Therapeutic Hypothermia After Cardiac Arrest

Lay, Cappi; Badjatia, Neeraj

doi:10.1007/s11883-010-0119-2

Cited by 14 publications

(7 citation statements)

References 39 publications

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“…The current protocols for inducing hypothermia rely on increasing heat loss by applying physical cooling, which is provided by surface or intravascular cooling devices (19). However, in conscious nonsedated subjects, cooling triggers compensatory cold-defensive responses, such as shivering, which increases metabolic rate and oxygen demand, thereby counteracting the cooling effect and preventing the drop in core temperature (19). Therefore, the successful use of TH for the treatment of stroke requires novel methods of lowering core temperature, which can be used in awake patients outside of intensive care units.…”

Section: Discussionmentioning

confidence: 99%

“…Within current protocols, hypothermia is induced through application of physical cooling (e.g., by cold water-perfused blankets or intravascular heat exchangers), with the resulting increase in heat loss (19). In conscious subjects, however, the decrease in both ambient and core temperatures activates compensatory responses to generate and retain heat, such as shivering and peripheral vasoconstriction, which make physical cooling ineffective in achieving hypothermia (32).…”

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confidence: 99%

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Shivering and tachycardic responses to external cooling in mice are substantially suppressed by TRPV1 activation but not by TRPM8 inhibition

Feketa

Balasubramanian

Flores

et al. 2013

American Journal of Physiology-Regulatory, Integrative and Comp

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Feketa VV, Balasubramanian A, Flores CM, Player MR, Marrelli SP. Shivering and tachycardic responses to external cooling in mice are substantially suppressed by TRPV1 activation but not by TRPM8 inhibition. Am J Physiol Regul Integr Comp Physiol 305: R1040-R1050, 2013. First published September 4, 2013 doi:10.1152/ajpregu.00296.2013.-Mild decrease of core temperature (32-34°C), also known as therapeutic hypothermia, is a highly effective strategy of neuroprotection from ischemia and holds significant promise in the treatment of stroke. However, induction of hypothermia in conscious stroke patients is complicated by cold-defensive responses, such as shivering and tachycardia. Although multiple thermoregulatory responses may be altered by modulators of thermosensitive ion channels, TRPM8 (transient receptor potential melastatin 8) and TRPV1 (TRP vanilloid 1), it is unknown whether these agents affect cold-induced shivering and tachycardia. The current study aimed to determine the effects of TRPM8 inhibition and TRPV1 activation on the shivering and tachycardic responses to external cooling. Conscious mice were treated with TRPM8 inhibitor compound 5 or TRPV1 agonist dihydrocapsaicin (DHC) and exposed to cooling at 10°C. Shivering was measured by electromyography using implanted electrodes in back muscles, tachycardic response by electrocardiography, and core temperature by wireless transmitters in the abdominal cavity. The role of TRPM8 was further determined using TRPM8 KO mice. TRPM8 ablation had no effect on total electromyographic muscle activity (vehicle: 24.0 Ϯ 1.8; compound 5: 23.8 Ϯ 2.0; TRPM8 KO: 19.7 Ϯ 1.9 V·s/min), tachycardia (⌬HR ϭ 124 Ϯ 31; 121 Ϯ 13; 121 Ϯ 31 beats/min) and drop in core temperature (Ϫ3.6 Ϯ 0.1; Ϫ3.4 Ϯ 0.4; Ϫ3.6 Ϯ 0.5°C) during cold exposure. TRPV1 activation substantially suppressed muscle activity (vehicle: 25.6 Ϯ 3.0 vs. DHC: 5.1 Ϯ 2.0 V·s/min), tachycardia (⌬HR ϭ 204 Ϯ 25 vs. 3 Ϯ 35 beats/min) and produced a profound drop in core temperature (Ϫ2.2 Ϯ 0.6 vs. Ϫ8.9 Ϯ 0.6°C). In conclusion, external cooling-induced shivering and tachycardia are suppressed by TRPV1 activation, but not by TRPM8 inhibition. This suggests that TRPV1 agonists may be combined with external physical cooling to achieve more rapid and effective hypothermia. therapeutic hypothermia; pharmacological hypothermia; shivering; transient receptor potential; physical cooling; electromyography; dihydrocapsaicin MILD DECREASE OF CORE TEMPERATURE to 32-34°C has been shown to effectively protect the brain from ischemia and has become a basis for the clinical method of therapeutic hypo-

