Changes in Local Cerebral Blood Flow, Glucose Utilization, and Mitochondrial Function Following Traumatic Brain Injury in Rats.

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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LOCAL CEREBRAL BLOOD FLOW AND GLUCOSE UTILIZATION IN SCHIZOPHRENIA. I. CATATONIC TYPE.

Clinical Neuropharmacology ◽

10.1097/00002826-199202001-00497 ◽

1992 ◽

Vol 15 ◽

pp. 258B

Author(s):

K. Satoh ◽

M. Narita ◽

T. Someya ◽

S. Takahashi ◽

T. Suzuki ◽

...

Keyword(s):

Blood Flow ◽

Cerebral Blood Flow ◽

Glucose Utilization ◽

Local Cerebral Blood Flow

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The Influence of Inhaled Nitric Oxide on Cerebral Blood Flow and Metabolism in a Child with Traumatic Brain Injury

Anesthesia & Analgesia ◽

10.1097/00000539-200108000-00023 ◽

2001 ◽

Vol 93 (2) ◽

pp. 351-353 ◽

Cited By ~ 3

Author(s):

Monica S. Vavilala ◽

Joan S. Roberts ◽

Anne E. Moore ◽

David W. Newell ◽

Arthur M. Lam

Keyword(s):

Nitric Oxide ◽

Traumatic Brain Injury ◽

Blood Flow ◽

Cerebral Blood Flow ◽

Brain Injury ◽

Inhaled Nitric Oxide

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Cerebral Metabolism and Blood Flow Following Traumatic Brain Injury

10.2310/vasc.2401 ◽

2018 ◽

Author(s):

Ryan Martin ◽

Lara Zimmermann ◽

Marike Zwienenberg ◽

Kee D Kim ◽

Kiarash Shahlaie

Keyword(s):

Traumatic Brain Injury ◽

Blood Flow ◽

Cerebral Blood Flow ◽

Brain Injury ◽

Intracranial Pressure ◽

Cerebral Autoregulation ◽

Cerebral Metabolism ◽

Elevated Intracranial Pressure ◽

Metabolic Demand ◽

Cerebral Metabolic Rate

The management of traumatic brain injury focuses on the prevention of second insults, which most often occur because of a supply/demand mismatch of the cerebral metabolism. The healthy brain has mechanisms of autoregulation to match the cerebral blood flow to the cerebral metabolic demand. After trauma, these mechanisms are disrupted, leaving the patient susceptible to episodes of hypotension, hypoxemia, and elevated intracranial pressure. Understanding the normal and pathologic states of the cerebral blood flow is critical for understanding the treatment choices for a patient with traumatic brain injury. In this chapter, we discuss the underlying physiologic principles that govern our approach to the treatment of traumatic brain injury. This review contains 3 figures, 1 table and 12 references Key Words: cerebral autoregulation, cerebral blood flow, cerebral metabolic rate, intracranial pressure, ischemia, reactivity, vasoconstriction, vasodilation, viscosity

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Cerebral Blood Flow Predicts Recovery in Children with Persistent Post-Concussion Symptoms after Mild Traumatic Brain Injury

Journal of Neurotrauma ◽

10.1089/neu.2020.7566 ◽

2021 ◽

Author(s):

Karen M. Barlow ◽

Kartik Iyer ◽

Tingting Yan ◽

Alex Scurfield ◽

Helen Carlson ◽

...

Keyword(s):

Traumatic Brain Injury ◽

Blood Flow ◽

Cerebral Blood Flow ◽

Brain Injury ◽

Mild Traumatic Brain Injury

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Cerebral blood flow, glucose use, and CSF ionic regulation in potassium-depleted rats

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1988.254.2.h250 ◽

1988 ◽

Vol 254 (2) ◽

pp. H250-H257

Author(s):

H. Schrock ◽

W. Kuschinsky

Keyword(s):

Blood Flow ◽

Cerebral Blood Flow ◽

Glucose Utilization ◽

Local Cerebral Blood Flow ◽

Arterial Pco2 ◽

Average Decrease ◽

K Concentration ◽

Low K ◽

The Brain ◽

K Depletion

Rats were kept on a low-K+ diet for 25 or 70 days. Local cerebral blood flow (LCBF) and local cerebral glucose utilization (LCGU) were measured in 31 different structures of the brain by means of the [14C]iodoantipyrine and [14C]2-deoxy-D-glucose method. After 25 and 70 days of K+ depletion LCBF was decreased significantly in 27 and 30 structures, respectively, the average decrease being 19 and 25%. In contrast, average LCGU was not changed. Cisternal cerebrospinal fluid (CSF) K+ concentration decreased significantly from 2.65 +/- 0.02 mM in controls to 2.55 +/- 0.02 mM and 2.47 +/- 0.02 mM in the two treated groups (P less than 0.01). CSF [HCO3-], pH, and PCO2 were increased in K+-depleted animals. These data show that K+ depletion induces an increase in CSF pH and a decrease in CSF K+ concentration, both of which cause a reduction in cerebral blood flow. The increased CSF PCO2 is secondary to the reduction of blood flow, since brain metabolism and arterial PCO2 remained constant.

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Local cerebral blood flow and glucose utilization after blood exchange with a hemoglobin-based O2 carrier in conscious rats

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1993.265.4.h1243 ◽

1993 ◽

Vol 265 (4) ◽

pp. H1243-H1248 ◽

Cited By ~ 1

Author(s):

K. Waschke ◽

H. Schrock ◽

D. M. Albrecht ◽

K. van Ackern ◽

W. Kuschinsky

Keyword(s):

Blood Flow ◽

Cerebral Blood Flow ◽

Glucose Utilization ◽

Brain Structures ◽

Control Group ◽

Local Cerebral Blood Flow ◽

Conscious Rats ◽

Cerebral Glucose Utilization ◽

Arterial Blood ◽

Blood Exchange

The effects of a blood exchange on cerebral blood flow and glucose utilization were studied. A near to total blood exchange (hematocrit < 3%) was achieved in conscious rats by isovolemic hemodilution. Ultrapurified, polymerized, bovine hemoglobin (UPBHB) served as a blood substitute. Local cerebral blood flow (LCBF) and local cerebral glucose utilization (LCGU) were measured in 34 brain structures of conscious rats by means of the ido[14C]antipyrine and the 2-[14C]-deoxy-D-glucose methods. A group of rats without blood exchange served as control. After blood exchange LCBF increased from 36 to 126% in the different brain structures resulting in a nearly doubled mean cerebral blood flow (+82%). LCGU increased only moderately by 0-24%. Significant increases in LCGU were observed in 16 brain structures. Mean cerebral glucose utilization slightly increased (+14%). The relationship between LCGU and LCBF was found to be tight both in the control group (r = 0.95) as well as after blood replacement (r = 0.94), although it was reset to a higher overall LCBF-to-LCGU ratio. The profound increases in LCBF observed after blood exchange, which were not paralleled by comparable increases in LCGU, might be explained by a reduction of blood viscosity after blood exchange. Additional effects of blood exchange observed in the present study were an increase of mean arterial blood pressure and a decline of heart rate. The results indicate that replacement of blood with the hemoglobin-based oxygen carrier UPBHB appears to meet the cerebral circulatory and metabolic demands of the brain tissue.

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