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PostSubject: increased cardiac ejection   Wed May 02, 2007 9:08 pm

It has been observed that pathological changes in the brain, heart, liver pregnant with PE resemble such as gipovolemii (31), while reducing woven blood flow typical of the early stages of the disease, and recorded well before its clinical manifestations (3). Risk convulsant epilepsy is highest when PE, and the HAG proteinuriey it below 8 times, as HAG without proteinurii it below 17 times (10). This indicates that rather gipoperfuziya bodies than vascular damage as a result of hypertension determine clinical picture of PE. The relative rarity of liver damage in PE, known as HELLP-sindrom is the feature of the body of blood from two sources : rivers, through the liver artery and portal veins. The organs affected by gipovolemii applies pregnant womb. So in pregnant women with VZRP already in the early stages, there are signs of decline in circulating blood : reducing the size of the left atrium, the concentration of sodium in the blood, spadenie bottom with the vena cava (14). There is suspicion on the involvement of RAAS in the processes going on in the pregnancy spiral arteries (Invasion trofoblasta in muscle layer), because they found wall renin gene expression, APF, angiotenzina receptors (25). A frequent occurrence in pregnant women with PE is a violation of cerebral circulation, which is the leading cause of maternal mortality in this disease. It is known that astrotsity brain, and proliferiruya migrating from the affected area vascular bed, recovering extracellular matriks and thus gemato-entsefalicheski barrier (GEB). Astrotsity deprived angiotenzinogena, poorly restored GEB, but you can update the introduction angiotenzina II and type IV (19). Insulin secretion blocking angiotenzinogena VIP cells (6) that, in excess insulin, provoked kontrinsulyarnymi hormones of pregnancy and obesity and metabolism angiotenzinogena inheritance defect may contribute to the development of PE, which is often a resistance to insulinu. It is worth noting that the processes relate to the mother body, because despite the fact that the components of RAAS : mRNK prorenin, angiotenzinogen, angiotenzina receptors, in platsente and endotelii fruit in all stages of pregnancy (13), signs of damage endoteliya receptacles fruit with PE has not been forthcoming. So the products of nitric oxide feto-platsentarnym set, the contents of the fetus is not reduced and the system it operates at a higher synthesis, kompensatornom mode (17). According to our records, there is a clear and direct relationship of fluid in the body pregnant, expressed in the form of impedance and length of daylight hours (20). In mid-latitudes which creates an impedance during the year (Figure 1). However, impedance changes and the frequency of PE. These changes can be imputed to submit a harmonic motion, the terms of which are about 20 weeks. This date in pregnant greatest growth in circulating blood (BCC), which is accompanied by increased cardiac ejection and lower round (24), increasing active plasma renin : 5 times (15). When this term pregnancy coincides with minimal or falling rates impedance, and frequency of PE is the lowest, and, accordingly, on the contrary. Figure 1. Changing Bodies pregnant impedance and frequency of PE in the year. Changing Bodies pregnant impedance and frequency pre-eclampsia during the year Figure 1 provides an alleged pathogenesis of PE and hypertension pregnant. The proposed concept needed clarifications : 1. It should be noted that the lack of RAAS and the reaction of the vascular bed gipovolemiyu an individual. It is possible pregnancy without hypertension, a leading, owing to a violation of the IPC, the VZRP and nedonashivaniyu. 2. If gipovolemii or clinically apparent vazospazma, increase blood viscosity violated "food" endoteliya in violation of its functions, which leads to a decline in production prostatsiklina and nitrogen oxide, activated platelets, imbalance prostatsiklin-trombok Brian and "closed" cycle vazospazm-endotely.

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