Abstract P139: A Paradoxical Increase in Brain Temperature Occurs Early During Cardiopulmonary Arrest.

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Manuel C Boller ◽  
Joseph M Katz ◽  
Lance B Becker
Keyword(s):  
Cardiac Arrest ◽  
Brain Temperature ◽  
Cardiopulmonary Arrest ◽  
Heat Removal ◽  
External Heat ◽  
Brain Cooling ◽  
The Face ◽  
The Brain ◽  
Domestic Swine ◽  
Recorded Temperature

Introduction : In patients with cardiac arrest, brain cooling is a powerful intervention to improve neurological outcome. However, brain temperature variation during the initial phase of untreated cardiac arrest has not been well characterized. Objective : To describe passive changes in brain temperature in early untreated cardiac arrest. Methods : Eleven domestic swine (35 kg) were anesthetized and routine respiratory and cardiovascular parameters were monitored and recorded. Temperature was recorded from various sites including the forebrain. External heat support was adjusted to maintain rectal temperature at 37±0.5 °C at baseline, but was discontinued thereafter. Ventricular fibrillation was then induced and cardiac arrest remained untreated for 15 minutes. During this phase, forebrain temperature was recorded every 60 seconds. Results : The brain temperature increased in all animals after induction of cardiac arrest and remained above baseline for the duration of the study period. Peak mean (±SEM) increase above baseline was 0.26 (±0.03) °C and was reached after 9 minutes. Brain temperature slowly declined thereafter. The maximum and minimum temperature increase in individual animals was 0.42 °C and 0.13 °C, respectively. Conclusions : Brain temperature consistently and rapidly increases in the early phase of untreated cardiac arrest in anesthetized swine. This may parallel ongoing, yet diminishing, heat production from cerebral metabolic activity in the face of cessation of convective heat removal via cerebral blood flow.

Selective regulation of brain and body temperatures in the squirrel monkey

1983 ◽  
Vol 245 (2) ◽  
pp. R293-R297 ◽  
Author(s):  
C. A. Fuller ◽  
M. A. Baker
Keyword(s):  
Squirrel Monkey ◽  
Brain Temperature ◽  
Human Subjects ◽  
Venous Blood ◽  
The Body ◽  
Body Core Temperature ◽  
Saimiri Sciureus ◽  
Brain Cooling ◽  
The Face ◽  
Body Core

Many panting mammals can cool the brain below body core temperature during heat stress. Studies on human subjects suggest that primates may also be able selectively to regulate brain temperature. We examined this possibility by measuring hypothalamic (Thy) and colonic (Tco) temperatures of unanesthetized squirrel monkeys (Saimiri sciureus) in two different experiments. First, Thy and Tco were examined at four different ambient temperatures (Ta) between 20 and 36 degrees C. Over this range of Ta, Thy was regulated within a narrower range than Tco. In the cold Ta, Tco was lower than Thy; whereas in warm Ta, Tco was higher than Thy. Second, monkeys maintained at 35 degrees C Ta were acutely exposed to cool air blown on the face or abdomen. Air directed at the face cooled Thy more and faster than Tco, whereas air directed at the abdomen cooled Tco and Thy at the same rate. The second experiment was repeated in anesthetized animals with a thermocouple in the right atrium, and the results showed that this brain cooling was not produced by cooling of blood in the body core. These data demonstrate that the squirrel monkey is capable of selectively regulating Thy. Further the results suggest that venous blood returning from the face may be involved in selective brain cooling in warm environments.

Bradycardia during face cooling in man may be produced by selective brain cooling

1979 ◽  
Vol 46 (5) ◽  
pp. 905-907 ◽  
Author(s):  
M. Caputa ◽  
M. Cabanac
Keyword(s):  
Venous Return ◽  
Human Subjects ◽  
Cardiac Response ◽  
Brain Cooling ◽  
Selective Brain Cooling ◽  
The Face ◽  
The Difference ◽  
The Brain ◽  
Face Cooling

In human subjects, bradycardia was produced by immersing the subjects' faces in water at 15 degrees C when they were hyperthermic. When they were hypothermic, the same face cooling produced tachycardia. It is suggested that the difference in cardiac response originates in selective brain cooling during hyperthermia, by venous return from the face to the brain, via ophthalmic veins.

