scholarly journals Model-derived assessment of cerebrovascular resistance and cerebral blood flow following traumatic brain injury

2010 ◽  
Vol 235 (4) ◽  
pp. 539-545 ◽  
Author(s):  
Michael L Daley ◽  
Nithya Narayanan ◽  
Charles W Leffler
Keyword(s):  
Traumatic Brain Injury ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Brain Injury ◽  
Cerebral Perfusion ◽  
The State ◽  
Cerebrovascular Resistance ◽  
Fluid Percussion ◽  
Arterial Blood ◽  
Cerebrovascular Regulation

The published guidelines point out the need for the development of methods that individualize patient cerebral perfusion management and minimize secondary ischemic complications associated with traumatic brain injury. A laboratory method has been developed to determine model-derived assessments of cerebrovascular resistance (mCVR) and cerebral blood flow (mCBF) from cerebrovascular pressure transmission, and the dynamic relationship between arterial blood pressure (ABP) and intracranial pressure (ICP). The aim of this two-fold study is to (1) evaluate relative changes in the model-derived parameters of mCVR and mCBF with the corresponding changes in the pial arteriolar vascular parameters of pial arteriolar resistance (PAR) and relative pial arteriolar blood flow (rPABF); and (2) examine the efficacy of the proposed modeling methodology for continuous assessment of the state of cerebrovascular regulation by evaluating relative changes in the model-derived parameters of CBF and cerebrovascular resistance in relation to changes of cerebral perfusion pressure prior to and following fluid percussion brain injury. Changes of ABP, ICP, PAR, relative arteriolar blood flow (rPABF) and the corresponding model-derived parameters of mCBF and mCVR induced by acute hypertensive challenge were evaluated before and following fluid percussion injury in piglets equipped with cranial windows. Before fluid percussion, hypertensive challenge resulted in a significant increase of PAR and mCVR, whereas both rPABF and mCBF remained constant. Following fluid percussion, hypertensive challenge resulted in a significant decrease of PAR and mCVR and consistent with impaired cerebrovascular regulation. Hypertensive challenge significantly increased both rPABF and mCBF, which approximately doubled with increased CPP with correlation values of r = 0.96 ( P < 0.01) and r = 0.97 ( P ≤ 0.01), respectively. The assessment of model-derived cerebrovascular resistance and CBF with changes of CPP provides a means to monitor continuously the state of cerebrovascular regulation.

Effects of fluid-percussion brain injury on regional cerebral blood flow and pial arteriolar diameter

1986 ◽  
Vol 64 (5) ◽  
pp. 787-794 ◽  
Author(s):  
Douglas S. DeWitt ◽  
Larry W. Jenkins ◽  
Enoch P. Wei ◽  
Harry Lutz ◽  
Donald P. Becker ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Brain Injury ◽  
Content Type ◽  
Cerebrovascular Resistance ◽  
Fluid Percussion ◽  
Arterial Blood ◽  
Pial Arterioles ◽  
High Level ◽  
Arteriolar Diameter

✓ The effects of two levels of fluid-percussion brain injury on cerebral blood flow (CBF) and pial arteriolar diameter were investigated in cats. Regional CBF was measured using the radioactive microsphere technique. Experimental brain injury resulted in changes in arterial blood pressure, CBF, and pial arteriolar diameter that were related to the severity of the injury. Low-level injury (1.88 ± 0.11 atm, mean ± standard error of the mean) resulted in a slight transient increase in CBF which had returned to preinjury levels by 30 minutes. High-level injury (2.68 ± 0.19 atm) resulted in larger, statistically significant (p < 0.01) increases in whole-brain CBF, decreases in cerebrovascular resistance, and increases in pial arteriolar diameter 1 minute postinjury. One hour after injury, CBF had returned to preinjury levels while cerebral perfusion pressure was significantly (p < 0.01) reduced. There was no evidence of reduced CBF in any region studied. Pial arterioles dilated during the posttraumatic hypertensive period and then returned to control diameters within 1 hour after injury. Changes in the diameter of pial arterioles were significantly correlated with posttraumatic changes in CBF.

