Integration of jugular venous return and circle of Willis in a theoretical human model of selective brain cooling

2007 ◽  
Vol 103 (5) ◽  
pp. 1837-1847 ◽  
Author(s):  
Matthew A. Neimark ◽  
Angelos-Aristeidis Konstas ◽  
Andrew F. Laine ◽  
John Pile-Spellman

A three-dimensional mathematical model was developed to examine the induction of selective brain cooling (SBC) in the human brain by intracarotid cold (2.8°C) saline infusion (ICSI) at 30 ml/min. The Pennes bioheat equation was used to propagate brain temperature. The effect of cooled jugular venous return was investigated, along with the effect of the circle of Willis (CoW) on the intracerebral temperature distribution. The complete CoW, missing A1 variant (mA1), and fetal P1 variant (fP1) were simulated. ICSI induced moderate hypothermia (defined as 32–34°C) in the internal carotid artery (ICA) territory within 5 min. Incorporation of the complete CoW resulted in a similar level of hypothermia in the ICA territory. In addition, the anterior communicating artery and ipsilateral posterior communicating artery distributed cool blood to the contralateral anterior and ipsilateral posterior territories, respectively, imparting mild hypothermia (35 and 35.5°C respectively). The mA1 and fP1 variants allowed for sufficient cooling of the middle cerebral territory (30–32°C). The simulations suggest that ICSI is feasible and may be the fastest method of inducing hypothermia. Moreover, the effect of convective heat transfer via the complete CoW and its variants underlies the important role of CoW anatomy in intracerebral temperature distributions during SBC.

2001 ◽  
Vol 281 (1) ◽  
pp. R108-R114 ◽  
Author(s):  
Shane K. Maloney ◽  
Andrea Fuller ◽  
Graham Mitchell ◽  
Duncan Mitchell

Selective brain cooling (SBC) is defined as a brain temperature cooler than the temperature of arterial blood from the trunk. Surrogate measures of arterial blood temperature have been used in many published studies on SBC. The use of a surrogate for arterial blood temperature has the potential to confound proper identification of SBC. We have measured brain, carotid blood, and rectal temperatures in conscious sheep exposed to 40, 22, and 5°C. Rectal temperature was consistently higher than arterial blood temperature. Brain temperature was consistently cooler than rectal temperature during all exposures. Brain temperature only fell below carotid blood temperature during the final few hours of 40°C exposure and not at all during the 5°C exposure. Consequently, using rectal temperature as a surrogate for arterial blood temperature does not provide a reliable indication of the status of the SBC effector. We also show that rapid suppression of SBC can result if the animals are disturbed.


2014 ◽  
Vol 34 (5) ◽  
pp. 743-752 ◽  
Author(s):  
Elga Esposito ◽  
Matthias Ebner ◽  
Ulf Ziemann ◽  
Sven Poli

Hypothermia is a promising therapeutic option for stroke patients and an established neuroprotective treatment for global cerebral ischemia after cardiac arrest. While whole body cooling is a feasible approach in intubated and sedated patients, its application in awake stroke patients is limited by severe side effects: Strong shivering rewarms the body and potentially worsens ischemic conditions because of increased O2 consumption. Drugs used for shivering control frequently cause sedation that increases the risk of aspiration and pneumonia. Selective brain cooling by intraarterial cold infusions (IACIs) has been proposed as an alternative strategy for patients suffering from acute ischemic stroke. Preclinical studies and early clinical experience indicate that IACI induce a highly selective brain temperature decrease within minutes and reach targeted hypothermia 10 to 30 times faster than conventional cooling methods. At the same time, body core temperature remains largely unaffected, thus systemic side effects are potentially diminished. This review critically discusses the limitations and side effects of current cooling techniques for neuroprotection from ischemic brain damage and summarizes the available evidence regarding advantages and potential risks of IACI.


2007 ◽  
Vol 293 (1) ◽  
pp. R438-R446 ◽  
Author(s):  
Andrea Fuller ◽  
Leith C. R. Meyer ◽  
Duncan Mitchell ◽  
Shane K. Maloney

By cooling the hypothalamus during hyperthermia, selective brain cooling reduces the drive on evaporative heat loss effectors, in so doing saving body water. To investigate whether selective brain cooling was increased in dehydrated sheep, we measured brain and carotid arterial blood temperatures at 5-min intervals in nine female Dorper sheep (41 ± 3 kg, means ± SD). The animals, housed in a climatic chamber at 23°C, were exposed for nine days to a cyclic protocol with daytime heat (40°C for 6 h). Drinking water was removed on the 3rd day and returned 5 days later. After 4 days of water deprivation, sheep had lost 16 ± 4% of body mass, and plasma osmolality had increased from 290 ± 8 to 323 ± 9 mmol/kg ( P < 0.0001). Although carotid blood temperature increased during heat exposure to similar levels during euhydration and dehydration, selective brain cooling was significantly greater in dehydration (0.38 ± 0.18°C) than in euhydration (−0.05 ± 0.14°C, P = 0.0008). The threshold temperature for selective brain cooling was not significantly different during euhydration (39.27°C) and dehydration (39.14°C, P = 0.62). However, the mean slope of lines of regression of brain temperature on carotid blood temperature above the threshold was significantly lower in dehydrated animals (0.40 ± 0.31) than in euhydrated animals (0.87 ± 0.11, P = 0.003). Return of drinking water at 39°C led to rapid cessation of selective brain cooling, and brain temperature exceeded carotid blood temperature throughout heat exposure on the following day. We conclude that for any given carotid blood temperature, dehydrated sheep exposed to heat exhibit selective brain cooling up to threefold greater than that when euhydrated.


