| Summary: | Placental hypoxia is commonly considered to play an important role in the development of several perinatal and neonatal diseases such as intrauterine growth retardation (IUGR) or preeclampsia. In this disertation we therefore tried to (at least partially) solve this problem by answering the question how do acute and chronic hypoxia affect fetoplacentar vasculature. Unlike all vascular beds with the exception of the pulmonary circulation, fetoplacental vessels respond to acute hypoxia with vasoconstriction ( HFPV). This mechanism presumably diverts blood flow from poorly oxygenated areas towards regions with better O2 supply. We already know, that hypoxia inhibits potassium channels and thus causes depolarization in fetoplacental vascular smooth muscle. We propose that this hypoxia-induced depolarization leads to vasoconstriction by activating voltage- dependent calcium (Ca) channels and Ca influx. We performed our first experiment on the preparation of dually perfused cotyledon of the human placenta, which we gained immediately after uncomplicated spontaneus deliveries or elective caesarian sections. The preparation was perfused with Krebs' saline with dextran and meclophenamate and gased with 40% O2, 5% CO2 a 55% N2. We compared HFPV, which was elicited by changing gasing of the perfusate to the...
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