Bayrak Sibel, Pehlivanoglu Bilge, Balkanci Zeynep Dicle, Ozyurek Hamit, Aksoy Yasemin, Atilla Pergin, Cakar Ayse Nur
Department of Physiology, Hacettepe University, Faculty of Medicine, Ankara, Turkey.
J Matern Fetal Neonatal Med. 2009 Jun;22(6):528-36. doi: 10.1080/14767050902822229.
Transient hypotension attacks, frequently experienced during pregnancy, have detrimental effects on maternal and fetal physiology. Despite the strong autoregulatory mechanisms, kidneys are remarkably sensitive to hypoperfusion. Transient hypotension together with high metabolic demand and increased oxygen requirement during pregnancy may disturb the oxidant status and natural course of nitric oxide (NO) metabolism. Therefore, we investigated in this study the effects of systemic hypotension during pregnancy on kidney oxidant status and morphology and plasma NO levels in an experimental hypotension model in rats.
Twenty-four rats were allocated into four groups as non-pregnant control (NPC), non-pregnant hypotensive (NPH), pregnant control (PC) and pregnant-hypotensive (PH). Blood pressure was monitored only (NPC, PC) or systemic hypotension by blood withdrawal (NPH, PH) was produced for 30 min following catheterisation on the 15th day of pregnancy or at a corresponding time in the control animals. Animals were sacrificed after 48 h of reperfusion. Malonyldialdehyde (MDA) and reduced glutathione (GSH) levels, superoxide dismutase and catalase activities in the kidneys and plasma NO levels were measured. Tissues were evaluated, histologically.
Hypotension and/or pregnancy elevated MDA levels, which was significant in the NPH and PH groups (p < 0.05). GSH levels were lower in all groups compared with the NPC group (p < 0.05). Pregnancy itself increased NO only in the control animals (p < 0.05), not in the hypotensive pregnant rats. Transient hypotension resulted in kidney damage in both hypotension groups, and damage was more prominent in renal cortical regions. The most severe effects were seen in the PH group (p < 0.05).
The findings of this study show that transient hypotension induces a kidney injury in pregnant rats. MDA and GSH in kidneys seem to play a role in the pathophysiology of this injury. However, the roles of antioxidant enzymes and NO and the other underlying mechanisms deserve and necessitate further investigation regarding the long-term health of the mother and fetus.
孕期经常出现的短暂性低血压发作会对母体和胎儿的生理机能产生不利影响。尽管存在强大的自动调节机制,但肾脏对低灌注非常敏感。孕期短暂性低血压加上高代谢需求和增加的氧气需求可能会扰乱氧化状态和一氧化氮(NO)代谢的自然进程。因此,我们在本研究中利用大鼠实验性低血压模型,研究孕期全身性低血压对肾脏氧化状态、形态以及血浆NO水平的影响。
将24只大鼠分为四组,即未孕对照组(NPC)、未孕低血压组(NPH)、孕对照组(PC)和孕低血压组(PH)。仅对未孕对照组和孕对照组监测血压,对未孕低血压组和孕低血压组在妊娠第15天或对照组相应时间进行插管后通过放血造成全身性低血压30分钟。再灌注48小时后处死动物。测量肾脏中丙二醛(MDA)和还原型谷胱甘肽(GSH)水平、超氧化物歧化酶和过氧化氢酶活性以及血浆NO水平。对组织进行组织学评估。
低血压和/或妊娠会升高MDA水平,在未孕低血压组和孕低血压组中这一升高具有显著性(p<0.05)。与未孕对照组相比,所有组的GSH水平均较低(p<0.05)。妊娠本身仅在对照动物中增加了NO(p<0.