医学
内科学
缺氧(环境)
血管收缩
心脏病学
发病机制
缺血
子痫前期
灌注
血压
怀孕
生物
化学
氧气
遗传学
有机化学
作者
Joey P. Granger,Babbette LaMarca,Kathy Cockrell,Mona Sedeek,Charles Balzi,Derrick Chandler,William A. Bennett
出处
期刊:Humana Press eBooks
[Humana Press]
日期:2006-06-30
卷期号:: 381-392
被引量:183
标识
DOI:10.1385/1-59259-989-3:381
摘要
Despite being one of the leading causes of maternal death and a major contributor of maternal and perinatal morbidity, the mechanisms responsible for the pathogenesis of preeclampsia are unknown. The initiating event in preeclampsia has been postulated to be reduced uteroplacental perfusion. Placental ischemia/hypoxia is thought to lead to widespread activation/dysfunction of the maternal vascular endothelium, vasoconstriction and hypertension. Experimental induction of chronic uteroplacental ischemia appears to be the most promising animal model to study potential mechanisms of preeclampsia since reductions in uteroplacental blood flow in a variety of animal models lead to a hypertensive state that closely resembles preeclampsia in women. This chapter details the methods we use in our laboratory to produce the reduced uterine perfusion pressure (RUPP) model in the pregnant rat.
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