Neutrophil Accumulation After Traumatic Brain Injury in Rats: Comparison of Weight Drop and Controlled Cortical Impact Models

Abstract

Previous work in our laboratory and others using the weight drop (WD) model of traumatic brain injury (TBI) has shown that neutrophils accumulate in brain tissue during the initial 24 h posttrauma as measured by myeloperoxidase (MPO) activity and immunohistochemistry. This study compares the acute inflammatory response to TBI over time, as measured by MPO activity, in the WD and controlled cortical impact (CCI) models. Anesthetized adult Sprague-Dawley rats were traumatized using WD (10-g weight dropped 5 cm) or CCI (4 m/sec, 2.5 mm depth). At 2, 24, 48, or 168 h after trauma, rats (n = 4-5/group at each time) were anesthetized and killed, the brains were removed, and 6-mm coronal slices from traumatized and contralateral hemispheres were assayed for MPO activity. Nontraumatized rats (n = 4) served as controls. Three additional rats underwent a more severe CCI (3 mm depth) with MPO activity assayed at 24 h. A separate group of rats (n = 6) was subjected to WD trauma and killed at 2 weeks after injury for analysis of lesion volume. MPO activity in the traumatized hemisphere was demonstrated at 24 and 48 h in both the WD (0.3152 +/- 0.0472 and 0.3017 +/- 0.0228 U/g, respectively, p < 0.05 vs controls) and CCI (0.1866 +/- 0.0225 and 0.1937 +/- 0.0772 U/g, respectively, p < 0.05 vs controls) models. MPO activity was below the sensitivity of the assay in the control, 2 h, and 168 h groups in both models.(ABSTRACT TRUNCATED AT 250 WORDS)

Nerve growth factor expression correlates with severity and outcome of traumatic brain injury in children

“…4,23,24 However, the specific relationship of cytokines and neurotrophins with the severity of brain injury and with the neurologic outcome remains still controversial. Recent studies have shown that increased levels of IL-1β are associated with increased severity and poor outcome in patients affected by meningitis, hypoxic-ischemic encephalopathy, and traumatic head injuries.…”

Differential acute and chronic responses of tumor necrosis factor-deficient mice to experimental brain injury

“…A profound inflammatory response has been documented, initiated immediately after experimental TBI (34,35), which is characterized by the release of several cytokines (4). It has been suggested that TNF plays a detrimental role in the acute pathophysiology of TBI and ischemia (2, 8, 16, 36, 37).…”

Pathophysiology of Cerebral Ischemia and Brain Trauma: Similarities and Differences

“…The inflammatory response in the CNS may have various consequences on outcome, depending upon the degree of inflammatory response and when it occurs (Blight, 1985;Benveniste, 1992). Both acute and chronic inflammatory processes have been shown to influence outcome in various experimental models of cerebral ischemia and trauma (Arvin et al, 1996;Clark et al, 1994;del Zoppo et al, 2000;Fan et al, 1995;Fan et al, 1996;Feuerstein et al, 1998;Kochanek and Hallenbeck, 1992). While acute inflammatory events may participate in secondary injury processes, more delayed inflammatory events may be reparative (Bethea and Dietrich, 2002;Kerschensteiner et al, 1999).…”