Afterdrop of body temperature during rewarming: an alternative explanation

Afterdrop, the continued fall of deep body temperatures during rewarming after hypothermia, is thought to endanger the heart by further cooling from cold blood presumed to be returning from the periphery. However, afterdrop is not always observed, depending on the circumstances. To explore this phenomenon, mild hypothermia was induced quantitatively with a suit calorimeter, using several patterns of cooling and rewarming. When cooling was rapid and followed immediately by rewarming, there were typical afterdrops in the temperatures measured in the rectum, auditory canal, and esophagus. However, when rewarming was delayed, or when cooling had been slow and prolonged, afterdrop was not seen. Afterdrops were then observed in two physical models that had no circulation: a bag of gelatin and a leg of beef. Central layers continued to give up heat as long as the surrounding layer was cooler. These results, together with recent findings by others that peripheral blood flow is low until afterdrop is complete, make this circulatory explanation of afterdrop improbable. Alternatively, afterdrop can be explained by the way heat moves through a mass of tissue.     

A second postcooling afterdrop: more evidence for a convective mechanism.

An attempt was made to demonstrate the importance of increased perfusion of cold tissue in core temperature afterdrop. Five male subjects were cooled twice in water (8 degrees C) for 53-80 min. They were then rewarmed by one of two methods (shivering thermogenesis or treadmill exercise) for another 40-65 min, after which they entered a warm bath (40 degrees C). Esophageal temperature (Tes) as well as thigh and calf muscle temperatures at three depths (1.5, 3.0, and 4.5 cm) were measured. Cold water immersion was terminated at Tes varying between 33.0 and 34.5 degrees C. For each subject this temperature was similar in both trials. The initial core temperature afterdrop was 58% greater during exercise (mean +/- SE, 0.65 +/- 0.10 degrees C) than shivering (0.41 +/- 0.06 degrees C) (P < 0.005). Within the first 5 min after subjects entered the warm bath the initial rate of rewarming (previously established during shivering or exercise, approximately 0.07 degrees C/min) decreased. The attenuation was 0.088 +/- 0.03 degrees C/min (P < 0.025) after shivering and 0.062 +/- 0.022 degrees C/min (P < 0.025) after exercise. In 4 of 10 trials (2 after shivering and 2 after exercise) a second afterdrop occurred during this period. We suggest that increased perfusion of cold tissue is one probable mechanism responsible for attenuation or reversal of the initial rewarming rate. These results have important implications for treatment of hypothermia victims, even when treatment commences long after removal from cold water.     

Effect of alcohol on thermal balance of man in cold water.

The effects of alcohol on core cooling rates (rectal and tympanic), skin temperatures, and metabolic rate were determined for 10 subjects rendered hypothermic by immersion for 45 min in 10 degrees C water. Experiments were duplicated with and without a 20-min period of exercise at the beginning of cold water immersion. Measurements were continued during rewarming in a hot bath. With blood alcohol concentrations averaging 82 mg 100 mL-1, core cooling rates and changes in skin temperatures were insignificantly different from controls, even if the exercise period was imposed. Alcohol reduced shivering metabolic rate by an overall mean of 13%, insufficient to affect cooling rate. Alcohol had no effect on metabolic rate during exercise. During rewarming by hot bath, the amount of 'afterdrop' and rate of increase in core temperature were unaffected by alcohol. It was concluded that alcohol in a moderate dosage does not influence the rate of progress into hypothermia or subsequent, efficient rewarming. This emphasizes that the high incidence of alcohol involvement in water-related fatalities is due to alcohol potentiation of accidents rather than any direct effects on cold water survival, although very high doses of alcohol leading to unconsciousness would increase rate of progress into hypothermia.     

