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Altered cerebrovascular CO2 reactivity following subarachnoid hemorrhage in cats
M N Diringer1, J R Kirsch, D F Hanley
1Department of Neurology, John Hopkins Medical Institutions, Baltimore, Maryland.
Insights
Subarachnoid hemorrhage (SAH) blunts cerebral blood flow (CBF) reactivity to carbon dioxide (CO2). Antifibrinolytic agents did not prevent this impairment in a feline model, suggesting vessel narrowing and impaired reactivity.
Area of Science:
- Neurology
- Vascular Physiology
Background:
- Subarachnoid hemorrhage (SAH) can lead to cerebrovascular complications.
- Cerebral blood flow (CBF) regulation is critical for brain function.
- The effect of SAH on CO2 reactivity is not fully understood.
Purpose of the Study:
- To investigate the hypothesis that CBF reactivity to CO2 is blunted after SAH.
- To evaluate the effect of an antifibrinolytic agent (AF) on CBF reactivity post-SAH.
Main Methods:
- SAH was induced in cats via cisterna magna blood injections.
- Control groups received saline or AF with saline.
- CBF reactivity was assessed by measuring regional CBF with radiolabeled microspheres across a range of PaCO2 levels (20-75 mm Hg).
- Basilar artery vasospasm was evaluated using angiography.
Main Results:
- Basilar artery vasospasm was present in the SAH group.
- Normocapnic CBF was similar across all groups.
- CBF reactivity to hypercarbia was blunted in the SAH group compared to controls.
- The antifibrinolytic agent did not restore normal CBF reactivity at high PaCO2 levels.
Conclusions:
- SAH, in this model, does not alter normocapnic CBF but impairs cerebrovascular reactivity to hypercarbia.
- Blunted reactivity may stem from proximal large vessel narrowing and/or impaired small vessel function.
- Antifibrinolytic agents did not mitigate this reactivity deficit.
Abstract:
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.