Bearchell M C, Redman C W, Pyne G J, Cadoux-Hudson T, Clark J F
Medical Research Council Clinical and Biochemical Magnetic Resonance Unit, Department of Biochemistry, University of Oxford, United Kingdom.
Am J Obstet Gynecol. 1998 Dec;179(6 Pt 1):1534-8. doi: 10.1016/s0002-9378(98)70020-1.
Preeclampsia is a complication of pregnancy that causes maternal vasoconstriction and hypertension. The disease may progress to eclampsia, which is thought to be related to cerebral vasospasm. Although there is evidence for more than one circulating factor that causes endothelial cell dysfunction in preeclampsia, little work has focused on the possibility that vascular smooth muscle function might be directly stimulated by a circulating factor. The aim of this study was to determine whether such a factor or factors could be detected by the vessels.
Excessive vascular smooth muscle oxygen consumption was used as a screen for metabolic stimulation because pathologic arterial constriction would require oxidative metabolism to generate adenosine triphosphate. De-endothelialized porcine carotid artery (a well-validated model of human arterial contractile function) was exposed to sera from patients with preeclampsia (1:30 dilution) in a sealed chamber with an oxygen electrode, and the rate of oxygen consumption by the tissue was measured. Comparisons with the effects of sera from matched normal pregnant patients and from nonpregnant women were made.
Exposure of vascular smooth muscle to sera from women with preeclampsia for 90 minutes resulted in greater oxygen consumption by the tissue (0.66 +/- 0.16 micromol O2 /min per gram of dry weight) than did exposure to sera of matched pregnant and nonpregnant control subjects (0.34 +/- 0.08 micromol O2 /min per gram of dry weight, P <.001, and 0.29 +/- 0.03 micromol O2 /min per gram of dry weight, P <.001, respectively). This stimulation was completely reversed by rinsing.
There is a factor in the circulation of women with preeclampsia that has the reversible effect on vascular smooth muscle of accelerating oxygen consumption. We discuss the implications of this observation in terms of known aspects of vascular smooth muscle contractile function.
子痫前期是一种妊娠并发症，可导致母体血管收缩和高血压。该疾病可能进展为子痫，子痫被认为与脑血管痉挛有关。尽管有证据表明不止一种循环因子会导致子痫前期的内皮细胞功能障碍，但很少有研究关注循环因子可能直接刺激血管平滑肌功能的可能性。本研究的目的是确定血管是否能检测到这样一种或多种因子。
由于病理性动脉收缩需要氧化代谢来生成三磷酸腺苷，因此将过量的血管平滑肌氧消耗用作代谢刺激的筛选指标。将去内皮的猪颈动脉（一种经过充分验证的人类动脉收缩功能模型）置于带有氧电极的密封室中，暴露于子痫前期患者的血清（1:30稀释）中，测量组织的氧消耗率。并与匹配的正常孕妇和非孕妇血清的作用进行比较。
将血管平滑肌暴露于子痫前期女性的血清90分钟后，组织的氧消耗（0.66±0.16微摩尔O2/每分钟每克干重）比暴露于匹配的孕妇和非孕妇对照受试者的血清时更高（分别为0.34±0.08微摩尔O2/每分钟每克干重，P<.001；以及0.29±0.03微摩尔O2/每分钟每克干重，P<.001）。通过冲洗可完全逆转这种刺激。
子痫前期女性的循环中存在一种因子，它对血管平滑肌具有加速氧消耗的可逆作用。我们根据血管平滑肌收缩功能的已知方面讨论了这一观察结果的意义。