Mechanism of afterdrop after cold water immersion

It was hypothesized that if afterdrop is a purely conductive phenomenon, the afterdrop during rewarming should proceed initially at a rate equal to the rate of cooling. Eight male subjects were cooled on three occasions in 22 degrees C water and rewarmed once by each of three procedures: spontaneous shivering, inhalation of heated (45 degrees C) and humidified air, and immersion up to the neck in 40 degrees C water. Deep body temperature was recorded at three sites: esophagus, auditory canal, and rectum. During spontaneous and inhalation rewarming, there were no significant differences between the cooling (final 30 min) and afterdrop (initial 10 min) rates as calculated for each deep body temperature site, thus supporting the hypothesis. During rapid rewarming, the afterdrop rate was significantly greater than during the preceding cooling, suggesting a convective component contributing to the increased rate of fall. The rapid reversal of the afterdrop also indicates that a convective component contributes to the rewarming process as well.     

Peripheral blood flow during rewarming from mild hypothermia in humans

During the initial stages of rewarming from hypothermia, there is a continued cooling of the core, or after-drop in temperature, that has been attributed to the return of cold blood due to peripheral vasodilatation, thus causing a further decrease of deep body temperature. To examine this possibility more carefully, subjects were immersed in cold water (17 degrees C), and then rewarmed from a mildly hypothermic state in a warm bath (40 degrees C). Measurements of hand blood flow were made by calorimetry and of forearm, calf, and foot blood flows by straingauge venous occlusion plethysmography at rest (Ta = 22 degrees C) and during rewarming. There was a small increase in skin blood flow during the falling phase of core temperature upon rewarming in the warm bath, but none in foot blood flow upon rewarming at room air, suggesting that skin blood flow seems to contribute to the after-drop, but only minimally. Limb blood flow changes during this phase suggest that a small muscle blood flow could also have contributed to the after-drop. It was concluded that the after-drop of core temperature during rewarming from mild hypothermia does not result from a large vasodilatation in the superficial parts of the periphery, as postulated. The possible contribution of mechanisms of heat conduction, heat convection, and cessation of shivering thermogenesis were discussed.     

Rewarming mice from hypothermia by exposure to 2450-MHz microwave radiation

Twenty- to forty-gram mice cooled to colonic temperatures of 17 to 30 °C were rewarmed to normothermia by exposure to whole-body 2450-MHz microwave radiation. Eighteen of nineteen mice survived rewarming at rates of 0.04 to as high as 0.65 °C/sec. Hot spots from microwaves exposure, as indicated by deep tissue burns, were found at the base of the tail in 12 of 19 animals. The maximum rate of rewarming in these experiments (0.65 °C/s) is much higher than warming rates achieved with external warming techniques such as immersion in warm water (~0.03 °C/s). It is concluded that when care is taken to avoid hot spots, whole-body microwave exposure at resonant wavelengths may be a potential means for rapidly rewarming experimental animals from hypothermia.     

Effect of occluded venous return on core temperature during cold water immersion

Recent studies using inanimate and animal models suggest that the afterdrop observed upon rewarming from hypothermia is based entirely on physical laws of heat flow without involvement of the returning cooled blood from the limbs. During the investigation of thermoregulatory responses to cold water immersion (15 degrees C), blood flow to the limbs (minimized by the effects of hydrostatic pressure and vasoconstriction) was occluded in 17 male subjects (age, 29.0 +/- 3.3 yr). Comparisons of rectal (Tre) and esophageal temperature (Tes) responses were made during the 5 min before occlusion, during the 10-min occlusion period, and for 5 min immediately after the release of the cuffs (postocclusion). In the preocclusion phase, Tre and Tes showed similar cooling rates. The occlusion of blood flow to the extremities significantly arrested the cooling of Tes (P less than 0.05) with little effect on Tre. Upon release of the pressure cuffs, the returning extremity blood flow resulted in an increased rate of cooling, that was three times greater at the esophageal site (-0:149 +/- 0.052 vs. -0.050 +/- 0.026 degrees C.min-1). These results suggest that the cooled peripheral circulation, minimized during cold water immersion, may dramatically affect esophageal temperature and the complete neglect of the circulatory component to the afterdrop phenomenon is not warranted.     

