Effects of temperature on cerebral tissue oxygen tension, carbon dioxide tension, and pH during transient global ischemia in rabbits

Andreas Bacher, Jae Young Kwon, Mark Zornow

Research output: Contribution to journalArticle

34 Citations (Scopus)

Abstract

Background: A decrease in brain temperature (T(brain)) causes a decrease in the cerebral metabolic rate for oxygen (CMRO2) and provides potent neuroprotection against ischemic damage. In the present study, the effects of mild to moderate hypothermia on cerebral tissue oxygen tension (P(O2) brain), carbon dioxide tension (P(CO2) brain), and pH (pH(brain)) were monitored during short episodes of global cerebral ischemia. Methods: After approval by the Animal Care and Use Committee, 10 New Zealand white rabbits were anesthetized (1% halothane in air) and mechanical ventilation was adjusted to maintain the arterial carbon dioxide tension at 35 mmHg (αstar). A sensor to measure P(O2) brain, P(CO2), brain, pH(brain), and T(brain) was inserted into the brain through a burr hole in the skull T(brain) was adjusted to 38°C, 34.4°C, and 29.4°C in a random sequence in each animal. P(O2) brain, P(CO2) brain, and pH(brain) (all variables are reported at the actual T(brain)) were recorded every 10 s during a 5-min baseline, 3 min of cerebral ischemia induced by inflation of a neck tourniquet, and 10 min of reperfusion at each level of T(brain). Analysis of variance and Dunnett's test were used for statistical analysis. Data are presented as means ± SD. Results: During ischemia, P(O2) brain decreased from 56 ± 3 to 33 ± 2 mmHg at 38°C, from 58 ± 3 to 32 ± 3 mmHg at 34.4°C, and from 51 ± 2 to 32 ± 2 mrnHg at 29.4°C (p = NS). P(CO2) brain increased by 6.7 ± 2 mmHg at 38°C, by 5.1 ± 1.4 mixing at 34.4°C, and by 2.3 ± 0.8 mmHg at 29.4°C. pH(brain) inversely followed the trend of P(CO2) brain. Conclusions: The attenuated increase in P(CO2) brain during hypothermic ischemia results from the reduced CMLRO2. The similar decrease in P(O2) brain at all temperature levels indicates that despite the reduction in CMRO2, P(O2) brain is no better preserved during brief episodes of hypothermic ischemia than during normothermic ischemia.

Original languageEnglish (US)
Pages (from-to)403-409
Number of pages7
JournalAnesthesiology
Volume88
Issue number2
DOIs
StatePublished - 1998
Externally publishedYes

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Carbon Dioxide
Ischemia
Oxygen
Rabbits
Temperature
Brain
Brain Ischemia
Animal Care Committees
Tourniquets

Keywords

  • Cerebral tissue
  • Extraction
  • Hypothermia
  • New Zealand white rabbit
  • Oxyhemoglobin dissociation

ASJC Scopus subject areas

  • Anesthesiology and Pain Medicine

Cite this

Effects of temperature on cerebral tissue oxygen tension, carbon dioxide tension, and pH during transient global ischemia in rabbits. / Bacher, Andreas; Kwon, Jae Young; Zornow, Mark.

In: Anesthesiology, Vol. 88, No. 2, 1998, p. 403-409.

Research output: Contribution to journalArticle

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abstract = "Background: A decrease in brain temperature (T(brain)) causes a decrease in the cerebral metabolic rate for oxygen (CMRO2) and provides potent neuroprotection against ischemic damage. In the present study, the effects of mild to moderate hypothermia on cerebral tissue oxygen tension (P(O2) brain), carbon dioxide tension (P(CO2) brain), and pH (pH(brain)) were monitored during short episodes of global cerebral ischemia. Methods: After approval by the Animal Care and Use Committee, 10 New Zealand white rabbits were anesthetized (1{\%} halothane in air) and mechanical ventilation was adjusted to maintain the arterial carbon dioxide tension at 35 mmHg (αstar). A sensor to measure P(O2) brain, P(CO2), brain, pH(brain), and T(brain) was inserted into the brain through a burr hole in the skull T(brain) was adjusted to 38°C, 34.4°C, and 29.4°C in a random sequence in each animal. P(O2) brain, P(CO2) brain, and pH(brain) (all variables are reported at the actual T(brain)) were recorded every 10 s during a 5-min baseline, 3 min of cerebral ischemia induced by inflation of a neck tourniquet, and 10 min of reperfusion at each level of T(brain). Analysis of variance and Dunnett's test were used for statistical analysis. Data are presented as means ± SD. Results: During ischemia, P(O2) brain decreased from 56 ± 3 to 33 ± 2 mmHg at 38°C, from 58 ± 3 to 32 ± 3 mmHg at 34.4°C, and from 51 ± 2 to 32 ± 2 mrnHg at 29.4°C (p = NS). P(CO2) brain increased by 6.7 ± 2 mmHg at 38°C, by 5.1 ± 1.4 mixing at 34.4°C, and by 2.3 ± 0.8 mmHg at 29.4°C. pH(brain) inversely followed the trend of P(CO2) brain. Conclusions: The attenuated increase in P(CO2) brain during hypothermic ischemia results from the reduced CMLRO2. The similar decrease in P(O2) brain at all temperature levels indicates that despite the reduction in CMRO2, P(O2) brain is no better preserved during brief episodes of hypothermic ischemia than during normothermic ischemia.",
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T1 - Effects of temperature on cerebral tissue oxygen tension, carbon dioxide tension, and pH during transient global ischemia in rabbits

