Wang Q, Paulson O B, Lassen N A
Department of Clinical Physiology/Nuclear Medicine, Bispebjerg Hospital, Copenhagen, Denmark.
J Cereb Blood Flow Metab. 1992 Nov;12(6):947-53. doi: 10.1038/jcbfm.1992.131.
The importance of nitric oxide (NO) for CBF variations associated with arterial carbon dioxide changes was investigated in halothane-anesthetized rats by using an inhibitor of nitric oxide synthase, NG-nitro-L-arginine (NOLAG). CBF was measured by intracarotid injection of 133Xe. In normocapnia, intracarotid infusion of 1.5, or 7.5, or 30 mg/kg NOLAG induced a dose-dependent increase of arterial blood pressure and a decrease of normocapnic CBF from 85 +/- 10 to 78 +/- 6, 64 +/- 5, and 52 +/- 5 ml 100 g-1 min-1, respectively. This effect lasted for at least 2 h. Raising PaCO2 from a control level of 40 to 68 mm Hg increased CBF to 230 +/- 27 ml 100 g-1 min-1, corresponding to a percentage CBF response (CO2 reactivity) of 3.7 +/- 0.6%/mm Hg PaCO2 in saline-treated rats. NOLAG attenuated this reactivity by 32, 49, and 51% at the three-dose levels. Hypercapnia combined with angiotensin to raise blood pressure to the same level as the highest dose of NOLAG did not affect the CBF response to hypercapnia. L-Arginine significantly prevented the effect of NOLAG on normocapnic CBF as well as blood pressure and also abolished its inhibitory effect on hypercapnic CBF. D-Arginine had no such effect. Decreasing PaCO2 to 20 mm Hg reduced control CBF to 46 +/- 3 ml 100 g-1 min-1 with no further reduction after NOLAG. Furthermore, NOLAG did not change the percentage CBF response to an extracellular acidosis induced by acetazolamide (50 mg/kg).(ABSTRACT TRUNCATED AT 250 WORDS)
通过使用一氧化氮合酶抑制剂NG-硝基-L-精氨酸（NOLAG），在氟烷麻醉的大鼠中研究了一氧化氮（NO）对于与动脉二氧化碳变化相关的脑血流量（CBF）变化的重要性。通过颈内动脉注射133Xe来测量CBF。在正常碳酸血症时，颈内动脉输注1.5、7.5或30mg/kg的NOLAG会引起动脉血压的剂量依赖性升高，并且正常碳酸血症时的CBF分别从85±10降至78±6、64±5和52±5ml·100g-1·min-1。这种效应持续至少2小时。将动脉血二氧化碳分压（PaCO2）从对照水平40mmHg升高至68mmHg会使CBF增加至230±27ml·100g-1·min-1，在生理盐水处理的大鼠中，对应于CBF反应百分比（二氧化碳反应性）为3.7±0.6%/mmHg PaCO2。在三个剂量水平下，NOLAG使这种反应性分别减弱了32%、49%和51%。高碳酸血症联合血管紧张素使血压升高至与最高剂量的NOLAG相同的水平，并未影响对高碳酸血症的CBF反应。L-精氨酸显著预防了NOLAG对正常碳酸血症时CBF以及血压的影响，并且也消除了其对高碳酸血症时CBF的抑制作用。D-精氨酸没有这种作用。将PaCO2降至20mmHg会使对照CBF降至46±3ml·100g-1·min-1，在使用NOLAG后没有进一步降低。此外，NOLAG没有改变对乙酰唑胺（50mg/kg）诱导的细胞外酸中毒的CBF反应百分比。（摘要截断于250字）
