Komuro T, Borsody M K, Ono S, Marton L S, Weir B K, Zhang Z D, Paik E, Macdonald R L
Section of Neurosurgery, Department of Surgery, The University of Chicago Medical Center, 5841 South Maryland Avenue, Chicago, IL 60637, USA.
Exp Biol Med (Maywood). 2001 Oct;226(9):860-5. doi: 10.1177/153537020122600909.
Carbon monoxide (CO) is known to increase cerebral blood flow, but the effect of CO on the vascular tone of large cerebral arteries is uncertain. We tested whether CO affects cerebral artery tone by measuring tension generated by ex vivo segments of dog basilar artery upon exposure to CO. In cerebral artery segments contracted with either KCl or prostaglandin F(2alpha), CO caused a concentration-related relaxation beginning with a concentration of 57 microM. Relaxation did not occur if CO was administered in the presence of bubbling carboxygen (95% O(2):5% CO(2)), which reduces greater than 99% of CO from the solution. Furthermore, the CO-induced relaxation of cerebral artery segments was reduced in the presence of the guanylyl cyclase inhibitor 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ, 10 microM)or the potassium channel blocker tetraethylammonium (TEA, 1 mM). Neither ODQ nor TEA completely eliminated the relaxation caused by CO and there was no additive effect if ODQ and TEA were administered together. These results suggest that cerebral arteries are directly relaxed by CO and that this relaxation depends upon the activation of guanylyl cyclase and the opening of potassium channels.
众所周知，一氧化碳（CO）可增加脑血流量，但CO对大脑大动脉血管张力的影响尚不确定。我们通过测量犬基底动脉离体节段在暴露于CO时产生的张力，来测试CO是否会影响脑动脉张力。在用氯化钾或前列腺素F（2α）收缩的脑动脉节段中，CO从57微摩尔的浓度开始引起浓度相关的舒张。如果在通入羧氧混合气（95%O₂：5%CO₂）的情况下给予CO，则不会发生舒张，羧氧混合气可使溶液中99%以上的CO减少。此外，在存在鸟苷酸环化酶抑制剂1H-[1,2,4]恶二唑并[4,3-a]喹喔啉-1-酮（ODQ，10微摩尔）或钾通道阻滞剂四乙铵（TEA，1毫摩尔）的情况下，CO诱导的脑动脉节段舒张减弱。ODQ和TEA均未完全消除CO引起的舒张，并且如果同时给予ODQ和TEA，也没有相加作用。这些结果表明，CO可直接使脑动脉舒张，且这种舒张依赖于鸟苷酸环化酶的激活和钾通道的开放。
