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Early polymorphonuclear leukocyte accumulation correlates with the development of posttraumatic cerebral edema in
R J Schoettle1, P M Kochanek, M J Magargee
1Department of Anesthesiology/Critical Care Medicine, University of Pittsburgh, Pennsylvania.
Abstract:
To evaluate the role of polymorphonuclear leukocytes (PMNs) in the development of posttraumatic cerebral edema, we quantitatively assessed the time course and magnitude of PMN accumulation and its relationship to cerebral edema formation after cerebral trauma in 78 rats. 111In-labeled PMN accumulation was measured in 26 rats in the first 8 h after right hemispheric percussive cerebral trauma or a sham control condition. 51Cr-labeled erythrocyte accumulation was measured simultaneously in 22 rats to assess the contribution of expansion of blood volume to early posttraumatic PMN accumulation. Edema formation [right-left (R-L) hemispheric difference in percent brain water], R-L hemispheric labeled-PMN accumulation, and blood volume index-adjusted PMN accumulation were measured between 0-2 h and 4-8 h posttrauma. PMN accumulation was elevated markedly in the first 2 h posttrauma compared with values in sham controls (13.45 +/- 2.53 vs -0.03 +/- 0.31, p less than 0.01) but not when adjusted for blood volume index (BVI), suggesting that PMN accumulation in the first 2 h posttrauma was due to expansion of blood volume. Between 4 and 8 h posttrauma, however, both total (2.56 +/- 0.82 vs -0.29 +/- 0.52) and BVI-adjusted (8.78 +/- 3.97 vs -0.48 +/- 0.79) PMN accumulation were elevated (p less than 0.05) compared with sham. Brain edema and total PMN accumulation were significantly correlated at both 2 h and 8 h posttrauma (r2 = 0.77, p less than 0.001, and r2 = 0.69, p less than 0.002, respectively), but a significant correlation between edema and BVI-adjusted PMN accumulation was observed only at 8 h posttrauma (r2 = 0.96, p less than 0.001). These data show that PMN accumulation after traumatic brain injury occurs with an initial phase explained by an increase in blood volume in the first 2 h posttrauma followed by a subsequent acute inflammatory phase. The significant correlation between PMN accumulation and the development of cerebral edema is the first quantitative relationship demonstrated between PMN accumulation and a relevant pathophysiological variable. A causal role for PMNs in the genesis of posttraumatic cerebral edema has yet to be proved.
Insights
Polymorphonuclear leukocytes (PMNs) contribute to brain swelling after injury. Early PMN accumulation is due to increased blood volume, while later accumulation correlates with cerebral edema, suggesting an inflammatory role.
Area of Science:
- Neuroscience
- Immunology
- Pathophysiology
Background:
- Traumatic brain injury (TBI) can lead to cerebral edema, a significant cause of secondary brain damage.
- Polymorphonuclear leukocytes (PMNs) are key inflammatory cells implicated in various tissue injuries.
Purpose of the Study:
- To quantitatively assess the role of PMN accumulation in the development of posttraumatic cerebral edema.
- To determine the temporal relationship between PMN infiltration and edema formation after experimental TBI.
Main Methods:
- Rats with percussive cerebral trauma underwent quantitative assessment of 111In-labeled PMN and 51Cr-labeled erythrocyte accumulation.
- Cerebral edema was measured by brain water content, and PMN accumulation was analyzed with and without blood volume index adjustment.
Main Results:
- PMN accumulation was elevated in the first 2 hours post-trauma, primarily due to increased blood volume.
- Between 4-8 hours post-trauma, both total and blood volume index-adjusted PMN accumulation were significantly increased.
- Significant correlations were found between total PMN accumulation and cerebral edema at 2 and 8 hours, and between adjusted PMN accumulation and edema at 8 hours.
Conclusions:
- PMN accumulation after TBI has an initial phase linked to blood volume expansion, followed by an acute inflammatory phase.
- A strong quantitative relationship exists between PMN accumulation and cerebral edema development, suggesting a causal role for PMNs in posttraumatic brain swelling.