Influence of early posttraumatic hypothermia therapy on local cerebral blood flow and glucose metabolism after fluid-percussion brain injury

Weizhao Zhao, Ofelia F. Alonso, Judith Y. Loor, Raul Busto, Myron Ginsberg

Research output: Contribution to journalArticle

23 Citations (Scopus)

Abstract

Object. Using autoradiographic image averaging, the authors recently described prominent foci of marked glucose metabolism-greater-than-blood- flow uncoupling in the acutely traumatized rat brain. Because hypothermia is known to ameliorate injury in this and other injury models, the authors designed the present study to assess the effects of posttraumatic therapeutic hypothermia on the local cerebral metabolic rate of glucose (LCMRglu) and local cerebral blood flow (LCBF) following moderate parasagittal fluid- percussion head injury (FPI) in rats. Methods. Either cranial hypothermia (30°C) or normothermia (37°C) was induced for 3 hours in matched groups of rats immediately after FPI; LCMRglu and LCBF were assessed 3 hours after concluding these temperature manipulations. In rats subjected to FPI, regardless of whether normothermia or hypothermia ensued, LCBF was reduced relative to the sham-injury groups. In addition, when FPI was followed by hypothermia (FPI-30°C group), the subsequent LCBF was significantly lower (35-38% on average) than in FPI-37°C rats. Statistical mapping of LCBF difference imaging data revealed confluent cortical and subcortical zones of significantly reduced LCBF (largely ipsilateral to the prior injury) in FPI- 30°C rats relative to the FPI-37°C group. Local glucose utilization was reduced in both hemispheres of FPI-37°C rats relative to the sham-injury group and was lower in the right (traumatized) hemisphere than in the left. However, LCMRglu values were largely unaffected by temperature manipulation in either the FPI or sham-injury groups. The LCMRglu/LCBF ratio was nearly doubled in FPI-30°C rats relative to the FPI-37°C group, in a diffuse and bihemispheric fashion. Linear regression analysis comparing LCMRglu and LCBF revealed that the FPI-37°C and FPI-30°C data sets were completely nonoverlapping, whereas the two sham-injury data sets were intermixed. Conclusions. Despite its proven neuroprotective efficacy, early posttraumatic hypothermia (30°C for 3 hours) nonetheless induces a moderate decline in cerebral perfusion without the (anticipated) improvement in cerebral glucose utilization, so that a state of mild metabolism-greater-than-blood-flow dissociation is perpetuated.

Original languageEnglish
Pages (from-to)510-519
Number of pages10
JournalJournal of Neurosurgery
Volume90
Issue number3
StatePublished - Mar 1 1999

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Cerebrovascular Circulation
Percussion
Hypothermia
Craniocerebral Trauma
Brain Injuries
Blood Glucose
Glucose
Wounds and Injuries
Therapeutics
Induced Hypothermia
Temperature

Keywords

  • Autoradiography
  • Brain temperature
  • Head injury
  • Hypoperfusion
  • Hypothermia
  • Image processing
  • Neuroprotection

ASJC Scopus subject areas

  • Clinical Neurology
  • Neuroscience(all)

Cite this

Influence of early posttraumatic hypothermia therapy on local cerebral blood flow and glucose metabolism after fluid-percussion brain injury. / Zhao, Weizhao; Alonso, Ofelia F.; Loor, Judith Y.; Busto, Raul; Ginsberg, Myron.

In: Journal of Neurosurgery, Vol. 90, No. 3, 01.03.1999, p. 510-519.

Research output: Contribution to journalArticle

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abstract = "Object. Using autoradiographic image averaging, the authors recently described prominent foci of marked glucose metabolism-greater-than-blood- flow uncoupling in the acutely traumatized rat brain. Because hypothermia is known to ameliorate injury in this and other injury models, the authors designed the present study to assess the effects of posttraumatic therapeutic hypothermia on the local cerebral metabolic rate of glucose (LCMRglu) and local cerebral blood flow (LCBF) following moderate parasagittal fluid- percussion head injury (FPI) in rats. Methods. Either cranial hypothermia (30°C) or normothermia (37°C) was induced for 3 hours in matched groups of rats immediately after FPI; LCMRglu and LCBF were assessed 3 hours after concluding these temperature manipulations. In rats subjected to FPI, regardless of whether normothermia or hypothermia ensued, LCBF was reduced relative to the sham-injury groups. In addition, when FPI was followed by hypothermia (FPI-30°C group), the subsequent LCBF was significantly lower (35-38{\%} on average) than in FPI-37°C rats. Statistical mapping of LCBF difference imaging data revealed confluent cortical and subcortical zones of significantly reduced LCBF (largely ipsilateral to the prior injury) in FPI- 30°C rats relative to the FPI-37°C group. Local glucose utilization was reduced in both hemispheres of FPI-37°C rats relative to the sham-injury group and was lower in the right (traumatized) hemisphere than in the left. However, LCMRglu values were largely unaffected by temperature manipulation in either the FPI or sham-injury groups. The LCMRglu/LCBF ratio was nearly doubled in FPI-30°C rats relative to the FPI-37°C group, in a diffuse and bihemispheric fashion. Linear regression analysis comparing LCMRglu and LCBF revealed that the FPI-37°C and FPI-30°C data sets were completely nonoverlapping, whereas the two sham-injury data sets were intermixed. Conclusions. Despite its proven neuroprotective efficacy, early posttraumatic hypothermia (30°C for 3 hours) nonetheless induces a moderate decline in cerebral perfusion without the (anticipated) improvement in cerebral glucose utilization, so that a state of mild metabolism-greater-than-blood-flow dissociation is perpetuated.",
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T1 - Influence of early posttraumatic hypothermia therapy on local cerebral blood flow and glucose metabolism after fluid-percussion brain injury

AU - Zhao, Weizhao

AU - Alonso, Ofelia F.

