placental insufficiency/kalium

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Placental insufficiency leads to developmental hypertension and mesenteric artery dysfunction in two generations of Sprague-Dawley rat offspring.

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It is generally accepted that preeclampsia results from reduction in perfusion to the uteroplacental unit leading to maternal hypertension and fetal growth restriction. Placental insufficiency creates an environment of fetal undernutriton, predisposing the fetus to the development of adult disease.

[The new directions in the physiotherapeutic applications of the natural potassium salts of the Western Ural].

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Salt therapy (halotherapy) as a non-traditional method for the treatment of various pathological conditions has become an increasingly popular therapeutic modality in Russia and abroad. The Perm region houses one of the largest sylvinite-bearing potash deposits in the world. These salts are

[Bulimia, induced vomiting, hypochloremic-hypokalemic alkalosis and fetal distress in the 33rd week of pregnancy. Obstetric and anesthesiologic management].

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A 39-year-old primigravida was admitted to the hospital in the 33rd week of pregnancy due to fetal retardation and placental insufficiency, malnutrition, decreased cutaneous turgor, and cardiotocographic (CTG) fetal distress. Body weight had increased subnormally through the 29th week of gestation

Effects of vasoactive agents on intracellular calcium and force in myometrial and subcutaneous resistance arteries isolated from preeclamptic, pregnant, and nonpregnant woman.

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OBJECTIVE Preeclampsia is a common and serious complication of pregnancy, characterized by maternal hypertension and proteinuria, placental insufficiency, and fetal growth restriction. The purpose of this study was to investigate whether intracellular Ca 2+ ([Ca 2+ ] i ) and contractile responses of

Mesenteric vascular responsiveness in a rat model of pregnancy-induced hypertension.

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Reduced perfusion to the placenta in early pregnancy is believed to be the initiating factor in the development of preeclampsia, triggering local ischemia and systemic vascular hyperresponsiveness. This sequence of events creates a predisposition to the development of altered vascular function and

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