The effects of convective cooling and rewarming on systemic and central nervous system physiology in isoflurane-anesthetized dogs

Lanier, William L.; Iaizzo, Paul A.; Murray, Michael J.

doi:10.1016/0300-9572(92)90197-k

Cited by 21 publications

(3 citation statements)

References 32 publications

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“…Patients 5 and 6 showed low T br (33.4°C 6 2.0) and negative DT br-rect (#22.9°C) due to failed temperature regulation. rent literature suggests in animals and in noninjured patients a 0.1-0.9°C higher brain temperature compared to the body temperature as well as an intracerebral thermal gradient (0.4-4°C), depending on the measured location (Baker et al, 1972;Hayward and Baker, 1968;Lanier et al, 1992;Marion et al, 1993;Mellergard andNordström, 1990a, 1991;Shiraki et al, 1998;Sternau et al, 1991;Stone et al, 1997). Several animal experiments investigated the brain temperature response after traumatic brain injury Jiang et al, 1991).…”

Section: Figmentioning

confidence: 95%

The Importance of Brain Temperature in Patients after Severe Head Injury: Relationship to Intracranial Pressure, Cerebral Perfusion Pressure, Cerebral Blood Flow, and Outcome

Soukup

Zauner

Doppenberg

et al. 2002

Journal of Neurotrauma

147

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Brain temperature was continuously measured in 58 patients after severe head injury and compared to rectal temperature, intracranial pressure, cerebral blood flow, and outcome after 3 months. The temperature difference between brain and rectal temperature was also calculated. Mild hypothermia (34-36 degrees C) was also used to treat uncontrollable intracranial pressure (ICP) above 20 mm Hg when other methods failed. Brain and rectal temperature were strongly correlated (r = 0.866; p < 0.001). Four groups were identified. The mean brain temperature ranged from 36.9 +/- 0.4 degrees C in the normothermic group to 38.2 +/- 0.5 degrees C in the hyperthermic group, 35.3 +/- 0.5 degrees C in the mild therapeutic hypothermia group, and 34.3 +/- 1.5 degrees C in the hypothermia group without active cooling. The mean DeltaT(br-rect) was positive for patients with a T(br) above 36.0 degrees C (0.0 +/- 0.5 degrees C) and negative for patients during mild therapeutic hypothermia (-0.2 +/- 0.6 degrees C) and also in those with a brain temperature below 36 degrees C without active cooling (0.8 +/- -1.4 degrees C) - the spontaneous hypothermic group. The cerebral perfusion pressure (CPP) was increased significantly by active cooling compared to the normothermic and hyperthermic groups. The mean cerebral blood flow (CBF) in patients with a brain temperature between 36.0 degrees C and 37.5 degrees C was 37.8 +/- 14.0 mL/100 g/min. The lowest CBF was measured in patients with a brain temperature <36.0 degrees C and a negative brain-rectal temperature difference (17.1 +/- 14.0 mL/100 g/min). A positive trend for improved outcome was seen in patients with mild hypothermia. Simultaneous monitoring of brain and rectal temperature provides important diagnostic and prognostic information to guide the treatment of patients after severe head injury (SHI) and the wide differentials that can develop between the brain and core temperature, especially during rapid cooling, strongly supports the use of brain temperature measurement if therapeutic hypothermia is considered for head injury care.

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Section: Figmentioning

confidence: 95%

The Importance of Brain Temperature in Patients after Severe Head Injury: Relationship to Intracranial Pressure, Cerebral Perfusion Pressure, Cerebral Blood Flow, and Outcome

Soukup

Zauner

Doppenberg

et al. 2002

Journal of Neurotrauma

147

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“…In adult dogs, rewarming from hypothermic cardiopulmonary bypass is associated with progressive recovery of normal continuous EEG activity (20); however, in this setting, there should seldom be underlying brain injury. In adult rats, although rapid rewarming over 30 min from moderate hypothermia was not associated with persistent biochemical or (21), there were greater early changes in cardiac output and heart rate, in a similar pattern to the present study, compared with slower rewarming over 2 h. Similarly, others have reported that rapid rewarming over 30 min can cause transient uncoupling of cerebral circulation and metabolism, with a transient increase in extracellular glutamate and lactate (22).…”