Whole-body temperature gradients under surface,perfusion, and combined surface/perfusion hypothermia

Using various methods of hypothermia and halothane-diethyl ether azeotrope anesthesia whole-body temperature gradients were evaluated in 20 adult mongrel dogs. Simultaneous measurements were taken of brain, rectal, esophageal, pharyngeal, liver, jugular vein, shoulder muscle, thigh muscle, and subcutaneous temperatures during (i) surface, (ii) perfusion (slow and rapid cooling), and (iii) combined surface/perfusion methods of hypothermia. Throughout cooling and rewarming core temperature gradients averaged 1.2 °C and during circulatory arrest core temperatures decreased an average of 0.3 °C under pure surface hypothermia. Animals, thermoregulated by extracorporeal methods only, developed larger core temperature gradients during cooling and a significant increase (average = 3.1 °C) was noted in core temperatures during circulatory arrest. This pattern was particularly pronounced during rapid perfusion cooling. Hypothermia induction by combined surface/perfusion, in contrast to pure perfusion methods, resulted in smaller gradients without remarkable increase in core temperature (average = 1.3 °C) during the arrest period. These findings when correlated with the shorter total operating time and ease of operative management and resuscitation lead us to the conclusion that combined surface/ perfusion hypothermia techniques have certain advantages over either pure surface or pure perfusion techniques alone.     

Influence of skeletal muscle glycogen on passive rewarming after hypothermia

To examine the influence of muscle glycogen on the thermal responses to passive rewarming subsequent to mild hypothermia, eight subjects completed two cold-water immersions (18 degrees C), followed by 75 min of passive rewarming (24 degrees C air, resting in blanket). The experiments followed several days of different exercise-diet regimens eliciting either low (LMG; 141.0 +/- 10.5 mmol.kg.dry wt-1) or normal (NMG; 526.2 +/- 44.2 mmol.kg.dry wt-1) prewarming muscle glycogen levels. Cold-water immersion was performed for 180 min or to a rectal temperature (Tre) of 35.5 degrees C. In four subjects (group A, body fat = 20 +/- 1%), postimmersion Tre was similar to preimmersion Tre for both trials (36.73 +/- 0.18 vs. 37.26 +/- 0.18 degrees C, respectively). Passive rewarming in group A resulted in an increase in Tre of only 0.13 +/- 0.08 degrees C. Conversely, initial rewarming Tre for the other four subjects (group B, body fat = 12 +/- 1%) averaged 35.50 +/- 0.05 degrees C for both trials. Rewarming increased Tre similarly in group B during both LMG (0.76 +/- 0.25 degrees C) and NMG (0.89 +/- 0.13 degrees C). Afterdrop responses, evident only in those individuals whose body core cooled during immersion (group B), were not different between LMG and NMG. These data support the contention that Tre responses during passive rewarming are related to body insulation. Furthermore these results indicate that low muscle glycogen levels do not impair rewarming time nor alter after-drop responses during passive rewarming after mild-to-moderate hypothermia.     

Effectiveness of three field treatments for induced mild (33.0 degrees C) hypothermia

Three field applicable treatments for hypothermia were compared. Subjects were cooled in stirred cold water (8.0 degrees C) to a core temperature (Tco) as low as 33 degrees C and rewarmed in a random order by each of three techniques: shivering, external heat, and treadmill exercise. Tco was monitored with an esophageal thermistor probe at the level of the heart. Treatment effectiveness was determined by calculating the amount of Tco afterdrop, length of afterdrop period, rate of Tco increase, and total recovery time. Rate of Tco increase for exercise (4.9 degrees C/h) was significantly higher (P less than 0.05) than shivering (3.5 degrees C/h) but not external heat (3.7 degrees C/h). Exercise afterdrop amount and afterdrop length values (0.95 degrees C and 24 min, respectively) were significantly higher (P less than 0.05) than both shivering (0.33 degrees C, 15 min) and external heat (0.32 degrees C, 14 min). Therefore, although rate of Tco increase during recovery for exercise was faster than for shivering or external heat, as it was preceded by a greater afterdrop length and amount, total recovery time did not differ among the three treatments.     