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Shivering and tachycardic responses to external cooling in mice are substantially suppressed by TRPV1 activation but not by TRPM8 inhibition

Feketa

Balasubramanian

Flores

et al. 2013

American Journal of Physiology-Regulatory, Integrative and Comp

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“…This strategy has become the basis of the current clinical protocols of therapeutic hypothermia. 35 A variety of practical implementations of the physical cooling strategy have been created, and new and improved methods are constantly being developed. 36 …”

Section: Altering Body Temperaturementioning

confidence: 99%

Induction of therapeutic hypothermia by pharmacological modulation of temperature-sensitive TRP channels: theoretical framework and practical considerations

Feketa

Marrelli

2015

Temperature

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Therapeutic hypothermia has emerged as a remarkably effective method of neuroprotection from ischemia and is being increasingly used in clinics. Accordingly, it is also a subject of considerable attention from a basic scientific research perspective. One of the fundamental problems, with which current studies are concerned, is the optimal method of inducing hypothermia. This review seeks to provide a broad theoretical framework for approaching this problem, and to discuss how a novel promising strategy of pharmacological modulation of the thermosensitive ion channels fits into this framework. Various physical, anatomical, physiological and molecular aspects of thermoregulation, which provide the foundation for this text, have been comprehensively reviewed and will not be discussed exhaustively here. Instead, the first part of the current review, which may be helpful for a broader readership outside of thermoregulation research, will build on this existing knowledge to outline possible opportunities and research directions aimed at controlling body temperature. The second part, aimed at a more specialist audience, will highlight the conceptual advantages and practical limitations of novel molecular agents targeting thermosensitive Transient Receptor Potential (TRP) channels in achieving this goal. Two particularly promising members of this channel family, namely TRP melastatin 8 (TRPM8) and TRP vanilloid 1 (TRPV1), will be discussed in greater detail.

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“…Cooling of the brain is of relevance for preventing cerebral ischemia during anesthesia and after cardiac arrest hypothermia may improve neurological outcome and even survival (Hoesch and Geocadin, 2007; Holzer, 2008, 2013; Lay and Badjatia, 2010; Harris et al, 2012). Cerebral cooling can be induced by global lowering of the body temperature as arterial blood will gradually lower brain temperature (Nybo et al, 2002; Holzer, 2008).…”

Section: Introductionmentioning

confidence: 99%

Influence of intranasal and carotid cooling on cerebral temperature balance and oxygenation

2014

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The present study evaluated the influence of intranasal cooling with balloon catheters, increased nasal ventilation, or percutaneous cooling of the carotid arteries on cerebral temperature balance and oxygenation in six healthy male subjects. Aortic arch and internal jugular venous blood temperatures were measured to assess the cerebral heat balance and corresponding paired blood samples were obtained to evaluate cerebral metabolism and oxygenation at rest, following 60 min of intranasal cooling, 5 min of nasal ventilation, and 15 min with carotid cooling. Intranasal cooling induced a parallel drop in jugular venous and arterial blood temperatures by 0.30 ± 0.08°C (mean ± SD), whereas nasal ventilation and carotid cooling failed to lower the jugular venous blood temperature. The magnitude of the arterio-venous temperature difference across the brain remained unchanged at −0.33 ± 0.05°C following intranasal and carotid cooling, but increased to −0.44 ± 0.11°C (P < 0.05) following nasal ventilation. Calculated cerebral capillary oxygen tension was 43 ± 3 mmHg at rest and remained unchanged during intranasal and carotid cooling, but decreased to 38 ± 2 mmHg (P < 0.05) following increased nasal ventilation. In conclusion, percutaneous cooling of the carotid arteries and intranasal cooling with balloon catheters are insufficient to influence cerebral oxygenation in normothermic subjects as the cooling rate is only 0.3°C per hour and neither intranasal nor carotid cooling is capable of inducing selective brain cooling.

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Therapeutic Hypothermia After Cardiac Arrest

Cited by 14 publications

References 39 publications

Shivering and tachycardic responses to external cooling in mice are substantially suppressed by TRPV1 activation but not by TRPM8 inhibition

Shivering and tachycardic responses to external cooling in mice are substantially suppressed by TRPV1 activation but not by TRPM8 inhibition

Induction of therapeutic hypothermia by pharmacological modulation of temperature-sensitive TRP channels: theoretical framework and practical considerations

Influence of intranasal and carotid cooling on cerebral temperature balance and oxygenation

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