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Endothelium-Dependent Responses in the Cerebral Circulation
腦循環之血管內皮依存性反應
摘要
血管內皮能經由舒張因子與收縮因子的釋放而影響血管對於一些刺激所引起之反應。據研究顯示，血管內皮依存性反應亦可發生於腦部之大、小血管。於離體實驗中，剝除腦部大血管之血管內皮會使其對一些刺激所引起的舒張反應消失。血管內皮舒張因子或一氧化氮的生成抑制劑N^G-單甲基-L-精胺酸於活體實驗中能減少由乙醯膽鹼所引起的基底動脈舒張。至於在腦部微循環方面的活體實驗，血管內皮的損傷會使得乙醯膽鹼、緩激肽、以及鈣離子通道劑A23187對軟腦膜細動脈的舒張作用減弱。在慢性高血壓大白鼠身上，以上諸血管內皮依存性刺激所引起的腦部大、小血管舒張反應均明顯變小，由此顯示慢性高壓會減弱內皮依存性腦血管舒張反應。血管內皮亦可能參與管制某些生理及病理情況下的腦循環。舉例而言，腦血管對管內壓力增加所引起的肌應性反應有賴於完整腦血管內皮的存在。另外，周邊血管與腦血管對血管加壓素的異質性反應可能影響血流之再分佈而有助於出血或休克時維持穩定之腦血流。腺核苷二磷酸，血清張力素，以及血漿血栓素為血小板凝集時所釋出的主要血管活性物質。腺核苷二磷酸在慢性高血壓大白鼠身上所引起的腦血管舒張反應較在正常血壓大白鼠身上所引起者為小。血清張力素以及血漿血栓素的同功劑U-46619則在慢性高血壓大白鼠身上較在正常血壓大白鼠身上引起類似甚至更大的腦血管收縮作用。由於對腺核苷二磷酸舒張反應的減弱以及對血清張力素和血漿血栓素的收縮反應呈正常甚或增加，因此在慢性高血壓大白鼠身上似乎較易引起腦血管收縮而導致腦缺血和中風。
並列摘要
The endothelium appears to play an important role in modulating vascular tone by releasing relaxing and contracting factors in response to a variety of stimuli. In the cerebral circulation, endothelium-dependent responses have been demonstrated in both large and small blood vessels. Dilator responses of large cerebral arteries to several agonists are abolished after denudation of the endothelium in vitro. N^G-monomethyl-L-arginine, which inhibits formation of endothelium-derived relaxing factor or nitric oxide, decreases dilatation of basilar artery to acetylcholine in vivo. In the cerebral microcirculation, dilatation of pial arterioles in response to acetylcholine, bradykinin, and the calcium ionophore A23187 is abolished after endothelial injury in vivo. In chronically hypertensive rats, dilator responses to these endothelium-dependent agonists are reduced in large and small cerebral blood vessels, suggesting that chronic hypertension impairs endothelium-dependent vasodilatation in the cerebral circulation. The endothelium may contribute to regulation of the cerebral circulation in physiological and pathophysiological conditions. For example, myogenic response of cerebral blood vessels to increases in intraluminal pressure depends on an intact endothelium. Also, heterogeneous responses of peripheral and cerebral blood vessels to vasopressin may contribute to redistribution of blood flow to maintain the cerebral perfusion during hemorrhage and shock. Adenosine diphosphate, serotonin, and thromboxane are the major vasoactive substances released during platelet aggregation. In the cerebral circulation, adenosine diphosphate produces less vasodilatation in chronically hypertensive rats than in normotensive rats. Serotonin and the thromboxane analogue U-46619 produce similar or even more constriction of cerebral blood vessels in hypertensive rats than in normotensive rats. Thus, impaired dilator responses to adenosine diphosphate, coupled with normal or increased constrictor responses to serotonin and thromboxane, would favor constriction of cerebral blood vessels and may predispose to ischemia and stroke in chronically hypertensive rats.