Section: Discussionmentioning

confidence: 99%

Epileptiform Activity During Rewarming from Moderate Cerebral Hypothermia in the Near-Term Fetal Sheep

et al. 2005

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Moderate hypothermia is consistently neuroprotective after hypoxic-ischemic insults and is the subject of ongoing clinical trials. In pilot studies, we observed rebound seizure activity in one infant during rewarming from a 72-h period of hypothermia. We therefore quantified the development of EEG-defined seizures during rewarming in an experimental paradigm of delayed cooling for cerebral ischemia. Moderate cerebral hypothermia (n ϭ 9) or sham cooling (n ϭ 13) was initiated 5.5 h after reperfusion from a 30-min period of bilateral carotid occlusion in near-term fetal sheep and continued for 72 h after the insult. During spontaneous rewarming, fetal extradural temperature rose from 32.5 Ϯ 0.6°C to control levels (39.4 Ϯ 0.1°C) in 47 Ϯ 6 min. Carotid blood flow and mean arterial blood pressure increased transiently during rewarming. The cooling group showed a significant increase in electrical seizure events 2, 3, and 5 h after rewarming, maximal at 2 h (2.9 Ϯ 1.2 versus 0.5 Ϯ 0.5 events/h; p Ͻ 0.05). From 6 h after rewarming, there was no significant difference between the groups. Individual seizures were typically short (28.8 Ϯ 5.8 s versus 29.0 Ϯ 6.8 s in sham cooled; NS), and of modest amplitude (35.9 Ϯ 2.8 versus 38.8 Ϯ 3.4 V; NS). Neuronal loss in the parasagittal cortex was significantly reduced in the cooled group (51 Ϯ 9% versus 91 Ϯ 5%; p Ͻ 0.002) and was not correlated with rebound epileptiform activity. In conclusion, rapid rewarming after a prolonged interval of therapeutic hypothermia can be associated with a transient increase in epileptiform events but does not seem to have significant adverse implications for neural outcome. There is now consistent experimental evidence that a sufficient interval of moderate cerebral hypothermia started shortly after severe perinatal hypoxia-ischemia can reduce secondary neuronal injury and improve functional outcomes (1). Although only pilot data are available in newborn infants (2), early induction of moderate hypothermia in adult patients after cardiac arrest improves neurologic recovery (3,4). Rewarming after cooling treatment for severe hypoxic-ischemic encephalopathy (HIE), however, is potentially a more complex process than the original induction of cooling: first because it might lead to destabilizing cardiovascular changes such as a loss of peripheral tone with an increased requirement for cardiac work (5) and second because damaging processes such as release of excitatory amino acid neurotransmitters that have been suppressed by hypothermia could become active again (6,7).In view of such considerations, clinical studies of therapeutic hypothermia typically have rewarmed infants at no more than 0.5°C/h (8 -10); however, there are few systematic data. During our early pilot studies of head-cooling with mild systemic hypothermia for neonatal HIE, we observed a case of an infant who exhibited transient clinical seizures during rewarming. To examine the hypothesis that rewarming from prolonged moderate hypothermia may be associated with rebound seizure activ...

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“…These findings indicated that reduction of global cerebral metabolism was not the sole mechanism involved in the beneficial effects of mild hypothermia. Indeed, a myriad of additional mechanisms of (mild) hypothermia have been unveiled since (Lanier et al, 1992), positively mitigating and modulating destructive processes associated with ischemia-reperfusion, for example, excitotoxicity, neuroinflammation, blood-brain barrier disruption, free radical production, apoptosis, and numerous others (for a detailed review on the mechanisms of action of hypothermia, see Polderman, 2009).…”

Section: Mild Hypothermia and Cerebral Protectionmentioning

confidence: 99%

Induction of Therapeutic Hypothermia Requires Modulation of Thermoregulatory Defenses

Bandschapp

Iaizzo²

2011

Therapeutic Hypothermia and Temperature Management

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Hypothermia has been linked to beneficial neurologic outcomes in different clinical situations and its therapeutic value is considered important. For example, in asphyctic neonates and in patients with out-of-hospital cardiac arrest (with ventricular fibrillation as the initial cardiac rhythm), rapid installation of hypothermia has been reported to add substantial therapeutic benefits over nonthermal standard treatments. Yet, in other groups of patients in which the application of therapeutic hypothermia may be applied with clinical benefits, the optimization of therapy remains less straightforward, as the body possesses vigorous defense mechanisms to protect it from inducing hypothermia, that is, especially in conscious patients and/or in those in which the hypothalamus remains intact, such as stroke patients or patients who suffer a myocardial infarction or spinal cord injury. This overview summarizes the body's primary reactions to hypothermia and the defense mechanisms available or evoked. Then, clinically applicable ways to overcome these forceful cold defenses of the body are described to ensure both an optimal induction process for therapeutic hypothermia and maximal subjective comfort for these conscious patients.

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The effects of convective cooling and rewarming on systemic and central nervous system physiology in isoflurane-anesthetized dogs

Cited by 21 publications

References 32 publications

The Importance of Brain Temperature in Patients after Severe Head Injury: Relationship to Intracranial Pressure, Cerebral Perfusion Pressure, Cerebral Blood Flow, and Outcome

The Importance of Brain Temperature in Patients after Severe Head Injury: Relationship to Intracranial Pressure, Cerebral Perfusion Pressure, Cerebral Blood Flow, and Outcome

Epileptiform Activity During Rewarming from Moderate Cerebral Hypothermia in the Near-Term Fetal Sheep

Induction of Therapeutic Hypothermia Requires Modulation of Thermoregulatory Defenses

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