scholarly journals Non-invasive Monitoring of Brain Temperature during Rapid Selective Brain Cooling by Zero-Heat-Flux Thermometry

2019 ◽  
Vol 3 (1) ◽  
pp. 1 ◽  
Author(s):  
Mohammad Fazel Bakhsheshi ◽  
Marjorie Ho ◽  
Lynn Keenliside ◽  
Ting-Yim Lee
Keyword(s):  
Heat Flux ◽  
Body Temperature ◽  
Rectal Temperature ◽  
Brain Temperature ◽  
Whole Body ◽  
Brain Cooling ◽  
Selective Brain Cooling ◽  
Non Invasive ◽  
Temperature Probe ◽  
The Brain

Introduction: Selective brain cooling can minimize systemic complications associated with whole body cooling but maximize neuroprotection. Recently, we developed a non-invasive, portable and inexpensive system for selectively cooling the brain rapidly and demonstrated its safety and efficacy in porcine models. However, the widespread application of this technique in the clinical setting requires a reliable, non-invasive and accurate method for measuring local brain temperature so that cooling and rewarming rates can be controlled during targeted temperature management. In this study, we evaluate the ability of a zero-heat-flux SpotOn sensor, mounted on three different locations, to measure brain temperature during selective brain cooling in a pig model. Computed Tomography (CT) was used to determine the position of the SpotOn patches relative to the brain at different placement locations.Methods and Results: Experiments were conducted on two juvenile pigs. Body temperature was measured using a rectal temperature probe while brain temperature with an intraparenchymal thermocouple probe. A SpotOn patch was taped to the pig’s head at three different locations: 1-2 cm posterior (Location #1, n=1), central forehead (Location #2, n=1); and 1-2 cm anterior and lateral to the bregma i.e., above the eye on the forehead (Location #3, n=1). This cooling system was able to rapidly cool the brain temperature to 33.7 ± 0.2°C within 15 minutes, and maintain the brain temperature within 33-34°C for 4-6 hours before slowly rewarming to 34.8 ± 1.1°C from 33.7 ± 0.2°C, while maintaining the core body temperature (as per rectal temperature probe) above 36°C. We measured a mean bias of -1.1°C, -0.2°C and 0.7°C during rapid cooling in induction phase, maintenance and rewarming phase, respectively. Amongst the three locations, location #2 had the highest correlation (R2 = 0.8) between the SpotOn sensor and the thermocouple probe.Conclusions: This SBC method is able to tightly control the rewarming rate within 0.52 ± 0.20°C/h. The SpotOn sensor placed on the center of the forehead provides a good measurement of brain temperature in comparison to the invasive needle probe.

Abstract 100: Neuroprotection Provided by Transnasal Airflow-Induced Brain Cooling in a Model of Pediatric Cardiac Arrest

Circulation ◽  
2019 ◽  
Vol 140 (Suppl_2) ◽  
Author(s):  
Zeng-Jin Yang ◽  
C. Danielle Hopkins ◽  
Shawn Adams ◽  
Ewa Kulikowicz ◽  
Harikrishna S Tandri ◽  
...  
Keyword(s):  
Cardiac Arrest ◽  
Sensorimotor Cortex ◽  
Brain Temperature ◽  
Low Cost ◽  
Venous Blood ◽  
Swine Model ◽  
Brain Cooling ◽  
Surface Cooling ◽  
Arterial Blood ◽  
Normothermic Group

