Tuor U I, Farrar J K
Am J Physiol. 1984 Jul;247(1 Pt 2):H40-51. doi: 10.1152/ajpheart.1984.247.1.H40.
We examined the relationship between cerebral blood flow (CBF) and pial vessel caliber responses to graded hemorrhagic hypotension at both normocapnia and hypercapnia in 31 anesthetized rabbits. Changes in CBF (hydrogen clearance) and pial arteriolar diameter (image splitting) were predictably related at all perfusion pressures (PP). Three autoregulatory regions were identified. 1) At PP greater than 65 mmHg, autoregulation was complete as CBF and the CBF response to hypercapnia remained at control levels. The pial vessels dilated progressively, and their response to hypercapnia increased. 2) At PP between 65 and 35 mmHg autoregulation continued but was incomplete. CBF decreased proportionately less than the corresponding reductions in PP due to continued pial vascular dilatation. Both the CBF and pial vessel responses to hypercapnia diminished. 3) At PP less than 35 mmHg, autoregulation was abolished. Pial arteriolar caliber and CBF decreased pressure passively, and there were no responses to hypercapnia. A comparison of changes in pial vascular resistance and total precapillary resistance indicated that the responses of pial vessels (particularly those less than 50 micron) paralleled the responses of the intraparenchymal arterioles.
我们在31只麻醉兔中,研究了在正常碳酸血症和高碳酸血症状态下,脑血流量(CBF)与软脑膜血管口径对分级出血性低血压的反应之间的关系。在所有灌注压(PP)下,CBF(氢清除法)的变化与软脑膜小动脉直径(图像分割法)的变化可预测地相关。确定了三个自动调节区域。1)在PP大于65 mmHg时,自动调节是完全的,因为CBF以及CBF对高碳酸血症的反应保持在对照水平。软脑膜血管逐渐扩张,并且它们对高碳酸血症的反应增强。2)在PP介于65和35 mmHg之间时,自动调节仍在继续但不完全。由于软脑膜血管持续扩张,CBF的降低幅度小于相应的PP降低幅度。CBF和软脑膜血管对高碳酸血症的反应均减弱。3)在PP小于35 mmHg时,自动调节被废除。软脑膜小动脉口径和CBF随压力被动降低,并且对高碳酸血症无反应。软脑膜血管阻力和总毛细血管前阻力变化的比较表明,软脑膜血管(特别是那些小于50微米的血管)的反应与脑实质内小动脉的反应平行。