降低子宫灌注压对妊娠大鼠血压和代谢因子的影响。
Effects of reduced uterine perfusion pressure on blood pressure and metabolic factors in pregnant rats.
作者信息
Gilbert Jeffrey, Dukes Matt, LaMarca Babbette, Cockrell Kathy, Babcock Sara, Granger Joey
机构信息
Department of Physiology and the Center for Excellence in Cardiovascular-Renal Research, University of Mississippi Medical Center, Jackson, MS 39216-4505, USA.
出版信息
Am J Hypertens. 2007 Jun;20(6):686-91. doi: 10.1016/j.amjhyper.2006.12.016.
BACKGROUND
Elements of metabolic syndrome (eg, dyslipidemia and impaired glucose metabolism) are often present in preeclamptic pregnancies. Currently it is unclear whether these metabolic aberrations presage preeclampsia, or if these manifestations result from placental ischemia and the ensuing proinflammatory state usually present in preeclampsia.
METHODS
The present study employed chronic reductions in uterine perfusion pressure (RUPP) to generate a rat model of pregnancy-induced hypertension (PIH) for the evaluation of fasting plasma concentrations of triglycerides (TGs), glucose, resistin, insulin, and glucose tolerance in late-gestation rats.
RESULTS
Mean arterial pressure was increased (130 +/- 2.1 mm Hg v 100 +/- 4.3 mm Hg; all values, mean +/- SEM), and fetal weight decreased (1.93 +/- 0.08 g v 2.19 +/- 0.06 g), in RUPP dams compared with normal pregnant (NP) control dams. Maternal fasting glucose (4.2 +/- 0.3 mmol L(-1) v 3.1 +/- 0.4 mmol L(-1); P < .05) was increased in RUPP compared with NP dams. Serum TGs (2.62 +/- 0.29 mmol L(-1) v 2.45 +/- 0.51 mmol L(-1)), insulin (9.9 +/- 0.7 microU mL(-1) v 8.5 +/- 0.7 microU mL(-1)), resistin (46.25 +/- 4.19 pg mL(-1) v 49.71 +/- 4.01 pg mL(-1)), and glucose area under the curve (650 +/- 35 mmol min L(-1) v 570 +/- 34 mmol min L(-1)) were not different between the RUPP and NP dams.
CONCLUSIONS
Although these findings do not rule out the hypothesis that preexisting symptoms of metabolic syndrome may contribute to the onset of preeclampsia, these data clearly show that pregnancy-induced hypertension resulting from RUPP does not elicit manifestations of metabolic syndrome in late-gestation rat dams.
背景
代谢综合征的要素（如血脂异常和糖代谢受损）在子痫前期妊娠中经常出现。目前尚不清楚这些代谢异常是子痫前期的先兆，还是这些表现是由胎盘缺血以及子痫前期通常存在的随之而来的促炎状态导致的。
方法
本研究采用慢性降低子宫灌注压（RUPP）来建立妊娠高血压（PIH）大鼠模型，以评估妊娠晚期大鼠空腹血浆甘油三酯（TGs）、葡萄糖、抵抗素、胰岛素浓度以及葡萄糖耐量。
结果
与正常妊娠（NP）对照母鼠相比，RUPP母鼠的平均动脉压升高（130±2.1 mmHg对100±4.3 mmHg；所有数值，均值±标准误），胎儿体重降低（1.93±0.08 g对2.19±0.06 g）。与NP母鼠相比，RUPP母鼠的母体空腹血糖升高（4.2±0.3 mmol L⁻¹对3.1±0.4 mmol L⁻¹；P<0.05）。RUPP母鼠与NP母鼠之间的血清TGs（2.62±0.29 mmol L⁻¹对2.45±0.51 mmol L⁻¹）、胰岛素（9.9±0.7 μU mL⁻¹对8.5±0.7 μU mL⁻¹）、抵抗素（46.25±4.19 pg mL⁻¹对49.71±4.01 pg mL⁻¹）以及葡萄糖曲线下面积（650±35 mmol min L⁻¹对570±34 mmol min L⁻¹）无差异。
结论
尽管这些发现不排除代谢综合征的现有症状可能导致子痫前期发病的假说，但这些数据清楚地表明，由RUPP导致的妊娠高血压不会在妊娠晚期大鼠母鼠中引发代谢综合征的表现。
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