Introduction: High transnasal airflow at ambient temperature increases evaporative cooling of the nasal passages and drives a countercurrent heat exchange between cooled venous blood draining the nasal turbinates with cephalic arterial blood. Hypothesis: High transnasal airflow is not inferior to standard surface cooling in protecting the brain in an infant swine model of asphyxic cardiac arrest. Methods: Arterial O2 saturation was decreased to ~35% for 45 min followed by 7 min airway occlusion to produce asphyxic cardiac arrest in 2-week-old anesthetized piglets (4 kg). Viable neuronal counts were assessed at 6 days of recovery in 6 groups (n=5-9): 1) sham surgery, 2) normothermic recovery, 3) surface cooling to decrease rectal temperature from 38.5 to 34C between 10-120 min 4) transnasal cooling with airflow of 32 L/min from 10-120 min, 5) surface cooling onset delayed until 120 min ROSC, and 6) transnasal cooling delayed by 120 min ROSC. In all 4 cooling groups, hypothermia was sustained at 34C with surface cooling until 20 h ROSC followed by 6-8 h of rewarming. Results: Nasal airflow of 32 L/min decreased brain temperature from 38.3±0.3°C to 33.8±0.6 within 60 min without spatial temperature gradients in these 45-g brains. Surface cooling and transnasal airflow rescued the number of viable neurons in putamen from 38±23% (% of sham viable neurons; ±SD) in the normothermic group to 67±33% and 76±36%, respectively, when initiated at 10 min ROSC, and to 72±30% and 61±25%, respectively, when initiated at 120 min. In sensorimotor cortex, surface cooling and transnasal airflow rescued neurons from 56±36% in the normothermic group to 89±37% and 89±29%, respectively, when initiated at 10 min ROSC, and to 84±19% and 81±28%, respectively, when initiated at 120 min. Conclusions: The use of a high transnasal airflow is as effective as standard surface cooling when initiated at 10 or 120 min after ROSC in protecting vulnerable putamen and sensorimotor cortex from asphyxic cardiac arrest in infant piglets. Because of its simplicity, portability, and low cost, we postulate that transnasal cooling potentially could be deployed in the field by first responders for early initiation of brain cooling prior to maintenance with standard surface cooling after pediatric cardiac arrest.

scholarly journals Brain Cooling: An Economy Mode of Temperature Regulation in Artiodactyls

Physiology ◽  
1998 ◽  
Vol 13 (6) ◽  
pp. 281-286 ◽  
Author(s):  
Claus Jessen
Keyword(s):  
Heat Stress ◽  
Body Temperature ◽  
Heat Loss ◽  
Temperature Regulation ◽  
Thermal Damage ◽  
Brain Temperature ◽  
Brain Cooling ◽  
Selective Brain Cooling ◽  
Free Ranging ◽  
The Brain

Artiodactyls employ selective brain cooling (SBC) regularly during experimental hyperthermia. In free-ranging antelopes, however, SBC often was present when body temperature was low but absent when brain temperature was near 42°C. The primary effect of SBC is to adjust the activity of the heat loss mechanisms to the magnitude of the heat stress rather than to the protection of the brain from thermal damage.

Brain cooling marginally increases maximum thermal tolerance in Atlantic cod

2019 ◽  
Author(s):  
Fredrik Jutfelt ◽  
Dominique G. Roche ◽  
Timothy D Clark ◽  
Tommy Norin ◽  
Sandra A. Binning ◽  
...  
Keyword(s):  
Thermal Effects ◽  
Thermal Tolerance ◽  
Gadus Morhua ◽  
Atlantic Cod ◽  
Brain Temperature ◽  
Brain Cooling ◽  
Local Cooling ◽  
Thermal Limits ◽  
The Difference ◽  
The Brain

ABSTRACTThe physiological mechanisms determining thermal limits in fishes are debated but remain elusive. It has been hypothesised that loss of motor function observed as a loss of equilibrium during an acute thermal challenge is due to direct thermal effects on brain neuronal function. To test this hypothesis, we mounted cooling plates on the head of Atlantic cod(Gadus morhua)and quantified whether local cooling of the brain increased whole-organism critical thermal maxima (CTmax). Brain cooling reduced brain temperature by 2–6°C and increased CTmaxby 0.5–0.7°C relative to instrumented and uninstrumented controls, suggesting that direct thermal effects on brain neurons might contribute to setting upper thermal limits in fish. However, the improvement in CTmaxwith brain cooling was small relative to the difference in brain temperature, demonstrating that other mechanisms (e.g., failure of spinal and peripheral neurons, or muscle) may also contribute to controlling acute thermal tolerance in fishes.Summary statementWe tested whether brain temperature sets the upper thermal limit in a fish. Selectively cooling the brain during whole-organism thermal ramping marginally increased thermal tolerance.

