Cardiovascular Drug Prescription in the Elderly
The Cerebellar Nodulus/Uvula Integrates Otolith Signals for the Translational Vestibulo-Ocular Reflex
Background: The otolith-driven translational vestibulo-ocular reflex (tVOR) generates compensatory eye movements to linear head accelerations. Studies in humans indicate that the cerebellum plays a critical role in the neural control of the tVOR, but little is known about mechanisms of this control or the functions of specific cerebellar structures. Here, we chose to investigate the contribution of the nodulus and uvula, which have been shown by prior studies to be involved in the processing of otolith signals in other contexts. Methodology/Principal Findings: We recorded eye movements in two rhesus monkeys during steps of linear motion along the interaural axis before and after surgical lesions of the cerebellar uvula and nodulus. The lesions strikingly reduced eye velocity during constant-velocity motion but had only a small effect on the response to initial head acceleration. We fit eye velocity to a linear combination of head acceleration and velocity and to a dynamic mathematical model of the tVOR that incorporated a specific integrator of head acceleration. Based on parameter optimization, the lesion decreased the gain of the pathway containing this new integrator by 62%. The component of eye velocity that depended directly on head acceleration changed little (gain decrease of 13%). In a final set of simulations, we compared our data to the predictions o
Electroreflectance spectroscopy in self-assembled quantum dots: lens symmetry
Modulated electroreflectance spectroscopy of semiconductor
self-assembled quantum dots is investigated. The structure is modeled as dots
with lens shape geometry and circular cross section. A microscopic description
of the electroreflectance spectrum and optical response in terms of an external
electric field () and lens geometry have been considered. The field
and lens symmetry dependence of all experimental parameters involved in the
spectrum have been considered. Using the effective mass formalism
the energies and the electronic states as a function of and dot
parameters are calculated. Also, in the framework of the strongly confined
regime general expressions for the excitonic binding energies are reported.
Optical selection rules are derived in the cases of the light wave vector
perpendicular and parallel to . Detailed calculation of the Seraphin
coefficients and electroreflectance spectrum are performed for the InAs and
CdSe nanostructures. Calculations show good agreement with measurements
recently performed on CdSe/ZnSe when statistical distribution on size is
considered, explaining the main observed characteristic in the
electroreflectance spectra
Antiarrhythmic agents
Los fármacos antiarritmicos son un grupo heterogéneo de sustancias que constituyen,
junto con la estimulación eléctrica programada, la implantación de marcapasos, la cirugÃa y
la fulguración, la base de la terapéutica antiarritmica actual. La mayor parte de las arritmias
observadas en la práctica clinica son debidas al fenómeno de reentrada, que representa una
alteración en la conducción del impulso cardiaco. Para que se produzca una arritmia por
reentrada debe: a) existir un obstáculo anatómico o funcional que defina el circuito de
reentrada, b) existir un área de bloqueo unidireccional y c) el tiempo que el impulso tarda en
recorrer el circuito debe ser mayor que el perÃodo refractario. Teóricamente, estas arritmias
pueden ser tratadas mediante dos tipos diferentes de maniobras: 1) disminuyendo la velocidad de conducción, de tal manera que convirtamos el área de bloqueo unidireccional
en bidireccional. Los fánnacos antiarritmicos que producen este efecto son aquellos que
actúan inhibiendo la corriente rápida de entrada de sodio (INa), o fánnacos antiarritmicos
del grupo 1. 2) Prolongando el perÃodo refractario, de tal modo que el frente de onda del
circuito se encuentre con tejido inexcitable. Recientes estudios clÃnicos (CAST, 1989)
han puesto en tela de juicio la eficacia de los fánnacos antiarrÃtmicos del grupo 1, dado
que dos de los fánnacos más potentes de este grupo (flecainida y encainida) no sólo no
disminuyeron, sino que aumentaron la mortalidad en pacientes con infarto de miocardio
previo y que presentaban más de 7 extrasÃstoles ventriculares tempranos. Estos resultados
obligaron a un replanteamiento en la terapéutica antiarritmica, y condujo a diferentes grupos
de investigación a la sÃntesis y caracterización de nuevos fármacos capaces de prolongar el
periodo refractario, o fármacos antiarritmicos del grupo m. El fármaco antiarritmico "ideal"
de este grupo serÃa aquél que produjera una mayor prolongación del perÃodo refractario a
frecuencias de estimulación más rápidas (más efectivo en taquicardia). Sin embargo, ningún
fármaco antiarritmico del grupo m presenta este perfil farmacológico. Por el contrario, son
más eficaces a frecuencias lentas (durante la bradiacardia) que a frecuencias rápidas. La
