Impaired Autoregulation of Cerebral Blood Flow in an Experimental Model of Traumatic Brain Injury

Abstract

In order to study the pathophysiology and the intracranial hemodynamics of traumatic brain injury, we have developed a modified closed-head injury model of impact-acceleration that expresses several features of severe head injury in humans, including acute and long-lasting intracranial hypertension, diffuse axonal injury, neuronal necrosis, bleeding, and edema. In view of the clinical relevance of impaired autoregulation of cerebral blood flow after traumatic brain injury, and aiming at further characterization of the model, we investigated the autoregulation efficiency 24 h after experimental closed-head injury. Cortical blood flow was continuously monitored with a laser-Doppler flowmeter, and the mean arterial blood pressure was progressively decreased by controlled hemorrhage. Relative laser-Doppler flow was plotted against the corresponding mean arterial blood pressure, and a two-line segmented model was applied to determine the break point and slopes of the autoregulation curves. The slope of the curve at the right hand of the break point was significantly increased in the closed head injury group (0.751 +/- 0.966%/mm Hg versus -0.104 +/- 0.425%/mm Hg,p = 0.028). The break point tended towards higher values in the closed head injury group (62.2 +/- 20.8 mm Hg versus 46.9 +/- 12.7 mm Hg; mean +/- SD, p = 0.198). It is concluded that cerebral autoregulation in this modified closed head injury model is impaired 24 h after traumatic brain injury. This finding, in addition to other characteristic features of severe head injury established earlier in this model, significantly contributes to its clinical relevance.

Acute, transient hemorrhagic hypotension does not aggravate structural damage or neurologic motor deficits but delays the long-term cognitive recovery following mild to moderate traumatic brain injury

“…Our results are partially in contrast to recent studies reporting a significant increase in focal tissue injury or sustained neurologic deficit related to the superimposed HH in more severe models of weight-drop brain injury in rats (37). Interestingly, using a mild FP brain injury model, Matushita et al (9) reported an exacerbation of tissue damage with the superimposed HH (MABP 50-60 mm Hg for 30 mins).…”

Vasopressin Increases Cerebral Perfusion Pressure but not Cerebral Blood Flow in Neurosurgical Patients with Catecholamine-Refractory Hypotension: A Preliminary Evaluation Using the Non-Invasive Quantix ND in Comparison to the Literature

“…This still is considered sufficient, at least in TBI patients according to the Brain Trauma Foundation guidelines. After TBI a dysfunction in cerebral autoregulation might occur [32] and also the microcirculation seems to be dysregulated leading to distended arterioles (Glushakova et al 2014 epub) and thus more intracerebral blood volume. As consequence ICP can be elevated.…”

Cerebral Blood Flow in Experimental and Clinical Neurotrauma: Quantitative Assessment

“…The caliber changes of the autoregulatory vessels are mediated by myogenic, metabolic, or neurogenic mechanisms (Brownlee & Langille, 1991;Bryan et al, 1995;Busto et al, 1997). The smaller arterioles dilate proportionately more than larger arterioles at a mean arterial blood pressure below physiological levels (Ellis et al, 1979;Engelborghs et al, 2000). However, larger arterioles tend to be more responsive than smaller arterioles at normal and increased levels of arterial pressure (Engelborghs et al, 2000).…”

“…The smaller arterioles dilate proportionately more than larger arterioles at a mean arterial blood pressure below physiological levels (Ellis et al, 1979;Engelborghs et al, 2000). However, larger arterioles tend to be more responsive than smaller arterioles at normal and increased levels of arterial pressure (Engelborghs et al, 2000). The other findings associated with CBF reduction at early time points after TBI is the increased cytokine expression and production, however the role of their activity changes is not clear yet (Ahn et al, 2004).…”