Accidental deep hypothermia with cardiac arrest. Prompt complete recovery after rewarming by extracorporeal circulation. Case report

BACKGROUND: Deep accidental hypothermia (core temperature <28 degrees C) is an uncommon medical emergency requiring rapid active core rewarming. Extracorporeal circulation has become the treatment of choice for deep hypothermic patients with cardiac arrest. CASE REPORT: We report on a 30-year-old patient who suffered from deep accidental hypothermia (core temperature 24.8 degrees C) and cardiac arrest by prolonged exposure to a cold urban environment as a consequence of severe ethylalcohol intoxication. The rewarming with the aid of extracorporeal circulation was initiated shortly after his arrival at the hospital. External cardiac massage was maintained until full ECC fl ow was established. The patient was weaned from extracorporeal circulation after 157 min, awaked 4 hours later and consequently extubated within 16 hours after rewarming with no neurological impairment. At 3-week follow-up, the patient was fully re-integrated in his work and personal life. CONCLUSION: This case demonstrates the excellent prognosis of a young victim in the case of deep accidental hypothermia with cardiac arrest, provided that deep hypothermia precedes the cardiac arrest and rewarming by extracorporeal circulation is immediately applied. Simultaneous ethyl alcohol intoxication can be considered a protective factor improving the patient's outcome. Complete recovery was achieved within 24 hours after the accident.     

Treatment of accidental hypothermia: a prospective clinical study.

A 15-year prospective study was carried out of 44 patients with accidental hypothermia (mean age 60 years) admitted to an intensive therapy unit. The lowest core temperature recorded in each patient ranged from 20.0 to 34.3 degrees C. The precipitating factors were poisoning (by drugs, alcohol, or coal gas) in 25 cases and various illnesses in 19. Rewarming was achieved in 42 patients by applying a radiant heat cradle over the torso, and in two patients by mediastinal irrigation with warmed fluids. Twelve patients died, but only two during the period of rewarming. Thus rewarming may be consistently and safely achieved irrespective of the cause of hypothermia, and normal body temperature may be regained as rapidly as is compatible with adequate tissue perfusion and oxygenation. Surface rewarming of the torso is perhaps the simplest technique available, but internal rewarming procedures may be desirable or essential in the presence of, for example, profound hypothermia, severe hypotension, or ventricular fibrillation. Mortality was attributable to underlying factors or disease and not to hypothermia.     

Cardiac arrhythmias during rewarming of patients with accidental hypothermia.

Accidental hypothermia has a high mortality and is associated with cardiac arrhythmias. To determine the incidence of arrhythmias and their importance 22 patients with accidental hypothermia (core temperature less than 35 degrees C) were studied by 12 lead electrocardiography and continuous recording of cardiac rhythm. Although 14 of the patients died (64%), only six died while hypothermic. Prolongation of the Q-T interval and the presence of J waves were related to the severity of the hypothermia. Supraventricular arrhythmias, including atrial fibrillation, were common (nine cases) and benign. Ventricular extrasystoles were also common (10 cases), but ventricular tachycardia or fibrillation did not occur during rewarming. In eight patients who died while being monitored the terminal rhythm was asystole. There was no correlation between the severity of hypothermia or the rate of rewarming and the clinical outcome. In the absence of malignant arrhythmias there is no indication for using prophylactic antiarrhythmic treatment in patients with accidental hypothermia. The presence or absence of severe underlying disease is the main determinant of prognosis.     

Is oxygen supply a limiting factor for survival during rewarming from profound hypothermia?

It has been postulated that unsuccessful resuscitation of victims of accidental hypothermia is caused by insufficient tissue oxygenation. The aim of this study was to test whether inadequate O2 supply and/or malfunctioning O2 extraction occur during rewarming from deep/profound hypothermia of different duration. Three groups of rats (n = 7 each) were used: group 1 served as normothermic control for 5 h; groups 2 and 3 were core cooled to 15 degrees C, kept at 15 degrees C for 1 and 5 h, respectively, and then rewarmed. In both hypothermic groups, cardiac output (CO) decreased spontaneously by > 50% in response to cooling. O2 consumption fell to less than one-third during cooling but recovered completely in both groups during rewarming. During hypothermia, circulating blood volume in both groups was reduced to approximately one-third of baseline, indicating that some vascular beds were critically perfused during hypothermia. CO recovered completely in animals rewarmed after 1 h (group 2) but recovered to only 60% in those rewarmed after 5 h (group 3), whereas blood volume increased to approximately three-fourths of baseline in both groups. Metabolic acidosis was observed only after 5 h of hypothermia (15 degrees C). A significant increase in myocardial tissue heat shock protein 70 after rewarming in group 3, but not in group 2, indicates an association with the duration of hypothermia. Thus mechanisms facilitating O2 extraction function well during deep/profound hypothermia, and, despite low CO, O2 supply was not a limiting factor for survival in the present experiments.     

