Effect of Posttraumatic Hyperglycemia on Contusion Volume and Neutrophil Accumulation after Moderate Fluid-Percussion Brain Injury in Rats
- 1 June 2002
- journal article
- research article
- Published by Mary Ann Liebert Inc in Journal of Neurotrauma
- Vol. 19 (6), 681-692
- https://doi.org/10.1089/08977150260139075
Abstract
The purpose of this study was to evaluate the effects of posttraumatic hyperglycemia on contusion volume and neutrophil accumulation following moderate traumatic brain injury (TBI) in rats. A parasagittal fluid-percussion (F-P) brain injury (1.8-2.1 atm) was induced in male Sprague-Dawley rats. Rats were then randomized into four trauma groups (n = 7/group) by the timing of dextrose injection (2.0 gm/kg/ip), which included (1) early (E) group: 5 min after TBI; (2) delayed (D) group: 4 h after TBI; (3) 24-h group: 24 h after TBI; or (4) control (C) group: no dextrose injection. A sham operated control group also received dextrose to document physiological parameters (n = 4). Rats were perfusion fixed 3 days following TBI, and the brains were processed for routine histopathological and immunocytochemical analysis. Contusion areas and volumes, as well as the frequency of myeloperoxidase immunoreactive polymorphonuclear leukocytes (PMNLs) were determined. Dextrose injections significantly increased blood glucose levels (p < 0.005) in all treated groups. Although acute hyperglycemia following TBI did not significantly affect total contusion volume, contusion area was significantly elevated in the early treatment group. In addition, early posttraumatic hyperglycemia enhanced neutrophil accumulation in the area of the cortical contusion (p < 0.005). In contrast, delayed induced hyperglycemia (i.e., 4 h, 24 h) did not significantly affect histopathological outcome or neutrophil accumulation. Taken together, these findings indicate that acute but not delayed hyperglycemia aggravates histopathological outcome and increased accumulation of PMNLs. Posttraumatic hyperglycemia in the acute phase may worsen traumatic outcome by enhancing secondary injury processes, including inflammation.Keywords
This publication has 81 references indexed in Scilit:
- Early White Blood Cell Dynamics after Traumatic Brain Injury: Effects on the Cerebral MicrocirculationJournal of Cerebral Blood Flow & Metabolism, 1997
- Temporal Thresholds for Hyperglycemia-Augmented Ischemic Brain Damage in RatsStroke, 1995
- Increased expression in vivo of VCAM-1 and E-selectin by the aortic endothelium of normolipemic and hyperlipemic diabetic rabbits.Arteriosclerosis and Thrombosis: A Journal of Vascular Biology, 1994
- Polymorphonuclear leukocytes and monocytes/macrophages in the pathogenesis of cerebral ischemia and stroke.Stroke, 1992
- Polymorphonuclear leukocytes occlude capillaries following middle cerebral artery occlusion and reperfusion in baboons.Stroke, 1991
- Effect of hyperglycemia on neuronal changes in a rabbit model of focal cerebral ischemia.Stroke, 1990
- Hyperglycemia enlarges infarct size in cerebrovascular occlusion in cats.Stroke, 1988
- Persistent nonketotic hyperglycemia as a grave prognostic sign in head-injured patientsCritical Care Medicine, 1981
- Deleterious effect of glucose pretreatment on recovery from diffuse cerebral ischemia in the cat. II. Regional metabolite levels.Stroke, 1980
- Deleterious effect of glucose pretreatment on recovery from diffuse cerebral ischemia in the cat. I. Local cerebral blood flow and glucose utilization.Stroke, 1980