Neuroscience 2005 Abstract
| Presentation Number: | 441.3 |
|---|---|
| Abstract Title: | Ischemic changes monitored by 1H-MRS and MRI in rats with permanent middle cerebral artery occlusion: protective effects of pyruvate. |
| Authors: |
Kim, T.*1
; Yi, J.1
; Koh, J.1,2
1CRI Center for the Study of CNS Zinc, Univ. Ulsan School of Medicine, Seoul, Democratic People's Republic of Korea 2Neurology, Univ. Ulsan School of Medicine, Seoul, Democratic People's Republic of Korea |
| Primary Theme and Topics |
Disorders of the Nervous System - Neurotoxicity, Inflammation, and Neuroprotection -- Neuroprotective mechanisms and treatments |
| Secondary Theme and Topics | Disorders of the Nervous System<br />- Ischemia<br />-- Neuroprotection and tolerance |
| Session: |
441. Vascular Pathobiology: Mechanisms and Treatments Poster |
| Presentation Time: | Monday, November 14, 2005 10:00 AM-11:00 AM |
| Location: | Washington Convention Center - Hall A-C, Board # TT9 |
| Keywords: | focal cerebral ischemia , DWI, T2-weighted imaging, lactate |
Monitoring metabolic changes during ischemia with 1H-MRS may provide additional insights into the efficacy and the mechanism of potential neuroprotective agents. Pyruvate is an endogenous glucose metabolite, which shows substantial neuroprotective effects against several brain insults. However, the mechanism is still not fully understood. As an attempt to gain some insights, in the present study, we examined with MRS the effect of pyruvate in a rat model of permanent MCAO.
Under general anesthesia, MCA was permanently occluded with fire-polished suture materials. Ischemic and non-ischemic contralateral brain regions (3 x 3 mm square with 2.5 mm thickness) were subjected to 1H-MRS. Pyruvate (125 mg/kg) was given intraperitoneally 30 min after the occlusion of MCA. In addition to MRS measurements, MR imagings, including diffusion-weighted imaging and T2-weighted imaging, were evaluated at 1, 2, and 6 hours following the ischemic onset. 24 h after MCAO, rats were sacrificed and their brains were stained with TTC to quantitate the infarct volume. The lactate peaks began to rise in ischemic areas 1or 2 h after MCA occlusion, and further increased at 6 h. In contrast, NAA peaks decreased at 6 h. Intriguingly, the average height of the lactate peak in the pyruvate group at 6 h of ischemia, was substantially lower, and that of NAA peaks was higher than those in the control group. Both DWI and T2-weighted lesion sizes in the pyruvate group matched infarct sizes, and were also reduced in the pyruvate group.
We monitored lactate peaks during ischemia along with infarct formation in vivo, and found that the brain-protective effect of pyruvate is associated with reduction of lactate levels in ischemic areas. This finding is a little surprising, because anoxic states would make pyruvate turn into lactate. Further studies may be warranted to investigate the mechanism of the lactate reduction by pyruvate during ishcemia.
Under general anesthesia, MCA was permanently occluded with fire-polished suture materials. Ischemic and non-ischemic contralateral brain regions (3 x 3 mm square with 2.5 mm thickness) were subjected to 1H-MRS. Pyruvate (125 mg/kg) was given intraperitoneally 30 min after the occlusion of MCA. In addition to MRS measurements, MR imagings, including diffusion-weighted imaging and T2-weighted imaging, were evaluated at 1, 2, and 6 hours following the ischemic onset. 24 h after MCAO, rats were sacrificed and their brains were stained with TTC to quantitate the infarct volume. The lactate peaks began to rise in ischemic areas 1or 2 h after MCA occlusion, and further increased at 6 h. In contrast, NAA peaks decreased at 6 h. Intriguingly, the average height of the lactate peak in the pyruvate group at 6 h of ischemia, was substantially lower, and that of NAA peaks was higher than those in the control group. Both DWI and T2-weighted lesion sizes in the pyruvate group matched infarct sizes, and were also reduced in the pyruvate group.
We monitored lactate peaks during ischemia along with infarct formation in vivo, and found that the brain-protective effect of pyruvate is associated with reduction of lactate levels in ischemic areas. This finding is a little surprising, because anoxic states would make pyruvate turn into lactate. Further studies may be warranted to investigate the mechanism of the lactate reduction by pyruvate during ishcemia.
Supported by Creative Research Initiatives of Korean Ministry of Science and Technology
Sample Citation:
[Authors]. [Abstract Title]. Program No. XXX.XX. 2005 Neuroscience Meeting Planner. Washington, DC: Society for Neuroscience, 2005. Online.
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