AU - Loor, Judith Y.

AU - Busto, Raul

AU - Ginsberg, Myron

PY - 1999/3/1

Y1 - 1999/3/1

N2 - Object. Using autoradiographic image averaging, the authors recently described prominent foci of marked glucose metabolism-greater-than-blood- flow uncoupling in the acutely traumatized rat brain. Because hypothermia is known to ameliorate injury in this and other injury models, the authors designed the present study to assess the effects of posttraumatic therapeutic hypothermia on the local cerebral metabolic rate of glucose (LCMRglu) and local cerebral blood flow (LCBF) following moderate parasagittal fluid- percussion head injury (FPI) in rats. Methods. Either cranial hypothermia (30°C) or normothermia (37°C) was induced for 3 hours in matched groups of rats immediately after FPI; LCMRglu and LCBF were assessed 3 hours after concluding these temperature manipulations. In rats subjected to FPI, regardless of whether normothermia or hypothermia ensued, LCBF was reduced relative to the sham-injury groups. In addition, when FPI was followed by hypothermia (FPI-30°C group), the subsequent LCBF was significantly lower (35-38% on average) than in FPI-37°C rats. Statistical mapping of LCBF difference imaging data revealed confluent cortical and subcortical zones of significantly reduced LCBF (largely ipsilateral to the prior injury) in FPI- 30°C rats relative to the FPI-37°C group. Local glucose utilization was reduced in both hemispheres of FPI-37°C rats relative to the sham-injury group and was lower in the right (traumatized) hemisphere than in the left. However, LCMRglu values were largely unaffected by temperature manipulation in either the FPI or sham-injury groups. The LCMRglu/LCBF ratio was nearly doubled in FPI-30°C rats relative to the FPI-37°C group, in a diffuse and bihemispheric fashion. Linear regression analysis comparing LCMRglu and LCBF revealed that the FPI-37°C and FPI-30°C data sets were completely nonoverlapping, whereas the two sham-injury data sets were intermixed. Conclusions. Despite its proven neuroprotective efficacy, early posttraumatic hypothermia (30°C for 3 hours) nonetheless induces a moderate decline in cerebral perfusion without the (anticipated) improvement in cerebral glucose utilization, so that a state of mild metabolism-greater-than-blood-flow dissociation is perpetuated.

AB - Object. Using autoradiographic image averaging, the authors recently described prominent foci of marked glucose metabolism-greater-than-blood- flow uncoupling in the acutely traumatized rat brain. Because hypothermia is known to ameliorate injury in this and other injury models, the authors designed the present study to assess the effects of posttraumatic therapeutic hypothermia on the local cerebral metabolic rate of glucose (LCMRglu) and local cerebral blood flow (LCBF) following moderate parasagittal fluid- percussion head injury (FPI) in rats. Methods. Either cranial hypothermia (30°C) or normothermia (37°C) was induced for 3 hours in matched groups of rats immediately after FPI; LCMRglu and LCBF were assessed 3 hours after concluding these temperature manipulations. In rats subjected to FPI, regardless of whether normothermia or hypothermia ensued, LCBF was reduced relative to the sham-injury groups. In addition, when FPI was followed by hypothermia (FPI-30°C group), the subsequent LCBF was significantly lower (35-38% on average) than in FPI-37°C rats. Statistical mapping of LCBF difference imaging data revealed confluent cortical and subcortical zones of significantly reduced LCBF (largely ipsilateral to the prior injury) in FPI- 30°C rats relative to the FPI-37°C group. Local glucose utilization was reduced in both hemispheres of FPI-37°C rats relative to the sham-injury group and was lower in the right (traumatized) hemisphere than in the left. However, LCMRglu values were largely unaffected by temperature manipulation in either the FPI or sham-injury groups. The LCMRglu/LCBF ratio was nearly doubled in FPI-30°C rats relative to the FPI-37°C group, in a diffuse and bihemispheric fashion. Linear regression analysis comparing LCMRglu and LCBF revealed that the FPI-37°C and FPI-30°C data sets were completely nonoverlapping, whereas the two sham-injury data sets were intermixed. Conclusions. Despite its proven neuroprotective efficacy, early posttraumatic hypothermia (30°C for 3 hours) nonetheless induces a moderate decline in cerebral perfusion without the (anticipated) improvement in cerebral glucose utilization, so that a state of mild metabolism-greater-than-blood-flow dissociation is perpetuated.

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KW - Brain temperature

KW - Head injury

KW - Hypoperfusion

KW - Hypothermia

KW - Image processing

KW - Neuroprotection

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