Cerebral Vascular and Metabolic Response to Sustained Systemic Inflammation in Ovine Traumatic Brain Injury

Abstract

Summary: Traumatic brain injury (TBI) is frequently accompanied by a systemic inflammatory response secondary to multiple trauma, shock, or infections. This study investigated the impact of sustained systemic inflammation on cerebral hemodynamics and metabolism in ovine traumatic brain injury. Fifteen sheep were investigated for 14 hours. Head injury was induced with a nonpenetrating stunner in anesthetized, ventilated animals. One group (TBI/Endo, n ‫ס‬ 6) subsequently received a continuous endotoxin infusion for 12 hours, whereas a second group (TBI, n ‫ס‬ 6) received the carrier. Three instrumented animals served as sham controls. Head impact significantly increased intracranial pressure from 9 ± 4 mm Hg to 21 ± 15 mm Hg (TBI/Endo) and from 10 ± 3 mm Hg to 24 ± 19 mm Hg (TBI) (means ± SD). Internal carotid blood flow increased and cerebral vascular resistance decreased (P < 0.05) during the hyperdynamic inflammatory response between 10 and 14 hours in the TBI/Endo group, whereas these parameters were at baseline level in the TBI group. Intracranial pressure remained unchanged during this period, but increased during hypercapnia. The CMRO 2 , PaCO 2 , and arterial hematocrit values were identical among the groups between 10 and 14 hours. It is concluded that chronic endotoxemia in ovine traumatic brain injury was associated with cerebral vasodilation uncoupled from global brain metabolism. Different mechanisms appear to induce cerebral vasodilation in response to inflammation and hypercapnia.

Increased carotid artery flow rate in a patient with Parry-Romberg syndrome

“…In this particular case, MR angiography did not reveal any collateral circulation between the internal and external carotid systems but we determined that the right ECA flow rate and volume had increased. This finding may be due to the increased chronic inflammation on the same side of the face, confirmed by Stubbe et al [10], showing that during the hyperdynamic inflammatory response ECA blood flow increased and cerebral vascular resistance decreased. Our patient also had decayed teeth and this may have contributed to the increased ECA flow rate, and may be explained by continuous chronic inflammation despite a normal erythrocyte sedimentation rate, C-reactive protein and leukocyte count.…”

Brain Trauma Leads to Enhanced Lung Inflammation and Injury: Evidence for Role of P4504Fs in Resolution

“…Indeed, development of acute lung injury is associated with the worst neurologic outcome in patients with severe brain trauma or hemorrhage (Holland et al , 2003; Mascia and Andrews 1998; Paine et al , 1952). While the episodes of hypoxia after head trauma do not correlate with lung injury (Holland et al , 2003), several pieces of evidence suggest it may occur as a result of a systemic inflammatory response (De Simoni et al , 1990; Stubbe et al , 2004; Woiciechowsky et al , 1998, 2002). Fisher et al (1999) have reported enhanced pulmonary inflammation in organ donors after fatal brain injury.…”

Closed Traumatic Brain Injury Model in Sheep Mimicking High-Velocity, Closed Head Trauma in Humans

“…In the presented experimental model, an initial increase of the mean ICP up to 20.5 mmHg was observed in the severe, closed TBI group. An immediate post-traumatic increase of the ICP has been shown in various experimental models [1,7] as well as in brain-injured patients. The regular use of multiparametric cerebral monitoring increases in brain-injured patients.…”

“…Traumatic brain injuries (TBI) are the leading cause of death and disability in the young [1] . Each year 1.4 million people in the United States of America are aff ected by traumatic brain injury.…”