Jones Stephen C, Easley Kirk A, Radinsky Carol R, Chyatte Douglas, Furlan Anthony J, Perez-Trepichio Alejandro D
Department of Anesthesiology, Allegheny General Hospital, Pittsburgh, Pennsylvania 15212, USA.
J Cereb Blood Flow Metab. 2003 Sep;23(9):1085-95. doi: 10.1097/01.WCB.0000081202.00668.FB.
Variations in the height of the CBF response to hypotension have been described recently in normal animals. The authors evaluated the effects of nitric oxide synthase (NOS) inhibition on these variations in height using laser Doppler flowmetry in 42 anesthetized (halothane and N2O) male Sprague-Dawley rats prepared with a superfused closed cranial window. In four groups (time control, enantiomer control, NOS inhibition, and reinfusion control) exsanguination to MABPs from 100 to 40 mm Hg was used to produce autoregulatory curves. For each curve the lower limit of autoregulation (the MABP at the first decrease in CBF) was identified; the pattern of autoregulation was classified as "peak" (15% increase in %CBF), "classic" (plateau with a decrease at the lower limit of autoregulation), or "none" (15% decrease in %CBF); and the autoregulatory height as the %CBF at 70 mm Hg (%CBF(70)) was determined. NOS inhibition decreased %CBF(70) in the NOS inhibition group (P = 0.014), in the control (combined time and enantiomer control) group (P = 0.015), and in the reinfusion control group (P = 0.025). NOS inhibition via superfusion depressed the autoregulatory pattern (P = 0.02, McNemar test on changes in autoregulatory pattern) compared with control (P = 0.375). Analysis of covariance showed that changes induced by NOS inhibition in the parameters of autoregulatory height are not related to changes in the lower limit, but are strongly (P < 0.001) related to each other. NOS inhibition depressed the autoregulatory pattern, decreasing the seemingly paradoxical increase in CBF as blood pressure decreases. These results suggest that nitric oxide increases CBF near the lower limit and augments the hypotensive portion of the autoregulatory curve.
最近在正常动物中已描述了脑血流（CBF）对低血压反应高度的变化。作者使用激光多普勒血流仪，在42只制备了超灌注闭合颅骨窗的麻醉（氟烷和一氧化二氮）雄性Sprague-Dawley大鼠中，评估了一氧化氮合酶（NOS）抑制对这些高度变化的影响。在四组（时间对照组、对映体对照组、NOS抑制组和再灌注对照组）中，通过放血使平均动脉压（MABP）从100降至40 mmHg以产生自动调节曲线。对于每条曲线，确定自动调节下限（CBF首次下降时的MABP）；自动调节模式分为“峰值”（CBF%增加15%）、“经典”（在自动调节下限处有下降的平台期）或“无”（CBF%下降15%）；并确定70 mmHg时的自动调节高度即CBF%（CBF(70)）。NOS抑制使NOS抑制组（P = 0.014）、对照组（时间和对映体对照组合并）（P = 0.015）以及再灌注对照组（P = 0.025）的CBF(70)降低。与对照组（P = 0.375）相比，通过超灌注进行的NOS抑制压低了自动调节模式（P = 0.02，对自动调节模式变化进行McNemar检验）。协方差分析表明，NOS抑制引起的自动调节高度参数变化与下限变化无关，但彼此密切相关（P < 0.001）。NOS抑制压低了自动调节模式，减少了血压降低时CBF看似矛盾的增加。这些结果表明，一氧化氮在接近下限处增加CBF并增强自动调节曲线的低血压部分。
