Abstract

Currently, preeclampsia is one of the most significant problems in obstetrics and gynecology. The significance of this pathology is determined by its high prevalence and pathological impact on the organism of both mother and fetus. The pathogenesis of preeclampsia is very complex, involving many different interrelated, complementary pathophysiological and biochemical reactions. One of the main mechanisms of preeclampsia development is the excessive synthesis of antiangiogenic factors that, among other effects, contribute to increased activity of a number of substances with vasoconstrictor action. These changes lead to the formation of placental insufficiency and the development of clinically overt disease. Among the most important substances that contribute to the formation of excessive uncontrolled vasospasm are endogenous digitalis-like factors (EDFs) which regulate the activity of Na+/K+-ATPase. The most important structural class of EDFs is represented by bufadienolides. The classic representative of this group is marinobufagenin. It selectively blocks the α-1 isoform of Na+/K+-ATPase, widely represented in the renal tubules thereby having the properties of potent.

Highlights

  • Среди ведущих проблем современной клиниче- с одной стороны, высокой частой встречаемости данской акушерско-гинекологической практики особое ного заболевания, а с другой стороны, ее способнозначение занимает преэклампсия

  • The significance of this pathology is determined by its high prevalence

  • of the main mechanisms of preeclampsia development is the excessive synthesis of antiangiogenic factors that

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Summary

Introduction

Среди ведущих проблем современной клиниче- с одной стороны, высокой частой встречаемости данской акушерско-гинекологической практики особое ного заболевания, а с другой стороны, ее способнозначение занимает преэклампсия. Что она способна провоцировать развитие ряда тяжелых синдромов, со стороны как организма матери, так и ребенка. Наблюдающихся на фоне ухудшения кровообращения, сопровождающегося понижением уровня кислорода в тканях при развитии преэклампсии, является запуск ишемического каскада, в рамках которого происходит формирование оксидантного стресса.

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