Effects of pH on brain energetics after hypothermic circulatory arrest

Aoki, Marcelo Saldanha; Nomura, Fumikazu; Stromski, Michael E.; Tsuji, Miles; Fackler, James C.; Hickey, Paul R.; Holtzman, David; Jonas, Richard A.

doi:10.1016/0003-4975(93)90014-9

Cited by 146 publications

(63 citation statements)

References 35 publications

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“…These authors interpreted their findings as evidence for "a net cellular oxygen deficit," although this suggestion is at variance with their own previous results (Aoki et al, 1993) on the increased levels of cerebral high-energy phosphate compounds in hypothermia, which are incompatible with tissue hypoxia. Moreover, because the energy state and the CMRO 2 were essentially the same in the two acid-base management strategies (Aoki et al, 1993), there is no obvious reason for the greater reduction of cytochrome aa3 reported with ␣-stat management (Hiramatsu et al, 1995). However, the technique of near-infrared spectroscopy does not yield quantitative results and is prone to multiple interferences (Sakamoto et al, 2001); hence it is possible that these observations do not reflect the true behavior of cytochrome oxidase but are an experimental artifact.…”

Section: Effect Of Temperature On Cerebral Atp Production and Cerebramentioning

confidence: 60%

“…It is, therefore, very surprising that a change in the redox state in the opposite direction (i.e., a reduction) was measured by near-infrared spectroscopy by Hiramatsu et al (1995) and Nomura et al (1996). These authors interpreted their findings as evidence for "a net cellular oxygen deficit," although this suggestion is at variance with their own previous results (Aoki et al, 1993) on the increased levels of cerebral high-energy phosphate compounds in hypothermia, which are incompatible with tissue hypoxia. Moreover, because the energy state and the CMRO 2 were essentially the same in the two acid-base management strategies (Aoki et al, 1993), there is no obvious reason for the greater reduction of cytochrome aa3 reported with ␣-stat management (Hiramatsu et al, 1995).…”

Section: Effect Of Temperature On Cerebral Atp Production and Cerebramentioning

confidence: 91%

“…Two other observations deserve mention: (1) the recovery of ATP and PCr during the first 30 minutes of postischemic reperfusion has been reported to be much faster in pH-stat than in ␣-stat management of acid-base balance (Aoki et al, 1993) and (2) the beneficial effect of even mild intrainsult hypothermia (32.5°C to 34°C) may be long-lived because ATP levels higher than those in noncooled controls were still maintained in cooled gerbils 1 week after total cerebral ischemia (Kimura et al, 2002;Welsh et al, 1990).…”

Section: Effect Of Temperature On the Recovery Of Brain Energy Paramementioning

confidence: 99%

“…Nevertheless, they did indicate an increase in phosphocreatine ([PCr]) and its ratio to creatine concentration ([PCr]/[Cr]) when temperature was lowered (Hägerdal et al, 1975b). More recent phosphorus 31 ( 31 P) NMR measurements on brains of hypothermic animals in vivo (Aoki et al, 1993;Johnson et al, 1989;Laptook et al, 1995;Swain et al, 1991a) have provided much more conclusive evidence that PCr/ATP and PCr/inorganic phosphate (Pi), and even ATP/Pi, are all elevated owing to increases in PCr and ATP and a decline in Pi. For example, Johnson et al (1989) reported a PCr/Pi of 1.53 at 37°C and 2.28 at 28°C, whereas Swain et al (1991a), who measured PCr/Pi as well as PCr/ATP and ATP/Pi, obtained figures for the three ratios of 1.74, 1.19, and 2.24, respectively in normothermia and of 2.10, 2.37, and 3.23, respectively at 18°C.…”

Section: High-energy Phosphate Compoundsmentioning

confidence: 99%

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Effects of Hypothermia on Energy Metabolism in Mammalian Central Nervous System

Erecińska

Thoresen

Silver

2003

J Cereb Blood Flow Metab

392

238

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Summary:This review analyzes, in some depth, results of studies on the effect of lowered temperatures on cerebral energy metabolism in animals under normal conditions and in some selected pathologic situations. In sedated and paralyzed mammals, acute uncomplicated 0.5-to 3-h hypothermia decreases the global cerebral metabolic rate for glucose (CMR glc ) and oxygen (CMRO 2 ) but maintains a slightly better energy level, which indicates that ATP breakdown is reduced more than its synthesis. Intracellular alkalinization stimulates glycolysis and independently enhances energy generation. Lowering of temperature during hypoxia-ischemia slows the rate of glucose, phosphocreatine, and ATP breakdown and lactate and inorganic phosphate formation, and improves recovery of energetic parameters during reperfusion. Mild hypothermia of 12 to 24-h duration after normothermic hypoxic-ischemic insults seems to prevent or ameliorate secondary failures in energy parameters. The authors conclude that lowered head temperatures help to protect and maintain normal CNS function by preserving brain ATP supply and level. Hypothermia may thus prove a promising avenue in the treatment of stroke and trauma and, in particular, of perinatal brain injury.

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Section: Effect Of Temperature On Cerebral Atp Production and Cerebramentioning

confidence: 60%

Section: Effect Of Temperature On Cerebral Atp Production and Cerebramentioning

confidence: 91%

Section: Effect Of Temperature On the Recovery Of Brain Energy Paramementioning

confidence: 99%

Section: High-energy Phosphate Compoundsmentioning

confidence: 99%

See 2 more Smart Citations

Effects of Hypothermia on Energy Metabolism in Mammalian Central Nervous System

Erecińska

Thoresen

Silver

2003

J Cereb Blood Flow Metab

392

238

View full text Add to dashboard Cite

show abstract

“…In the uninjured brain, CBF and cerebral metabolic rate are closely coupled from 33-35 ℃; with that coupling becoming inconsistent between 28-33 ℃ [67,93,103,[191][192][193][194] . The 2011 consensus review of TTM in critical care contends the uncertainty of the mechanism of action for ICP reduction in TTM precludes an affirmative recommendation.…”

Section: Increased Intracerebral Pressurementioning

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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Cardiac surgery in the young infant: An in vivo model for the study of hypoxic-ischemic brain injury?

Plessis

1997

Ment. Retard. Dev. Disabil. Res. Rev.

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The remarkable advances in survival of infants with congenital heart disease who undergo cardiac surgery are due in large part to techniques that require periods of markedly decreased or arrested circulation. An obvious prerequisite has been the development of techniques that protect critical organ systems, particularly the nervous system, during the often prolonged periods of attenuated oxygen delivery. Despite the manifest success of current neuroprotective strategies, a substantial postoperative neurologic morbidity persists in these infants. The planned periods of hypoperfusion provide a unique clinical opportunity for the prospective, in vivo study of cerebral responses to hypoxic‐ischemic stress. Furthermore, the potential for pretreatment intervention is likely to make this an active setting for the clinical trial of future neuroprotective strategies. This article will evaluate the strengths and limitations of this clinical model, with particular reference to the mechanisms of hypoxia‐ischemia and potential interventions. MRDD Research Reviews 3:49–58, 1997. © 1997 Wiley‐Liss, Inc.

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Effects of pH on brain energetics after hypothermic circulatory arrest

Cited by 146 publications

References 35 publications

Effects of Hypothermia on Energy Metabolism in Mammalian Central Nervous System

Effects of Hypothermia on Energy Metabolism in Mammalian Central Nervous System

Use of hypothermia in the intensive care unit

Cardiac surgery in the young infant: An in vivo model for the study of hypoxic-ischemic brain injury?

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