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asbryobvrz · Wysłany: Pon 8:00, 07 Mar 2011

,[link widoczny dla zalogowanych]
Hemodialysis in uremic patients in the clinical study the mechanism of hypertension

extracellular fluid volume expansion is the development of hypertension in dialysis patients the main pathophysiological mechanism of E2]. study found that about 50% of hemodialysis patients with high blood pressure to some extent dependent on the capacity,[link widoczny dla zalogowanych], the resulting high blood pressure more Question of the weight gain seen in dialysis patients significantly. but some still do not fully satisfactory blood pressure control in dialysis patients, suggesting that Shuinazhuliu is not the only reason for high blood pressure. In addition, RAS system, an abnormal increase in the activity of the sympathetic nervous system over-excitement E33, excessive secretion of vasoactive substances and other factors are also associated. there are found, ET1 also with end-stage kidney disease hypertension. dialysis plasma levels of ET-1 decreased, so the full body of dialysis to avoid the level of ET-1 the vasoconstriction caused by high blood pressure [. In this study,[link widoczny dla zalogowanych], as far as possible to maintain dialysis adequacy based on the observation of the occurrence of hypertension during dialysis with the RAS, endothelial derived factor between the question and found that Kt / v values in the There were no significant differences between the groups, hypertension, plasma PRA levels in patients before and after dialysis at the dialysis blood pressure were significantly higher than normal, but blood pressure in the dialysis group only in dialysis than predialysis blood pressure is not found significantly higher increase in plasma Ang-II levels in the blood pressure before dialysis was significantly higher than normal, each group after dialysis was no significant difference; ET-1 levels in plasma before dialysis than in the group significantly higher than normal blood pressure. hemodialysis PRA increased blood pressure group than in predialysis blood pressure did not increase after dialysis were significantly increased, plasma Ang-II levels in the blood pressure before dialysis after dialysis did not increase more significantly increased, but plasma levels of ET-1 through blood pressure did not increase after the group difference was not statistically significant. In this study, each group PRA, Ang-II and ET-1 were lower than dialysis after dialysis,[link widoczny dla zalogowanych], and this mainly related to their molecular weight. We use dialyzer as poly methyl methacrylate film (PMMA), the largest molecular weight retention 34720IH, molecular weight renin 39680I1J, it is not removed by the dialyzer, and Ang-II relative molecular mass of 962. 5Iu, ET-1 relative molecular mass 2380.8I1J, are in the molecular substance, it can be partially removed. Therefore, the plasma Ang-II and ET-1 levels in all groups after dialysis were not significantly different, while plasma renin activity in hypertensive dialysis before and after dialysis group were significantly higher than normal blood pressure. It is worth mentioning that the study not only found that plasma renin activity and levels of Ang-II not only in the hypertensive group and normotensive group Q are different, and in blood pressure after dialysis,[link widoczny dla zalogowanych], after dialysis group with normal blood pressure are more significant differences between groups, to clarify RAS system activation in dialysis related hypertension play a role in the pathogenesis of this study did not find a plasma ET 1 Levels of blood pressure after dialysis group and blood pressure did not increase after dialysis the difference between the groups. In short, high blood pressure in hemodialysis patients in the high incidence, inadequate dialysis is known to cause high blood pressure one of the reasons adequate dialysis patients in this group were found on the basis of dialysis related hypertension and renin-angiotensin system and excessive activation of ET for the future of the system to provide a theoretical basis for drug intervention.