Horvath I, Sandor N T, Ruttner Z, McLaughlin A C
National Institute on Alcohol Abuse and Alcoholism, Rockville, Maryland.
J Cereb Blood Flow Metab. 1994 May;14(3):503-9. doi: 10.1038/jcbfm.1994.62.
The effect of the nitric oxide (NO) synthase inhibitor N omega-nitro-L-arginine methyl ester (L-NAME) on the response of cerebrocortical oxygen consumption (CMRO2) and blood flow (CBF) to two levels of hypercapnia (PaCO2 approximately 60 mm Hg and PaCO2 approximately 90 mm Hg) was investigated in ketamine-anesthetized rats. CBF was calculated using the Kety-Schmidt approach and CMRO2 was calculated from the product of CBF and the arteriovenous (superior sagittal sinus) difference for oxygen. L-NAME treatment did not have a significant effect on either CMRO2 or CBF under normocapnic conditions but inhibited the hypercapnic increase of CMRO2 and the hypercapnic increase in CBF. These results suggest that NO plays a role in the response of CMRO2 and CBF during hypercapnia and are consistent with the suggestion that at least part of the increase in CBF observed during hypercapnia is coupled to an increase in CMRO2.
在氯胺酮麻醉的大鼠中，研究了一氧化氮（NO）合酶抑制剂Nω-硝基-L-精氨酸甲酯（L-NAME）对脑皮质氧耗（CMRO2）和血流（CBF）对两种高碳酸血症水平（动脉血二氧化碳分压[PaCO2]约为60 mmHg和PaCO2约为90 mmHg）的反应的影响。使用凯蒂-施密特方法计算CBF，并根据CBF与氧的动静脉（上矢状窦）差值的乘积计算CMRO2。在正常碳酸血症条件下，L-NAME处理对CMRO2或CBF均无显著影响，但抑制了高碳酸血症时CMRO2的增加以及高碳酸血症时CBF的增加。这些结果表明，NO在高碳酸血症期间CMRO2和CBF的反应中起作用，并且与以下观点一致：在高碳酸血症期间观察到的CBF增加至少部分与CMRO2的增加相关。
