LAUSR

Purpose: Immediate pial collateral recruitment during acute ischemic stroke is an endogenous response limiting permanent tissue damage due to proximal cerebral artery occlusion. There is presently no known way to predict the degree of pial collateral recruitment. This work sought to determine if cerebrovascular reactivity (CVR) to CO 2 predicts pial collateral recruitment in an experimental model of cerebral ischemia. Methods: Eight mongrel dogs underwent cerebral blood flow (CBF) measurements using stable isotope neutron activated microspheres during normocapnia (PaCO 2 30-35mmHg) using medical air, and subsequently during hypercapnia (PaCO 2 60-70mmHg) using 7% CO 2 . Anesthesia (propofol, remifentanil, rocuronium and 1% isofluorane) and normal range physiologic parameters were maintained to avoid undue influence on CO 2 reactivity. Animals underwent middle cerebral artery occlusion using a previously described endovascular method. Pial collateral recruitment was angiographically assessed using a previously published 11-point scale. Animals subsequently underwent MRI to derive 4-hour infarct volumes calculated using an automated threshold technique using mean diffusivity maps. Bivariate linear fit analyses were used to assess correlations between CVR versus pial collateral score and infarct volume. Results: CBF values derived from cortical gray matter during simultaneous CO 2 challenge demonstrate a statistically significant correlation to infarct volumes (p=0.0041, r 2 adj= 0.734) and pial collateral recruitment (p=0.0006, r 2 adj= 0.856) (figure 1). CBF at PaCO 2 of 65mmHg was secondarily found to correlate with infarct volume (p=0.0013, r 2 adj= 0.817) and pial collateral recruitment (p=0.0005, r 2 adj= 0.862). Conclusion: Preliminary data presented suggest that cerebrovascular reactivity to CO 2 may be predictive of pial collateral recruitment and infarct volumes during acute ischemic stroke