Activation of N-methyl-D-aspartate (NMDA) and kainate (KAI) receptors dilates cerebral arterioles. In a previous study, we found that cerebral vasodilation to NMDA is reduced after hypoxic/anoxic insults (AJP 270: H1225, 1996 & Stroke 27:1634, 1996). The purpose of this study was to examine the effects of ischemia on cerebral arteriolar dilation to KAI. Pial arteriolar diameter was determined in anesthetized piglets via intravital microscopy. Baseline arteriolar diameters were ∼ 100 μm. Cerebral ischemia was induced by raising intracranial pressure for 10 min. Topical application of KAI at concentrations of 5×10-5 and 10-4 mol/l dilated pial arterioles by 16±2% and 28±3% above baseline, respectively (p<0.05, n=6). Cerebral vasodilation to KAI was sustained for 30-45 minutes. Application of MK 801 (10-5 mol/l), a NMDA antagonist, did not influence responses to KAI (13±3% and 25±3%; p>0.05, n=4). One hour after ischemia, pial arteriolar reactivity to KAI was not substantially modified (16±4% and 21±5%; p>0.05, n=6). Application of KAI after ischemia resulted in edema formation by 2-4 hours. We conclude that reduced NMDA- but intact KAI-vascular responsiveness would alter glutamate influences on the cerebral circulation after ischemic stress.
|Publication status||Published - Dec 1 1997|
ASJC Scopus subject areas
- Molecular Biology