Anim-Nyame N, Sooranna S R, Johnson M R, Sullivan M H, Gamble J, Steer P J
Academic Department of Obstetrics and Gynaecology, Faculty of Medicine, Imperial College of Science, Technology and Medicine, Chelsea and Westminster Hospital, 369 Fulham Road, London SW10 9NH, UK.
Clin Sci (Lond). 2004 Jan;106(1):19-25. doi: 10.1042/CS20030045.
There is evidence that tissue blood flow is regulated by retrograde transmission of signals initiated at capillary and post-capillary sites, and transmitted via the endothelium to modulate pre-capillary resistance. We have used pre-eclampsia as a model to test the hypothesis that normal endothelium is required to enable adjustment of blood flow to match tissue requirements. Integrity of the endothelial pathway was assessed by measuring calf blood flow at increasing venous pressures, using an established small cumulative-step venous-congestion plethysmography protocol in ten women with pre-eclampsia, 17 normal pregnant controls and ten non-pregnant women. Endothelial cell activation was assessed by measuring plasma levels of the cell adhesion molecules, intercellular cell-adhesion molecule-1 (ICAM-1), vascular cell-adhesion molecule-1 (VCAM-1) and E-selectin. Baseline calf blood flow was significantly lower in pre-eclampsia than in the other two groups (P<0.0001; ANOVA). In the pre-eclampsia group, there was a fall in blood flow as venous congestion pressure was raised (P<0.0001; ANOVA). No such change was observed in the other two groups. A significant inverse correlation was observed between the reduction in blood flow in pre-eclampsia and the levels of E-selectin (r=-0.92, P=0.0002), VCAM-1 (r=-0.93, P=0.0008) and ICAM-1 (r=-0.86, P=0.001). The differences between the pre-eclamptic women and the other two groups support the notion that the failure to sustain blood flow during a cumulative pressure step protocol in the pre-eclamptic group might be influenced by interference with the retrograde transmission of signals via the endothelium in these patients.
有证据表明，组织血流受始于毛细血管和毛细血管后部位的信号逆行传递调节，并通过内皮细胞传递以调节毛细血管前阻力。我们以先兆子痫作为模型来检验这一假说，即需要正常的内皮细胞来使血流调节以匹配组织需求。通过在10例先兆子痫女性、17例正常妊娠对照和10例非妊娠女性中使用既定的小累积步长静脉充血体积描记术方案，在逐渐升高的静脉压力下测量小腿血流量，评估内皮途径的完整性。通过测量细胞黏附分子细胞间细胞黏附分子-1（ICAM-1）、血管细胞黏附分子-1（VCAM-1）和E-选择素的血浆水平来评估内皮细胞活化。先兆子痫患者的基线小腿血流量显著低于其他两组（P<0.0001；方差分析）。在先兆子痫组中，随着静脉充血压力升高，血流量下降（P<0.0001；方差分析）。在其他两组中未观察到这种变化。先兆子痫患者血流量减少与E-选择素水平（r=-0.92，P=0.0002）、VCAM-1水平（r=-0.93，P=0.0008）和ICAM-1水平（r=-0.86，P=0.001）之间存在显著负相关。先兆子痫女性与其他两组之间的差异支持这样一种观点，即先兆子痫组在累积压力步长方案期间无法维持血流可能受到这些患者中通过内皮细胞的信号逆行传递受到干扰的影响。