Pathophysiology and causes of cardiac arrest

2016 ◽  
Author(s):  
Peter Thomas Morley
Keyword(s):  
Cardiac Arrest ◽  
Cardiopulmonary Arrest ◽  
The Body ◽  
Biochemical Pathways ◽  
Initial Rhythm ◽  
Underlying Causes ◽  
Children And Young Adults ◽  
The Brain ◽  
Post Cardiac Arrest Syndrome ◽  
Respiratory Causes

Sudden cardiopulmonary arrest (CPA) is still the commonest cause of death globally. CPAs are usually categorized according to where they occur, with out-of-hospital arrests accounting for approximately 75% of CPA deaths and in-hospital the remaining 25%. The arrests are also sub-categorized according to the initial rhythm, with the best outcomes associated with shockable rhythms. Large registries have demonstrated a variable incidence of out-of-hospital CPAs in adults (50–150/100,000 person years), with a range of outcomes (3–16% survival to hospital discharge). The majority of CPAs in adults are due to cardiac causes, but teaching surrounding the management of cardiac arrests now includes an increased focus on the identification and correction of underlying causes, irrespective of the rhythm. While identifying an underlying cause is often challenging, this is probably one of reasons explaining the improved survival seen with in-hospital compared with the out-of-hospital CPA. The incidence of CPAs in children is highest in infants, and decreases with age. The majority of CPAs in children are due to respiratory causes. Cardiac causes in children and young adults include a variety of familial, genetic, and acquired conditions. The pathophysiology of cardiac arrests is also now better understood. A large number of biochemical pathways are activated as a result of the CPA. These result in the post-cardiac arrest syndrome, which affects many systems in the body, but in particular the brain, heart, and kidneys.

scholarly journals Guttural pouches, brain temperature and exercise in horses

2006 ◽  
Vol 2 (3) ◽  
pp. 475-477 ◽  
Author(s):  
Graham Mitchell ◽  
Andrea Fuller ◽  
Shane K Maloney ◽  
Nicola Rump ◽  
Duncan Mitchell
Keyword(s):  
Brain Temperature ◽  
Brain Cooling ◽  
Selective Brain Cooling ◽  
Free Living ◽  
Heat Injury ◽  
Blood Temperature ◽  
Arterial Blood ◽  
Exchange Function ◽  
The Brain ◽  
Arterial Blood Temperature

Selective brain cooling (SBC) is defined as the lowering of brain temperature below arterial blood temperature. Artiodactyls employ a carotid rete, an anatomical heat exchanger, to cool arterial blood shortly before it enters the brain. The survival advantage of this anatomy traditionally is believed to be a protection of brain tissue from heat injury, especially during exercise. Perissodactyls such as horses do not possess a carotid rete, and it has been proposed that their guttural pouches serve the heat-exchange function of the carotid rete by cooling the blood that traverses them, thus protecting the brain from heat injury. We have tested this proposal by measuring brain and carotid artery temperature simultaneously in free-living horses. We found that despite evidence of cranial cooling, brain temperature increased by about 2.5 °C during exercise, and consistently exceeded carotid temperature by 0.2–0.5 °C. We conclude that cerebral blood flow removes heat from the brain by convection, but since SBC does not occur in horses, the guttural pouches are not surrogate carotid retes.

About the Brain, the Face, and Emotion

1984 ◽  
Vol 29 (7) ◽  
pp. 567-568
Author(s):  
Gilles Kirouac
Keyword(s):  
The Face ◽  
The Brain

scholarly journals Time to Be SHY? Some Comments on Sleep and Synaptic Homeostasis

2012 ◽  
Vol 2012 ◽  
pp. 1-12 ◽  
Author(s):  
Giulio Tononi ◽  
Chiara Cirelli
Keyword(s):  
Synaptic Strength ◽  
Universal Function ◽  
Systematic Bias ◽  
Synaptic Homeostasis ◽  
The Face ◽  
Essential Function ◽  
Function Of Sleep ◽  
The Brain

Sleep must serve an essential, universal function, one that offsets the risk of being disconnected from the environment. The synaptic homeostasis hypothesis (SHY) is an attempt to identify this essential function. Its core claim is that sleep is needed to reestablish synaptic homeostasis, which is challenged by the remarkable plasticity of the brain. In other words, sleep is “the price we pay for plasticity.” In this issue, M. G. Frank reviewed several aspects of the hypothesis and raised several issues. The comments below provide a brief summary of the motivations underlying SHY and clarify that SHY is a hypothesis not about specific mechanisms, but about a universal, essential function of sleep. This function is the preservation of synaptic homeostasis in the face of a systematic bias toward a net increase in synaptic strength—a challenge that is posed by learning during adult wake, and by massive synaptogenesis during development.

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