excepción es la arniodarona (el primer fánnaco antiarritmico de este grupo, con propie dades antiarritmicas del grupo 1, B-bloqueantes y antagonistas del calcio) que prolonga
el perÃodo refractario a cualquier frecuencia de estimulación: es independiente de la
frecuencia. La utilización de técnicas de BiologÃa Molecular que nos permitan conocer
la estructura de los canales iónicos involucrados en la r epolarización del potencial de
acción, asà como estudios realizados en miocitos cardiacos humanos nos proporcionarán
una gran ayuda para diseñar nuevos fánnacos antiarritmicos sobre bases más racionales.Antiarchythmic agents are a very hoterogenous group of drugs which, together with
programmed electrical stimulation, pacemaker implantation, ablation and surgery, constitute
the basis of the antiarrhythmic therapy. Most clinical arrhythmias are due to reentry,
which represents an alteration of the cardiac impulse. The basis for reentry are: a) an
anatornical or functional obstacle which defines the circus movement, b) an area of
unidirectional block, and c) the length of path must exceed the wave length deterrnined
by effective refractoriness. Theoretically, reentrant arrhythmias can be suppressed by: 1)
decreasing the conduction velocity, so that the area of unidirectional block becomes an
area or bidirectional block. Antiaarrhythmic drugs acting by this mechanism include
those that decrease the fast inward sodium current (INal), the so-caHed class 1 antiarrythmic
drugs. 2) Lengthenin of the effective refractory period, in such a way that the wavefront
encroaches in its own refractory period and the cardiac impulse cannot be propagated
anymore. Drugs that selectively prolonged the effective refractory period are included as
class III antiarrhytmics. Recent clinical studies (CAST, 1989) have warned the scientific
community about the effectiveness and safety of class 1 antiarrhythmic drugs, since two
of them (flecainide and encainide) did not de crease, but increased mortality in patients
which previous myocardial infarction and asymptomatic ventricular extrasystoles. These
results led numerous work groups and pharmaceutical companies to develop new class
III antiarrhythmic drugs. The "ideal" class III antiarrhythmic drug would be that which
produced rninirnal effect in sinus rhythm but produced a marked prolongationof the
effective refractory period when the heart rate increased (i.e. during tachycardia). However,
none of the available class III antiarrhythmic drugs exhibit this pharrnacological profile.
On the contrary, they prolonged cardiac refractoriness more at low frequencies of stimulation
(bradycardia) than at higher stimulation rates. Only arniodarone, the first class ID antiarrhythmic
drug, which exhibits class 1, 11 (B-adrenoceptor blockade) and IV (calcium antagonist)
properties produced a prolongation of the effective refractory period at aH cardiac rates,
i.e. its effect is frequency-independent. The use of Molecular Biology techniques which
allow us to determine the structure of the ionic channels involved in the repolarization
of the cardiac action potential, as well as the studies performed in isolated human cardiac
myocytes will afford the basis for a more rational design of new antiarrhythmic drugs
Processing and characterisation of II-VI ZnCdMgSe thin film gain structures
Lattice-matched II-VI selenide quantum well (QW) structures grown on InP substrates can be designed for emission throughout the visible spectrum. InP has, however, strong visible-light absorption, so that a method for epitaxial lift-off and transfer to transparent substrates is desirable for vertically-integrated devices. We have designed and grown, via molecular beam epitaxy, ZnCdSe/ZnCdMgSe multi-QW gain regions for vertical emission, with the QWs positioned for resonant periodic gain. The release of the 2.7 μm-thick ZnCdSe/ZnCdMgSe multi-QW film is achieved via selective wet etching of the substrate and buffer layers leaving only the epitaxial layers, which are subsequently transferred to transparent substrates, including glass and thermally-conductive diamond. Post-transfer properties are investigated, with power and temperature-dependent surface and edge-emitting photoluminescence measurements demonstrating no observable strain relaxation effects or significant shift in comparison to unprocessed samples. The temperature dependant quantum well emission shift is found experimentally to be 0.13 nm/K. Samples capillary-bonded epitaxial-side to glass exhibited a 6 nm redshift under optical pumping of up to 35 mW at 405 nm, corresponding to a 46 K temperature increase in the pumped region; whereas those bonded to diamond exhibited no shift in quantum well emission, and thus efficient transfer of the heat from the pumped region. Atomic force microscopy analysis of the etched surface reveals a root-mean-square roughness of 3.6 nm. High quality optical interfaces are required to establish a good thermal and optical contact for high power optically pumped laser applications
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