Abstract
Objective: We investigated the effect of ischemia and reperfusion on the vasoactive function of penetrating brain parenchymal arterioles under pressurized conditions.
Methods: Parenchymal arterioles (<50 μm in diameter) from within the middle cerebral artery territory were dissected from male Wistar rats that were either nonischemic control (n = 16) or ischemic for one hour and reperfused for 24 hours (n = 16) by temporary filament occlusion of the middle cerebral artery. Arterioles were mounted on glass cannulas within an arteriograph chamber that allowed for the measurement of lumen diameter and control over intravascular pressure.
Results: After one hour of equilibration at 10 mmHg, spontaneous myogenic tone developed in both groups of animals, constricting control arterioles from 69 ± 9 to 49 ± 11 μm (29.5 ± 10.2%) and ischemic arterioles from 66 ± 9 to 45 ± 11 μm (33.1 ± 14.1%); p > 0.05. Contraction to the nitric oxide synthase inhibitor nitro-L-arginine (10–4M) was significantly diminished in ischemic arterioles, constricting only 3.2 ± 3.3 vs. 15.6 ± 12.5% in control arterioles (p = 0.017). Both groups dilated to nifedipine; however, the response was significantly diminished after ischemia. The EC50 for nifedipine in control arterioles was 3.54 ± 0.11 vs. 9.90 ± 0.71 nM for ischemic arterioles (p = 0.024).
Conclusions: These findings demonstrate that functional changes occur in brain parenchymal arterioles after ischemia and reperfusion, a result that may significantly influence stroke outcome by altering blood flow to an ischemic region.
ACKNOWLEDGMENTS
This work was supported by the NIH, National Institute of Neurologic Disorders, and Stroke grant nos. NS40071 (MJC) and NS043316 (MJC). The authors would also like to acknowledge the generous support of the Totman Medical Research Trust.
This study was supported by NINDS grant nos. RO1 NS40071 and RO1 NS043316 (to MJC) and the Totman Medical Research Trust