RESUMO
Heart failure is the second pathology of importance in long-lived dogs. It has been suggested that heart failure can be considered as a neurohormonal or neuroendocrine model, in which heart failure progresses as a result of over-expression of biologically active molecules that are able to exert a deleterious effect on the heart and circulation. Among these molecules is the rennin angiotensin aldosterone and its main effector peptide: the angiotensin II. In recent years, the pathophysiological consequences of the system have been the main focus of attention, being more relevant the alternative routes of angiotensin II synthesis and the participation of other enzymes such as the angiotensin converting enzyme. Therefore, this review aimed to describe the pathophysiological importance of the renin angiotensin aldosterone on Congestive Heart Failure.
La insuficiencia cardiaca es la segunda patología en perros longevos. Se ha sugerido que la insuficiencia cardiaca puede ser vista como un modelo neurohormonal o neuroendocrino, ya que la progresión de la enfermedad se da como resultado de la sobreexpresión de moléculas activadas biológicamente que son capaces de ejercer un efecto deletéreo sobre el corazón y la circulación. Dentro de estas moléculas está el Sistema Renina Angiotensina Aldosterona y su principal péptido efector, la angiotensina II. En los últimos años, las consecuencias fisiopatológicas del sistema han sido el foco principal de atención, siendo más relevantes las vías alternativas de síntesis de la angiotensina II y la participación de otras enzimas similares a la enzima convertidora de angiotensina. Por lo tanto, esta revisión pretende describir el valor fisiopatológico del sistema renina angiotensina aldosterona sobre la Insuficiencia Cardíaca Congestiva.
A insuficiência cardíaca é a segunda doença em cães longevos. Tem sido sugerido que a insuficiência cardíaca pode ser vista como um modelo neurohormonal ou neuroendócrino, já que a progressão da doença apresenta-se como um resultado da sobre-expressão de moléculas activadas biologicamente que são capazes de exercer um efeito deletério sobre o coração e a circulação. Dentre estas moléculas está o sistema renina-angiotensina-aldosterona e o seu peptídeo efetor principal, a angiotensina II. Nos últimos anos, as consequências fisiopatológicas deste sistema têm sido o foco principal de interesse, tendo maior relevância a síntese da angiotensina II e o envolvimento de outras enzimas como a enzima conversora da angiotensina. Portanto, esta revisão tem como objetivo descrever o valor fisiopatológico que tem o sistema renina-angiotensina-aldosterona sobre a insuficiência cardíaca congestiva.
RESUMO
Objecfive To investigate the effects of endotoxin on nuclear factor-κB p65(NF-κB p65)mRNA expression and ahtosteron secretion in rat hepatic stellate cells(HSCs).Methods Cultured rat HSCs(HSC-T6)were divided into endotoxin-treated group and control group.Cells in endotoxin-treated group were exposure to 1 mg/ml.endotoxin.Aldosteron secretions of HSCs were determined by radioimmunoassay,and NF-κB p65 mRNA expressions of HSCs were detected by one-step RT-PCR.Results At 6,12,24 and 48 h,aldosteron secretions in endotoxin-treated group were significantly hisher than those in the control group(t=3.063,4.577,6.847 and 9.317,P<0.05),and the expressions of NF-κB p65 mRNA in endotoxin-treated group were also higher than those in control group(t=5.155,6.095,7.875 and 9.313,P<0.01).Aldosteron secretions and NF-κB p65 mRNA expressions in HSCs displayed a positive correlation(r=0.886,P<0.01).Conclusion Endotoxin can up-regulate the aldosteron secretion and NF-κB p65 mRNA expression in rat HSCs,which may be one of the mechanisms of liver fibrosis induced by endotoxin.
RESUMO
La ascitis es el acúmulo anormal de líquido en la cavidad abdominal, que en el caso del paciente cirrótico obedece a una conjugación de factores determinantes. Diversas teorías se han elaborado al respecto a lo largo de las décadas anteriores, sin embargo el concepto actual es que el principal mecanismo patofisiológico de formación de ascitis es un estado de vasodilatación periférica permanente en el cirrótico, asociado a una relativa hipoperfusión renal que a su vez determina la activación de una serie de mecanismos retenedores de sodio y agua. Es un fenómeno progresivo cuya historia natural se puede ver como un espectro de enfermedad, teniendo como evento extremo al síndrome hepato-renal, con ascitis refractaria al tratamiento diurético y la mayor frecuencia de colonización bacteriana del líquido ascítico, fenómeno conocido como peritonitis bacteriana espontánea. El siguiente artículo revisa la patofisiología, diagnóstico, complicaciones y aspectos terapéuticos de la ascitis en el paciente cirrótico.
Ascites is the abnormal accumulation of fluid into the peritoneal cavity, which in the cirrhotic patient is due to a number of determinant factors. Many theories have been elaborated in that regard during the previous decades, however the current concept states that the chief pathophysiologic mechamism of ascites formation is a permanent state of peripheral vasodilation in the cirrhotic patient, associated with a relative renal hypoperfusion, which in turn activates a host of sodium and water retaining mechanisms. It is a progressive phenomenon and its natural history can be viewed as a spectrum of disease, having at one end of the spectrum the so called hepatorenal syndrome, with ascites refractory to diuretic treatment and a higher frequency of bacterial colonization of the ascitic fluid, so called spontaneous bacterial peritonitis. This article reviews the pathophysiology, diagnosis, complications and therapeutic aspects of ascites in the cirrhotic patient.
RESUMO
Objective To report the clinical characteristics, biochemical profiles, diagnosis and treatment of one Chinese pedigree with glucocorticoid remediable aldosteronism. Methods Plasma and urine aldo~sterone and cortisol and plasma renin activity were dynamically tested and diagnostic therapy was undergone in 3 affected subjects. Results All of 4 affected members had hypertension, hypokalemia, 3 patients had low basic and provoked renin activity (0.017?0.015 vs 0.13?0.08)?g?L -1 ?h -1 . 3 patients were treated with 2 mg dexamethasone for 5～7 days, then the medication was reduced gradually and maintained at 0.5～0.75 mg per day after 1～1.5 month(s). 5 days after treatment, the plasma aldosterone concentrations (PACs) decreased significantly from (192?9)ng/L to (87?7)ng/L (P