Neonatal ischemie neuroprotection by modest hypothermia is associated with attenuated brain acidosis

Abbot R. Laptook, Ron J T Corbett, Dennis Burns, Rick Sterett

Research output: Contribution to journalArticle

43 Citations (Scopus)

Abstract

Background and Purpose: A 2.9°C reduction in the intraischemic rectal temperature of neonatal piglets is associated with less brain damage compared with animals with normothermic rectal temperatures. This investigation studied one potential mechanism for this observation: better maintenance of energy stores and less brain acidosis secondary to reduced metabolic activity associated with modest hypothermia. Methods: 31P MR spectroscopy was used to study piglets before, during, and after 15 minutes of partial brain ischemia with intraischemic rectal temperatures of either 38.3±0.4°C (n=10, normothermic) or 35.4±0.5°C (n=10, hypothermic). Animals were followed up for up to 72 hours after ischemia and were evaluated clinically and by brain histology. Results: Values for pHi remained 0.15 to 0.20 pH units greater in modestly hypothermic than in normothermic piglets during ischemia and the initial 30 minutes after ischemia (P=.049, group effect). Phosphocreatine, β-ATP, and inorganic phosphorus were similar between groups. The relationship between the intraischemic energy state and subsequent clinical evidence of brain damage (irrespective of group assignment) revealed lower pHi over the last 7 minutes of ischemia for abnormal compared with normal piglets (5.98±0.22 versus 6.39±0.24, respectively; P=.002). In contrast, intraischemic β-ATP (41±19% versus 57±21% of control) and inorganic phosphorus (273±31% versus 224±92% of control) for abnormal and normal piglets, respectively, did not differ between groups. Conclusions: Intraischemic modest hypothermia attenuates the severity of brain acidosis during and 30 minutes after ischemia compared with normothermic animals and supports the concept that attenuated brain acidosis is a potential mechanism by which hypothermia may reduce ischemic brain damage.

Original languageEnglish (US)
Pages (from-to)1240-1246
Number of pages7
JournalStroke
Volume26
Issue number7
StatePublished - Jul 1995

Fingerprint

Acidosis
Hypothermia
Ischemia
Brain
Phosphorus
Temperature
Adenosine Triphosphate
Phosphocreatine
Neuroprotection
Brain Ischemia
Histology
Magnetic Resonance Spectroscopy
Maintenance

Keywords

  • Acidosis
  • Cerebral ischemia
  • Hypothermia
  • Spectroscopy, nuclear magnetic resonance

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine
  • Neuroscience(all)

Cite this

Laptook, A. R., Corbett, R. J. T., Burns, D., & Sterett, R. (1995). Neonatal ischemie neuroprotection by modest hypothermia is associated with attenuated brain acidosis. Stroke, 26(7), 1240-1246.

Neonatal ischemie neuroprotection by modest hypothermia is associated with attenuated brain acidosis. / Laptook, Abbot R.; Corbett, Ron J T; Burns, Dennis; Sterett, Rick.

In: Stroke, Vol. 26, No. 7, 07.1995, p. 1240-1246.

Research output: Contribution to journalArticle

Laptook, AR, Corbett, RJT, Burns, D & Sterett, R 1995, 'Neonatal ischemie neuroprotection by modest hypothermia is associated with attenuated brain acidosis', Stroke, vol. 26, no. 7, pp. 1240-1246.
Laptook, Abbot R. ; Corbett, Ron J T ; Burns, Dennis ; Sterett, Rick. / Neonatal ischemie neuroprotection by modest hypothermia is associated with attenuated brain acidosis. In: Stroke. 1995 ; Vol. 26, No. 7. pp. 1240-1246.
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abstract = "Background and Purpose: A 2.9°C reduction in the intraischemic rectal temperature of neonatal piglets is associated with less brain damage compared with animals with normothermic rectal temperatures. This investigation studied one potential mechanism for this observation: better maintenance of energy stores and less brain acidosis secondary to reduced metabolic activity associated with modest hypothermia. Methods: 31P MR spectroscopy was used to study piglets before, during, and after 15 minutes of partial brain ischemia with intraischemic rectal temperatures of either 38.3±0.4°C (n=10, normothermic) or 35.4±0.5°C (n=10, hypothermic). Animals were followed up for up to 72 hours after ischemia and were evaluated clinically and by brain histology. Results: Values for pHi remained 0.15 to 0.20 pH units greater in modestly hypothermic than in normothermic piglets during ischemia and the initial 30 minutes after ischemia (P=.049, group effect). Phosphocreatine, β-ATP, and inorganic phosphorus were similar between groups. The relationship between the intraischemic energy state and subsequent clinical evidence of brain damage (irrespective of group assignment) revealed lower pHi over the last 7 minutes of ischemia for abnormal compared with normal piglets (5.98±0.22 versus 6.39±0.24, respectively; P=.002). In contrast, intraischemic β-ATP (41±19{\%} versus 57±21{\%} of control) and inorganic phosphorus (273±31{\%} versus 224±92{\%} of control) for abnormal and normal piglets, respectively, did not differ between groups. Conclusions: Intraischemic modest hypothermia attenuates the severity of brain acidosis during and 30 minutes after ischemia compared with normothermic animals and supports the concept that attenuated brain acidosis is a potential mechanism by which hypothermia may reduce ischemic brain damage.",
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AB - Background and Purpose: A 2.9°C reduction in the intraischemic rectal temperature of neonatal piglets is associated with less brain damage compared with animals with normothermic rectal temperatures. This investigation studied one potential mechanism for this observation: better maintenance of energy stores and less brain acidosis secondary to reduced metabolic activity associated with modest hypothermia. Methods: 31P MR spectroscopy was used to study piglets before, during, and after 15 minutes of partial brain ischemia with intraischemic rectal temperatures of either 38.3±0.4°C (n=10, normothermic) or 35.4±0.5°C (n=10, hypothermic). Animals were followed up for up to 72 hours after ischemia and were evaluated clinically and by brain histology. Results: Values for pHi remained 0.15 to 0.20 pH units greater in modestly hypothermic than in normothermic piglets during ischemia and the initial 30 minutes after ischemia (P=.049, group effect). Phosphocreatine, β-ATP, and inorganic phosphorus were similar between groups. The relationship between the intraischemic energy state and subsequent clinical evidence of brain damage (irrespective of group assignment) revealed lower pHi over the last 7 minutes of ischemia for abnormal compared with normal piglets (5.98±0.22 versus 6.39±0.24, respectively; P=.002). In contrast, intraischemic β-ATP (41±19% versus 57±21% of control) and inorganic phosphorus (273±31% versus 224±92% of control) for abnormal and normal piglets, respectively, did not differ between groups. Conclusions: Intraischemic modest hypothermia attenuates the severity of brain acidosis during and 30 minutes after ischemia compared with normothermic animals and supports the concept that attenuated brain acidosis is a potential mechanism by which hypothermia may reduce ischemic brain damage.

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