Yoshioka J, Clower B R, Smith R R
Stroke. 1984 Mar-Apr;15(2):288-94. doi: 10.1161/01.str.15.2.288.
Subarachnoid hemorrhage (SAH) due to rupture of the right middle cerebral artery (RMCA) produced specific anatomical and biophysiological responses in the involved feline vessels. The RMCA showed morphological alterations that became progressively more severe with time and were widespread within the cerebral vascular tree. SAH also resulted in an acute depletion of vessel catecholamine levels which remained depressed over a 30 day period. When the cerebral vessels of cats were severely depleted of catecholamines (using reserpine) prior to induced SAH, morphological alterations were significantly reduced both in severity and in degree of spread within the cerebral vascular network. The results of this study suggest that the concentration of norepinephrine within the vessel at the time of hemorrhage plays a significant role in the production of the angiopathy that follows SAH.
右侧大脑中动脉(RMCA)破裂导致的蛛网膜下腔出血(SAH)在受累猫血管中产生了特定的解剖学和生物生理学反应。RMCA出现了形态学改变,且随着时间推移逐渐加重,并在脑血管树中广泛存在。SAH还导致血管儿茶酚胺水平急性耗竭,且在30天内一直处于低水平。在诱导SAH之前,若猫的脑血管儿茶酚胺严重耗竭(使用利血平),则形态学改变在严重程度和脑血管网络内的扩散程度上均显著降低。本研究结果表明,出血时血管内去甲肾上腺素的浓度在SAH后血管病变的发生中起重要作用。