Efficacy of forced-air and inhalation rewarming by using a human model for severe hypothermia

Goheen, M. S. L., M. B. Ducharme, G. P. Kenny, C. E. Johnston, John Frim, Gerald K. Bristow, and Gordon G. Giesbrecht. Efficacy of forced-air and inhalation rewarming by using a humanmodel for severe hypothermia. J. Appl.Physiol. 83(5): 1635-1640, 1997.We recentlydeveloped a nonshivering human model for severe hypothermia by usingmeperidine to inhibit shivering in mildly hypothermic subjects. Thisthermal model was used to evaluate warming techniques. On threeoccasions, eight subjects were immersed for ~25 min in 9°C water.Meperidine (1.5 mg/kg) was injected before the subjects exited thewater. Subjects were then removed, insulated, and rewarmed in anambient temperature of 20°C with either1) spontaneous rewarming (control),2) inhalation rewarming withsaturated air at ~43°C, or 3)forced-air warming. Additional meperidine (to a maximumcumulative dose of 2.5 mg/kg) was given to maintain shiveringinhibition. The core temperature afterdrop was 30-40% less duringforced-air warming (0.9°C) than during control (1.4°C) andinhalation rewarming (1.2°C) (P < 0.05). Rewarming rate was 6- to 10-fold greater during forced-airwarming (2.40°C/h) than during control (0.41°C/h) andinhalation rewarming (0.23°C/h) (P < 0.05). In nonshivering hypothermic subjects, forced-air warming provided a rewarming advantage, but inhalation rewarming did not.

     

Radio frequency (13.56 MHz) energy enhances recovery from mild hypothermia

The rate of warming after hypothermia depends on the method of rewarming. This study compared the effectiveness of radio frequency (RF) energy against hot (41 degrees C) water immersion (HW) and an insulated cocoon (IC) for rewarming hypothermic men. Six men fasted overnight and were rewarmed for 1 h after attaining a 0.5 degree C reduction in rectal temperature (Tre). Tre and esophageal (Tes) temperature were recorded every 5 min with nonmetallic thermal probes. The base-line value for Tre and Tes just before rewarming was subtracted from each 5 min Tre and Tes during rewarming to give delta Tre and delta Tes. The 12 delta Tes values were averaged for each individual and were compared using analysis of variance. The average delta Tes for RF (1.15 +/- 0.22 degrees C/h) was faster (P less than 0.001) than either IC (0.37 +/- 0.16 degrees C/h) or HW (0.18 +/- 0.09 degree C/h). The present study shows the superiority of RF energy for rewarming mildly hypothermic men.     

Inhibition of shivering increases core temperature afterdrop and attenuates rewarming in hypothermic humans

Giesbrecht, Gordon G., M. S. L. Goheen, C. E. Johnston, G. P. Kenny, Gerald K. Bristow, and John S. Hayward. Inhibition ofshivering increases core temperature afterdrop and attenuates rewarmingin hypothermic humans. J. Appl.Physiol. 83(5): 1630-1634, 1997.During severehypothermia, shivering is absent. To simulate severe hypothermia,shivering in eight mildly hypothermic subjects was inhibited withmeperidine (1.5 mg/kg). Subjects were cooled twice (meperidine andcontrol trials) in 8°C water to a core temperature of 35.9 ± 0.5 (SD) °C, dried, and then placed in sleeping bags. Meperidinecaused a 3.2-fold increase in core temperature afterdrop (1.1 ± 0.6 vs. 0.4 ± 0.2°C), a 4.3-fold increase in afterdrop duration(89.4 ± 31.4 vs. 20.9 ± 5.7 min), and a 37% decrease inrewarming rate (1.2 ± 0.5 vs. 1.9 ± 0.9°C/h).Meperidine inhibited overt shivering. Oxygen consumption, minuteventilation, and heart rate decreased after meperidine injection butsubsequently returned toward preinjection values after 45 minpostimmersion. This was likely due to the increased thermoregulatorydrive with the greater afterdrop and the short half-life ofmeperidine. These results demonstrate the effectiveness of shiveringheat production in attenuating the postcooling afterdrop of coretemperature and potentiating core rewarming. The meperidine protocolmay be valuable for comparing the efficacy of various hypothermiarewarming methods in the absence of shivering.

