Effect of hyperglycemia on neuronal changes in a rabbit model of focal cerebral ischemia
- PMID: 2309269
- DOI: 10.1161/01.str.21.3.447
Effect of hyperglycemia on neuronal changes in a rabbit model of focal cerebral ischemia
Abstract
In clinical medicine, cerebral ischemia is frequently due to a focal, rather than global, insult. The effect of hyperglycemia in focal cerebral ischemia is not well defined. We studied the effect of hyperglycemia on neuropathologic changes in a rabbit model of focal cerebral ischemia. Rabbits were randomized to receive saline (n = 12) or glucose (n = 12) infusions. The left anterior cerebral and left internal carotid arteries were clipped after the infusion began. After 6 hours of occlusion, the area of severe ischemic neuronal damage in the left neocortex and striatum on two standard sections of brain was calculated and expressed as a percentage of the total area of the left cortex or striatum. The mean +/- SEM cortical area of severe ischemic neuronal damage was 22.1 +/- 2.8% in the glucose-treated rabbits and 34.0 +/- 4.6% in the saline-treated rabbits (p less than 0.05). The cortical area of severe ischemic neuronal damage was inversely correlated with plasma glucose concentration at the time of arterial clipping (p less than 0.05). We conclude that hyperglycemia is associated with decreased histologic neuronal injury in this model of focal cerebral ischemia and may be protective when cerebral ischemia occurs from a focal insult.
Similar articles
-
Hyperglycemia decreases acute neuronal ischemic changes after middle cerebral artery occlusion in cats.Stroke. 1989 Apr;20(4):519-23. doi: 10.1161/01.str.20.4.519. Stroke. 1989. PMID: 2929029
-
Cerebral damage caused by interrupted, repeated arterial occlusion versus uninterrupted occlusion in a focal ischemic model.J Neurosurg. 1994 Oct;81(4):554-9. doi: 10.3171/jns.1994.81.4.0554. J Neurosurg. 1994. PMID: 7931589
-
Protection after transient focal cerebral ischemia by the N-methyl-D-aspartate antagonist dextrorphan is dependent upon plasma and brain levels.J Cereb Blood Flow Metab. 1991 Nov;11(6):1015-24. doi: 10.1038/jcbfm.1991.169. J Cereb Blood Flow Metab. 1991. PMID: 1939379
-
[Potential of the Cerebral Sodium-Glucose Transporter as a Novel Therapeutic Target in Cerebral Ischemia].Yakugaku Zasshi. 2018;138(7):955-962. doi: 10.1248/yakushi.17-00223-4. Yakugaku Zasshi. 2018. PMID: 29962475 Review. Japanese.
-
Blood glucose level and morphological brain damage following cerebral ischemia.Cerebrovasc Brain Metab Rev. 1991 Spring;3(1):29-38. Cerebrovasc Brain Metab Rev. 1991. PMID: 2036299 Review.
Cited by
-
Hyperglycaemia and infarct size in animal models of middle cerebral artery occlusion: systematic review and meta-analysis.J Cereb Blood Flow Metab. 2011 Mar;31(3):807-18. doi: 10.1038/jcbfm.2010.210. Epub 2010 Dec 15. J Cereb Blood Flow Metab. 2011. PMID: 21157471 Free PMC article.
-
Animal models of stroke: translational potential at present and in 2050.Future Neurol. 2014 Sep;9(5):541-551. doi: 10.2217/fnl.14.44. Future Neurol. 2014. PMID: 25530721 Free PMC article.
-
Spreading depression-induced cyclooxygenase-2 expression in the cortex.Neurochem Res. 2000 May;25(5):645-51. doi: 10.1023/a:1007559003261. Neurochem Res. 2000. PMID: 10905626 Review.
-
Does hyperglycaemia play a role on the outcome of acute ischaemic stroke patients?J Neurol. 1992 Aug;239(7):382-6. doi: 10.1007/BF00812155. J Neurol. 1992. PMID: 1403020
-
Association between stress hyperglycemia ratio with short-term and long-term mortality in critically ill patients with ischemic stroke.Acta Diabetol. 2024 Jul;61(7):859-868. doi: 10.1007/s00592-024-02259-4. Epub 2024 Mar 19. Acta Diabetol. 2024. PMID: 38499778
MeSH terms
Substances
LinkOut - more resources
Full Text Sources
Medical