Electrophysiological Properties of CA1 Neurons Protected by Postischemic Hypothermia in Gerbils

Dong, Hui; Moody-Corbett, F; Colbourne, Frederick; Pittman, Quentin J.; Corbett, Dale

doi:10.1161/01.str.32.3.788

Cited by 23 publications

(14 citation statements)

References 36 publications

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“…However, it remains clear that delayed hypothermia does provide benefit, as shown by recent cardiac arrest trials and in other systems by a number of recent investigations. 17,18 The timing of hypothermia will be a critical consideration for future clinical trials. Table 1.…”

Section: Discussionmentioning

confidence: 99%

Intra-Arrest Cooling Improves Outcomes in a Murine Cardiac Arrest Model

et al. 2004

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Background-Recent clinical studies have demonstrated that hypothermia to 32°to 34°C provides significant clinical benefit when induced after resuscitation from cardiac arrest. However, cooling during the postresuscitation period was slow, requiring 4 to 8 hours to achieve target temperatures after return of spontaneous circulation (ROSC). Whether more rapid cooling would further improve survival remains unclear. We sought to determine whether cooling during cardiac arrest before ROSC (ie, "intra-arrest" hypothermia) has survival benefit over more delayed post-ROSC cooling, using a murine cardiac arrest model. Methods and Results-A model of potassium-induced cardiac arrest was established in C57BL/6 mice. After 8 minutes of untreated cardiac arrest, resuscitation was attempted with chest compression, ventilation, and intravenous fluid. Mice were randomized to 3 treatment groups (nϭ10 each): an intra-arrest hypothermia group, in which mice were cooled to 30°C just before attempted resuscitation, and then rewarmed after 1 hour; a post-ROSC hypothermia group, in which mice were kept at 37°C for 20 minutes after successful ROSC and then were cooled to 30°C for 1 hour; and a normothermic control group, in which mice were kept at 37°C. The intra-arrest hypothermia group demonstrated better 72-hour survival than delayed hypothermia and normothermia groups (6/10 versus 1/10 and 1/10 survivors, respectively, PϽ0.05), with similar differences seen at 6-hour survival and on neurological scoring. Conclusions-Timing of hypothermia is a crucial determinant of survival in the murine arrest model. Early intra-arrest cooling appears to be significantly better than delayed post-ROSC cooling or normothermic resuscitation. (Circulation.

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Section: Discussionmentioning

confidence: 99%

Intra-Arrest Cooling Improves Outcomes in a Murine Cardiac Arrest Model

et al. 2004

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“…In early studies, a 3 day survival or less were commonly used as an indicator of protection. Most recently, more clinically relevant survival periods have been examined and have been shown to be a critical factor in determining the long-term effects of hypothermic therapy (Corbett et al, 1997;Dong et al, 2001). In one study, postischemic hypothermia was shown to be protective after a 3 day survival, yet no protection was documented at 2 months after the ischemic insult (Dietrich et al, 1993).…”

Section: Postischemic Hypothermiamentioning

confidence: 99%

Protection in Animal Models of Brain and Spinal Cord Injury with Mild to Moderate Hypothermia

Dietrich

Atkins

Bramlett

2009

Journal of Neurotrauma

130

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For the past 20 years, various laboratories throughout the world have shown that mild to moderate levels of hypothermia lead to neuroprotection and improved functional outcome in various models of brain and spinal cord injury (SCI). Although the potential neuroprotective effects of profound hypothermia during and following central nervous system (CNS) injury have long been recognized, more recent studies have described clinically feasible strategies for protecting the brain and spinal cord using hypothermia following a variety of CNS insults. In some cases, only a one or two degree decrease in brain or core temperature can be effective in protecting the CNS from injury. Alternatively, raising brain temperature only a couple of degrees above normothermia levels worsens outcome in a variety of injury models. Based on these data, resurgence has occurred in the potential use of therapeutic hypothermia in experimental and clinical settings. The study of therapeutic hypothermia is now an international area of investigation with scientists and clinicians from every part of the world contributing to this important, promising therapeutic intervention. This paper reviews the experimental data obtained in animal models of brain and SCI demonstrating the benefits of mild to moderate hypothermia. These studies have provided critical data for the translation of this therapy to the clinical arena. The mechanisms underlying the beneficial effects of mild hypothermia are also summarized.

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“…Additionally, postischemic hypothermia preserved the electrophysiological properties of CA1 neurons, which relects the functional preservation of neural networks [149]. Moreover, mice subjected to ischemia followed by hypothermia treatment showed neuroprotection against ischemia-induced long-term potentiation (LTP) impairment as well as synaptic plasticity [150].…”

Section: Preservation Of the Integrity Of Neural Networkmentioning

confidence: 99%

Hypothermia in Stroke Therapy: Systemic versus Local Application

Huber¹,

Duan²,

Chandra³

et al. 2017

Hypoxia and Human Diseases

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Presently, there are no efective, widely applicable therapies for ischemic stroke. There is strong clinical evidence for the neuroprotective beneits of hypothermia, and surfacecooling methods have been utilized for decades in the treatment of cerebral ischemia during cardiac arrest, but complications with hypothermia induction have hindered its clinical acceptance in ischemic stroke therapy. Recently, the microcatheter-based local endovascular infusion (LEVI) of cold saline directly to the infarct site has been proposed as a solution to the drawbacks of surface cooling. The safety and eicacy of LEVI in rat models have been established, and implementation in larger animals has been similarly encouraging. A recent pilot study even established the safety of LEVI in humans. This review seeks to outline the major research on LEVI, discusses the mechanisms that mediate its superior neuroprotection over surface and systemic cooling, and identiies areas that warrant further investigation. While LEVI features improvements on surface cooling, its core mechanisms of neuroprotection are still largely shared with therapeutic hypothermia in general. As such, the mechanisms of hypothermia-based neuroprotection are discussed as well.

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Electrophysiological Properties of CA1 Neurons Protected by Postischemic Hypothermia in Gerbils

Cited by 23 publications

References 36 publications

Intra-Arrest Cooling Improves Outcomes in a Murine Cardiac Arrest Model

Intra-Arrest Cooling Improves Outcomes in a Murine Cardiac Arrest Model

Protection in Animal Models of Brain and Spinal Cord Injury with Mild to Moderate Hypothermia

Hypothermia in Stroke Therapy: Systemic versus Local Application

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