AU - Bacher, Andreas

AU - Kwon, Jae Young

AU - Zornow, Mark

PY - 1998

Y1 - 1998

N2 - Background: A decrease in brain temperature (T(brain)) causes a decrease in the cerebral metabolic rate for oxygen (CMRO2) and provides potent neuroprotection against ischemic damage. In the present study, the effects of mild to moderate hypothermia on cerebral tissue oxygen tension (P(O2) brain), carbon dioxide tension (P(CO2) brain), and pH (pH(brain)) were monitored during short episodes of global cerebral ischemia. Methods: After approval by the Animal Care and Use Committee, 10 New Zealand white rabbits were anesthetized (1% halothane in air) and mechanical ventilation was adjusted to maintain the arterial carbon dioxide tension at 35 mmHg (αstar). A sensor to measure P(O2) brain, P(CO2), brain, pH(brain), and T(brain) was inserted into the brain through a burr hole in the skull T(brain) was adjusted to 38°C, 34.4°C, and 29.4°C in a random sequence in each animal. P(O2) brain, P(CO2) brain, and pH(brain) (all variables are reported at the actual T(brain)) were recorded every 10 s during a 5-min baseline, 3 min of cerebral ischemia induced by inflation of a neck tourniquet, and 10 min of reperfusion at each level of T(brain). Analysis of variance and Dunnett's test were used for statistical analysis. Data are presented as means ± SD. Results: During ischemia, P(O2) brain decreased from 56 ± 3 to 33 ± 2 mmHg at 38°C, from 58 ± 3 to 32 ± 3 mmHg at 34.4°C, and from 51 ± 2 to 32 ± 2 mrnHg at 29.4°C (p = NS). P(CO2) brain increased by 6.7 ± 2 mmHg at 38°C, by 5.1 ± 1.4 mixing at 34.4°C, and by 2.3 ± 0.8 mmHg at 29.4°C. pH(brain) inversely followed the trend of P(CO2) brain. Conclusions: The attenuated increase in P(CO2) brain during hypothermic ischemia results from the reduced CMLRO2. The similar decrease in P(O2) brain at all temperature levels indicates that despite the reduction in CMRO2, P(O2) brain is no better preserved during brief episodes of hypothermic ischemia than during normothermic ischemia.

AB - Background: A decrease in brain temperature (T(brain)) causes a decrease in the cerebral metabolic rate for oxygen (CMRO2) and provides potent neuroprotection against ischemic damage. In the present study, the effects of mild to moderate hypothermia on cerebral tissue oxygen tension (P(O2) brain), carbon dioxide tension (P(CO2) brain), and pH (pH(brain)) were monitored during short episodes of global cerebral ischemia. Methods: After approval by the Animal Care and Use Committee, 10 New Zealand white rabbits were anesthetized (1% halothane in air) and mechanical ventilation was adjusted to maintain the arterial carbon dioxide tension at 35 mmHg (αstar). A sensor to measure P(O2) brain, P(CO2), brain, pH(brain), and T(brain) was inserted into the brain through a burr hole in the skull T(brain) was adjusted to 38°C, 34.4°C, and 29.4°C in a random sequence in each animal. P(O2) brain, P(CO2) brain, and pH(brain) (all variables are reported at the actual T(brain)) were recorded every 10 s during a 5-min baseline, 3 min of cerebral ischemia induced by inflation of a neck tourniquet, and 10 min of reperfusion at each level of T(brain). Analysis of variance and Dunnett's test were used for statistical analysis. Data are presented as means ± SD. Results: During ischemia, P(O2) brain decreased from 56 ± 3 to 33 ± 2 mmHg at 38°C, from 58 ± 3 to 32 ± 3 mmHg at 34.4°C, and from 51 ± 2 to 32 ± 2 mrnHg at 29.4°C (p = NS). P(CO2) brain increased by 6.7 ± 2 mmHg at 38°C, by 5.1 ± 1.4 mixing at 34.4°C, and by 2.3 ± 0.8 mmHg at 29.4°C. pH(brain) inversely followed the trend of P(CO2) brain. Conclusions: The attenuated increase in P(CO2) brain during hypothermic ischemia results from the reduced CMLRO2. The similar decrease in P(O2) brain at all temperature levels indicates that despite the reduction in CMRO2, P(O2) brain is no better preserved during brief episodes of hypothermic ischemia than during normothermic ischemia.

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KW - Extraction

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KW - Oxyhemoglobin dissociation

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