Altered cerebrovascular CO₂ reactivity following subarachnoid hemorrhage in cats

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.