Cerebral blood flow decreased by adrenergic stimulation of cerebral vessels in anesthetized newborn pigs with traumatic brain injury

1993 ◽  
Vol 79 (5) ◽  
pp. 696-704 ◽  
Author(s):  
Masaaki Shibata ◽  
Stephanie Einhaus ◽  
John B. Schweitzer ◽  
Samuel Zuckerman ◽  
Charles W. Leffler
Keyword(s):  
Blood Pressure ◽  
Traumatic Brain Injury ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Brain Injury ◽  
Parietal Cortex ◽  
Adrenergic Blockade ◽  
Fluid Percussion ◽  
Arterial Blood ◽  
Arteriolar Diameter

✓ Changes in cerebral blood flow (CBF), pial arteriolar diameter, and arterial blood pressure, gases, and pH were examined before and for 3 hours after fluid-percussion brain injury in α-chloralose-anesthetized piglets. The brain injury was induced by a percussion of 2.28 ± 0.06 atm applied for 23.7 ± 0.5 msec to the right parietal cortex. Regional CBF was measured with radiolabeled microspheres, and changes in pial arteriolar diameter were monitored in the left parietal cortex using closed cranial windows. Immediately following brain injury, mean blood pressure transiently (for approximately 10 minutes) either increased or decreased and then exhibited a prolonged decrease in all of the animals. The brains showed changes consistent with traumatic brain injury such as subarachnoid hemorrhage, contusions, or reactive axonal swelling; none showed histological evidence of a global alternative pathogenetic mechanism such as hypoxic ischemic damage. While CBF of uninjured control animals did not change over a 3-hour observation period, after brain injury blood flow decreased 30% ± 1% below the baseline level within 10 minutes and remained there for 2 to 3 hours posttrauma. After adrenergic blockade, CBF did not decrease at any time during the 3-hour period in either the uninjured control or the injured animals. Concomitant with the decreased blood flow after brain injury, pial arteriolar diameter decreased 14% below the preinjury level. However, in piglets treated with adrenoceptor antagonists, uninjured control and brain-injured animals did not show a decrease in pial arteriolar diameter. The present results support the hypothesis that increased sympathetic outflow to the cephalic vasculature following the fluid-percussion brain injury causes cerebral vasoconstriction decreasing pial arteriolar diameter and regional CBF.

Autoregulation of cerebral blood flow after experimental fluid percussion injury of the brain

1980 ◽  
Vol 53 (4) ◽  
pp. 500-511 ◽  
Author(s):  
W. Lewelt ◽  
L. W. Jenkins ◽  
J. Douglas Miller
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Brain Injury ◽  
Intracranial Pressure ◽  
Severe Injury ◽  
Content Type ◽  
Fluid Percussion ◽  
Arterial Blood ◽  
Fluid Percussion Injury ◽  
The Brain

✓ To test the hypothesis that concussive brain injury impairs autoregulation of cerebral blood flow (CBF), 24 cats were subjected to hemorrhagic hypotension in 10-mm Hg increments while measurements were made of arterial and intracranial pressure, CBF, and arterial blood gases. Eight cats served as controls, while eight were subjected to mild fluid percussion injury of the brain (1.5 to 2.2 atmospheres) and eight to severe injury (2.8 to 4.8 atmospheres). Injury produced only transient changes in arterial and intracranial pressure, and no change in resting CBF. Impairment of autoregulation was found in injured animals, more pronounced in the severe-injury group. This could not be explained on the basis of intracranial hypertension, hypoxemia, hypercarbia, or brain damage localized to the area of the blood flow electrodes. It is, therefore, concluded that concussive brain injury produces a generalized loss of autoregulation for at least several hours following injury.