2003 ◽  
Vol 99 (1) ◽  
pp. 47-51 ◽  
Author(s):  
Tadahiko Shiozaki ◽  
Yoshikazu Nakajima ◽  
Mamoru Taneda ◽  
Osamu Tasaki ◽  
Yoshiaki Inoue ◽  
...  

Object. This study was performed to determine whether moderate hypothermia (31°C) improves clinical outcome in severely head injured patients whose intracranial hypertension cannot be controlled using mild hypothermia (34°C). Methods. Twenty-two consecutive severely head injured patients who fulfilled the following criteria were included in this study: an intracranial pressure (ICP) that remained higher than 40 mm Hg despite the use of mild hypothermia combined with conventional therapies; and a Glasgow Coma Scale score of 8 or less on admission. After the failure of mild hypothermia in combination with conventional therapies; patients were exposed to moderate hypothermia as quickly as possible. As brain temperature was reduced from 34 to 31°C, the volume of intravenous fluid infusion was increased significantly from 1.9 ± 0.9 to 2.6 ± 1.2 mg/kg/hr (p < 0.01), and the dose of dopamine infusion increased significantly from 4.3 ± 3.1 to 8.2 ± 4.4 µg/kg/min (p < 0.01). Nevertheless, mean arterial blood pressure and heart rate decreased significantly from 97.1 ± 13.1 to 85.1 ± 10.5 mm Hg (p < 0.01) and from 92.2 ± 13.8 to 72.2 ± 14.3 beats/minute at (p < 0.01) at 34 and 31°C, respectively. Arterial base excess was significantly aggravated from −3.3 ± 4 at 34°C to −5.6 ± 5.4 mEq/L (at 31°C; p < 0.05). Likewise, serum potassium concentration, white blood cell counts, and platelet counts at 31°C decreased significantly compared with those at 34°C (p < 0.01). In 19 (86%) of 22 patients, elevation of ICP could not be prevented using moderate hypothermia. In the remaining three patients, ICP was maintained below 40 mm Hg by inducing moderate hypothermia; however, these three patients died of multiple organ failure. These results clearly indicate that moderate hypothermia induces complications more severe than those induced by mild hypothermia without improving outcomes. Conclusions. The authors concluded that moderate hypothermia is not effective in improving clinical outcomes in severely head injured patients whose ICP remains higher than 40 mm Hg after treatment with mild hypothermia combined with conventional therapies.


1979 ◽  
Vol 46 (5) ◽  
pp. 905-907 ◽  
Author(s):  
M. Caputa ◽  
M. Cabanac

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.


2019 ◽  
Vol 3 (1) ◽  
pp. 1 ◽  
Author(s):  
Mohammad Fazel Bakhsheshi ◽  
Marjorie Ho ◽  
Lynn Keenliside ◽  
Ting-Yim Lee

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.


Physiology ◽  
1998 ◽  
Vol 13 (6) ◽  
pp. 281-286 ◽  
Author(s):  
Claus Jessen

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.


1994 ◽  
Vol 267 (6) ◽  
pp. R1528-R1536 ◽  
Author(s):  
C. Jessen ◽  
H. P. Laburn ◽  
M. H. Knight ◽  
G. Kuhnen ◽  
K. Goelst ◽  
...  

Using miniature data loggers, we measured the temperatures of carotid blood and brain in four wildebeest (Connochaetes gnou) every 2 min for 3 wk and every 5 min, in two of the animals, for a further 6 wk. The animals ranged freely in their natural habitat, in which there was no shelter. They were subject to intense radiant heat (maximum approximately 1,000 W/m2) during the day. Arterial blood temperature showed a circadian rhythm with low amplitude (< 1 degree C) and peaked in early evening. Brain temperature was usually within 0.2 degrees C of arterial blood temperature. Above a threshold between 38.8 and 39.2 degrees C, brain temperature tended to plateau so that the animals exhibited selective brain cooling. However, selective brain cooling sometimes was absent even when blood temperature was high and present when it was low. During helicopter chases, selective brain cooling was absent, even though brain temperature was near 42 degrees C. We believe that selective brain cooling is controlled by brain temperature but is modulated by sympathetic nervous system status. In particular, selective brain cooling may be abolished by high sympathetic activity even at high brain temperatures.


1993 ◽  
Vol 265 (3) ◽  
pp. H824-H827 ◽  
Author(s):  
J. W. Kuluz ◽  
R. Prado ◽  
J. Chang ◽  
M. D. Ginsberg ◽  
C. L. Schleien ◽  
...  

To evaluate the effect of selective brain cooling on cortical cerebral blood flow, we reduced brain temperature in nitrous oxide anesthetized adult rats using a high speed fan while keeping rectal temperature at 37-38 degrees C. During selective brain cooling, cortical cerebral blood flow, as measured by laser-Doppler flowmetry, increased to 215 +/- 26% (mean +/- SE) of baseline at a cortical brain temperature of 30.9 +/- 0.5 degrees C and a rectal temperature of 37.5 +/- 0.1 degrees C. During rewarming, as brain temperature increased, cortical cerebral blood flow decreased. The cerebral vasodilatory response to hypothermia may explain its protective effects during and after cerebral ischemia.


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