Diringer M N, Kirsch J R, Hanley D F, Traystman R J
Department of Neurology, John Hopkins Medical Institutions, Baltimore, Maryland.
J Neurosurg. 1993 Jun;78(6):915-21. doi: 10.3171/jns.1993.78.6.0915.
The authors tested the hypothesis that cerebral blood flow (CBF) reactivity to CO2 was blunted following subarachnoid hemorrhage (SAH). Subarachnoid hemorrhage was produced in five cats by performing four cisterna magna injections of blood in each (SAH Group). A second group of six cats was treated with an antifibrinolytic agent (AF) in addition to four cisterna magna blood injections (SAH+AF Group). Four cats received AF and four cisterna magna injections of saline (Control Group). The presence or absence of basilar artery vasospasm was determined by comparing baseline and follow-up selective angiograms. Cerebral blood flow reactivity was determined by randomly varying the concentration of inspired CO2 to alter PaCO2 from 20 to 75 mm Hg. Regional CBF was measured with radiolabeled microspheres. Basilar artery vasospasm was seen following subarachnoid injection of blood but not of saline. Normocapnic CBF was similar in all three groups in the brain stem (mean +/- standard error of the mean: SAH Group 46 +/- 6, SAH+AF Group 46 +/- 6, and Control Group 44 +/- 9 ml/min/100 gm) and in the supratentorial compartment (SAH Group 53 +/- 8, SAH+AF Group 61 +/- 9, and Control Group 51 +/- 13 ml/min/100 gm). At intermediate levels of hypercarbia (PaCO2 50 +/- 3 mm Hg), CBF increased similarly in all three groups (SAH Group 161% +/- 32%, SAH+AF Group 118% +/- 33%, and Control Group 174% +/- 19% compared to baseline); at higher levels of PaCO2 (60 +/- 3 mm Hg), CBF values were SAH Group 265% +/- 50%, SAH+AF Group 205% +/- 47%, and Control Group 159% +/- 30% of baseline. At the highest level of PaCO2 (75 +/- 6 mm Hg), supratentorial CBF did not increase as much in the SAH+AF Group as in the Control Group (179% +/- 59% vs. 463% +/- 58% of baseline, respectively). The authors conclude that, in this model of SAH, there is no change in normocapnic CBF; however, blood flow reactivity to hypercarbia is blunted. It is possible that this may result from a combination of narrowing of proximal large vessels and globally impaired reactivity of small vessels.
作者检验了蛛网膜下腔出血（SAH）后大脑血流（CBF）对二氧化碳的反应性减弱这一假设。通过对五只猫的枕大池进行四次注血来制造蛛网膜下腔出血（SAH组）。第二组六只猫除了进行四次枕大池注血外还接受了抗纤溶药物（AF）治疗（SAH+AF组）。四只猫接受AF和四次枕大池注射生理盐水（对照组）。通过比较基线和随访时的选择性血管造影来确定基底动脉是否存在血管痉挛。通过随机改变吸入二氧化碳的浓度使动脉血二氧化碳分压（PaCO2）从20毫米汞柱变化到75毫米汞柱来测定大脑血流反应性。用放射性微球测量局部脑血流量。蛛网膜下腔注射血液后可见基底动脉血管痉挛，而注射生理盐水后未见。三组动物脑干的正常碳酸血症时的脑血流量相似（平均值±平均标准误：SAH组46±6，SAH+AF组46±6，对照组44±9毫升/分钟/100克），幕上腔的情况也相似（SAH组53±8，SAH+AF组61±9，对照组51±13毫升/分钟/100克）。在中度高碳酸血症水平（PaCO2 50±3毫米汞柱）时，三组的脑血流量增加情况相似（与基线相比，SAH组增加161%±32%，SAH+AF组增加118%±33%，对照组增加174%±19%）；在更高的PaCO2水平（60±3毫米汞柱）时，脑血流量值分别为SAH组是基线的265%±50%，SAH+AF组是基线的205%±47%，对照组是基线的159%±30%。在最高的PaCO2水平（75±6毫米汞柱）时，SAH+AF组幕上脑血流量的增加不如对照组多（分别是基线的179%±59%和463%±58%）。作者得出结论，在这个SAH模型中，正常碳酸血症时的脑血流量没有变化；然而，对高碳酸血症的血流反应性减弱。这可能是近端大血管狭窄和小血管整体反应性受损共同作用的结果。
