Podjarny Eduardo, Losonczy Gyorgy, Baylis Chris
Department of Nephrology and Hypertension, Meir Hospital, Sackler Faculty of Medicine, Tel-Aviv University, Israel.
Semin Nephrol. 2004 Nov;24(6):596-606. doi: 10.1016/s0270-9295(04)00131-7.
There have been many attempts to produce animal models that mimic the hypertensive disorders of pregnancy, especially preeclampsia, but most are incomplete when compared to the full spectrum of the human disease. This review assesses a number of these models, organized according to the investigators attempt to focus on a specific pathogenic mechanism believed to play a role in the human disease. These mechanisms include uterine ischemia, impairments in the nitric oxide system, insulin resistance, overactivity of the autonomic nervous and/or renin-angiotensin systems, activation of a systemic inflammatory response, and most recently, activation of circulating proteins that interfere with angiogenesis. In addition a model of renal disease that mimics superimposed preeclampsia is discussed. Defining these animal models should help in our quest to understand the cause, as well as to test preventative and therapeutic strategies in the management of these hypertensive disorders of pregnancy.
人们已进行了许多尝试来建立模拟妊娠高血压疾病(尤其是先兆子痫)的动物模型,但与人类疾病的全貌相比,大多数模型并不完善。本综述评估了其中一些模型,这些模型是根据研究人员试图聚焦于一种被认为在人类疾病中起作用的特定致病机制来组织的。这些机制包括子宫缺血、一氧化氮系统功能受损、胰岛素抵抗、自主神经和/或肾素 - 血管紧张素系统过度活跃、全身炎症反应激活,以及最近发现的干扰血管生成的循环蛋白激活。此外,还讨论了一种模拟叠加先兆子痫的肾脏疾病模型。明确这些动物模型应有助于我们探寻病因,并测试这些妊娠高血压疾病管理中的预防和治疗策略。