Neonatal Ischemic Neuroprotection by Modest Hypothermia Is Associated With Attenuated Brain Acidosis

Laptook, Abbot R.; Corbett, Ronald J. T.; Burns, Dennis K.; Sterett, Rick

doi:10.1161/01.str.26.7.1240

Cited by 50 publications

(20 citation statements)

References 32 publications

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“…In our laboratory, an intraischemic temperature difference of 2.9"C between normothermic and modestly hypothermic piglets was associated with a trend for greater preservation of brain ATP in cooler animals (57 versus 43% of control for hypothermic versus normothermic, p = 0.11) (4). These results suggest that even reductions in temperature of 2-3°C may alter brain energy utilization rate.…”

Section: Laptook Et Almentioning

confidence: 58%

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Quantitative Relationship between Brain Temperature and Energy Utilization Rate Measured in Vivo Using 31P AND 1H Magnetic Resonance Spectroscopy

et al. 1995

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In neonatal and adult animals, modest reduction in brain temperature (2-3°C) during ischemia and hypoxia-ischemia provides partial or complete neuroprotection. One potential mechanism for this effect is a decrease in brain energy (1) and rat pups (2, of ischemia-induced brain injury. For example, modest hypo-3 ) have demonstrated that relatively small reductions in tem-thermia attenuates the extent of brain acidosis during and perature (2-3°C) during brain ischemia or hypoxia-ischemia immediately after brain ischemia in neonatal piglets (4). Modprovides partial neuroprotection. There are multiple mecha-est hypothermia blunts the increase in concentration of excitanisms by which modest hypothermia may modulate the extent tory amino acids in brain extracellular fluid during ischemia in adult rats (5). Another potential benefit of intraischemic hypothermia is preservation of brain ATP. The latter has been Received October 10, 1994; accepted A U~U S~ 3, 1995. confirmed in adult and neonatal animals when temperature is perature also preserve brain ATP. In adult cats and rats,

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Section: Laptook Et Almentioning

confidence: 58%

“…These results suggest that the differences in ATP concentration are secondary to temperatureassociated changes in energy utilization. In our earlier study (4) …”

Section: Discussionmentioning

confidence: 86%

Quantitative Relationship between Brain Temperature and Energy Utilization Rate Measured in Vivo Using 31P AND 1H Magnetic Resonance Spectroscopy

et al. 1995

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“…In the post ischemic period, hypothermic animals and humans demonstrated faster recovery of pH [97] . Studies with magnetic resonance spectroscopy (MRS) have suggested HT attenuates the development of acidosis in long-term ischemia and decreases the decline of high energy phosphates approximate 5% per 1 ℃ [98,99] . Although lactate levels still increase, HI animal models treated with HT demonstrate faster clearance of lactate, improved glucose utilization, resolution of pH, and quicker recovery of high-energy phosphates compared with normothermic (NT) controls [73] .…”

Section: Early Phase Protective Physiologymentioning

confidence: 99%

Use of hypothermia in the intensive care unit

Corry¹

2012

WJCCM

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Used for over 3600 years, hypothermia, or targeted temperature management (TTM), remains an ill defined medical therapy. Currently, the strongest evidence for TTM in adults are for out-of-hospital ventricular tachycardia/ventricular fibrillation cardiac arrest, intracerebral pressure control, and normothermia in the neurocritical care population. Even in these disease processes, a number of questions exist. Data on disease specific therapeutic markers, therapeutic depth and duration, and prognostication are limited. Despite ample experimental data, clinical evidence for stroke, refractory status epilepticus, hepatic encephalopathy, and intensive care unit is only at the safety and proof-of-concept stage. This review explores the deleterious nature of fever, the theoretical role of TTM in the critically ill, and summarizes the clinical evidence for TTM in adults.

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“…This was recently confirmed in human subjects who, when cooled from 37°C to 27°C, showed a decrease in CMRO2 by a factor of 1 / 2.3 [31]. This decrease in oxygen demand likely corresponds to a decreased rate of intracellular energy metabolism, resulting in or from a slower rate of ATP consumption [32], diminished acidosis [33], and improved glucose metabolism [34].…”

Section: Hypothermiamentioning

confidence: 73%

Hypothermia for neuroprotection after cardiac arrest: Mechanisms, clinical trials and patient care

Froehler

Geocadin

2007

Journal of the Neurological Sciences

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Neonatal Ischemic Neuroprotection by Modest Hypothermia Is Associated With Attenuated Brain Acidosis

Abstract: 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.

Cited by 50 publications

References 32 publications

Quantitative Relationship between Brain Temperature and Energy Utilization Rate Measured in Vivo Using 31P AND 1H Magnetic Resonance Spectroscopy

Quantitative Relationship between Brain Temperature and Energy Utilization Rate Measured in Vivo Using 31P AND 1H Magnetic Resonance Spectroscopy

Use of hypothermia in the intensive care unit

Hypothermia for neuroprotection after cardiac arrest: Mechanisms, clinical trials and patient care

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