Effect of intracisternal phentolamine on cerebral blood flow after subarachnoid injection of blood

1976 ◽  
Vol 44 (3) ◽  
pp. 353-358 ◽  
Author(s):  
Albert N. Martins ◽  
Norwyn Newby ◽  
Thomas F. Doyle ◽  
Arthur I. Kobrine ◽  
Archimedes Ramirez
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Cerebral Perfusion ◽  
Perfusion Pressure ◽  
Content Type ◽  
Cerebrovascular Resistance ◽  
Arterial Blood ◽  
Subarachnoid Injection ◽  
Ischemic Encephalopathy ◽  
Hydrogen Clearance

✓ The hydrogen clearance method was used to measure total and focal cerebral blood flow (CBF) in the monkey before and for 5 hours after a simulated subarachnoid hemorrhage (SAH). Some monkeys also received 0.2 to 1.0 mg/kg phentolamine intracisternally 3 hours after SAH. Results show that SAH did not change cerebrovascular resistance, but as cerebral perfusion pressure decreased, CBF fell transiently. Phentolamine injected intracisternally 3 hours after SAH produced a significant fall in arterial blood pressure; cerebrovascular resistance did not change but CBF decreased significantly. These data indicate that intracisternal phentolamine cannot be considered potentially useful to treat ischemic encephalopathy after SAH.

scholarly journals Quantitative cerebral blood flow using xenon-enhanced CT after decompressive craniectomy in traumatic brain injury

2018 ◽  
Vol 129 (1) ◽  
pp. 241-246 ◽  
Author(s):  
Aditya Vedantam ◽  
Claudia S. Robertson ◽  
Shankar P. Gopinath
Keyword(s):  
Traumatic Brain Injury ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Brain Injury ◽  
Clinical Outcome ◽  
Decompressive Craniectomy ◽  
Decompressive Surgery ◽  
Hemodynamic Parameters ◽  
Enhanced Ct ◽  
The Mean

OBJECTIVEFew studies have reported on changes in quantitative cerebral blood flow (CBF) after decompressive craniectomy and the impact of these measures on clinical outcome. The aim of the present study was to evaluate global and regional CBF patterns in relation to cerebral hemodynamic parameters in patients after decompressive craniectomy for traumatic brain injury (TBI).METHODSThe authors studied clinical and imaging data of patients who underwent xenon-enhanced CT (XeCT) CBF studies after decompressive craniectomy for evacuation of a mass lesion and/or to relieve intractable intracranial hypertension. Cerebral hemodynamic parameters prior to decompressive craniectomy and at the time of the XeCT CBF study were recorded. Global and regional CBF after decompressive craniectomy was measured using XeCT. Regional cortical CBF was measured under the craniectomy defect as well as for each cerebral hemisphere. Associations between CBF, cerebral hemodynamics, and early clinical outcome were assessed.RESULTSTwenty-seven patients were included in this study. The majority of patients (88.9%) had an initial Glasgow Coma Scale score ≤ 8. The median time between injury and decompressive surgery was 9 hours. Primary decompressive surgery (within 24 hours) was performed in the majority of patients (n = 18, 66.7%). Six patients had died by the time of discharge. XeCT CBF studies were performed a median of 51 hours after decompressive surgery. The mean global CBF after decompressive craniectomy was 49.9 ± 21.3 ml/100 g/min. The mean cortical CBF under the craniectomy defect was 46.0 ± 21.7 ml/100 g/min. Patients who were dead at discharge had significantly lower postcraniectomy CBF under the craniectomy defect (30.1 ± 22.9 vs 50.6 ± 19.6 ml/100 g/min; p = 0.039). These patients also had lower global CBF (36.7 ± 23.4 vs 53.7 ± 19.7 ml/100 g/min; p = 0.09), as well as lower CBF for the ipsilateral (33.3 ± 27.2 vs 51.8 ± 19.7 ml/100 g/min; p = 0.07) and contralateral (36.7 ± 19.2 vs 55.2 ± 21.9 ml/100 g/min; p = 0.08) hemispheres, but these differences were not statistically significant. The patients who died also had significantly lower cerebral perfusion pressure (52 ± 17.4 vs 75.3 ± 10.9 mm Hg; p = 0.001).CONCLUSIONSIn the presence of global hypoperfusion, regional cerebral hypoperfusion under the craniectomy defect is associated with early mortality in patients with TBI. Further study is needed to determine the value of incorporating CBF studies into clinical decision making for severe traumatic brain injury.

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