     

Effects of moderate hypothermia on in situ cardiac sympathetic nerve endings

Although hypothermia is known to alter neuronal control of circulation, it has been uncertain whether clinically used hypothermia (moderate hypothermia) affects in situ cardiac sympathetic nerve endings. We examined the effects of moderate hypothermia on cardiac sympathetic nerve ending function in anesthetized cats. By use of a cardiac dialysis technique, we implanted dialysis probes in the midwall of the left ventricle and monitored dialysate norepinephrine (NE) levels as an index of NE output from cardiac sympathetic nerve endings. Hypothermia (27.0+/-0.5 degrees C) induced decreases in dialysate NE levels. Dialysate NE levels did not return to the control level at normothermia after rewarming. Dialysate NE response to inferior vena cava occlusion was attenuated at hypothermia but restored at normothermia after rewarming. Dialysate NE response to high K(+) (100 mM) was attenuated at hypothermia and was not restored at normothermia after rewarming. Hypothermia induced increases in dialysate dihydroxyphenylglycol (DHPG) levels. There were no differences in desipramine (neuronal NE uptake blocker, 10 microM) induced increment in dialysate NE level among control, hypothermia, and normothermia after rewarming. However, hypothermia induced an increase in DHPG/NE ratio. These data suggest that hypothermia impairs vesicle NE mobilization rather than membrane NE uptake. We conclude that moderate hypothermia suppresses exocytotic NE release via central mediated reflex and regional depolarization.     

Effect of Mild Hypothermia on the Coagulation-Fibrinolysis System and Physiological Anticoagulants after Cardiopulmonary Resuscitation in a Porcine Model

The aim of this study was to evaluate the effect of mild hypothermia on the coagulation-fibrinolysis system and physiological anticoagulants after cardiopulmonary resuscitation (CPR). A total of 20 male Wuzhishan miniature pigs underwent 8 min of untreated ventricular fibrillation and CPR. Of these, 16 were successfully resuscitated and were randomized into the mild hypothermia group (MH, n = 8) or the control normothermia group (CN, n = 8). Mild hypothermia (33°C) was induced intravascularly, and this temperature was maintained for 12 h before pigs were actively rewarmed. The CN group received normothermic post-cardiac arrest (CA) care for 72 h. Four animals were in the sham operation group (SO). Blood samples were taken at baseline, and 0.5, 6, 12, 24, and 72 h after ROSC. Whole-body mild hypothermia impaired blood coagulation during cooling, but attenuated blood coagulation impairment at 72 h after ROSC. Mild hypothermia also increased serum levels of physiological anticoagulants, such as PRO C and AT-III during cooling and after rewarming, decreased EPCR and TFPI levels during cooling but not after rewarming, and inhibited fibrinolysis and platelet activation during cooling and after rewarming. Finally, mild hypothermia did not affect coagulation-fibrinolysis, physiological anticoagulants, or platelet activation during rewarming. Thus, our findings indicate that mild hypothermia exerted an anticoagulant effect during cooling, which may have inhibitory effects on microthrombus formation. Furthermore, mild hypothermia inhibited fibrinolysis and platelet activation during cooling and attenuated blood coagulation impairment after rewarming. Slow rewarming had no obvious adverse effects on blood coagulation.     

Effects of regional body temperature variation during asphyxial cardiac arrest on mortality and brain damage in a rat model

To date, hypothermia has focused on improving rates of resuscitation to increase survival in patients sustaining cardiac arrest (CA). Towards this end, the role of body temperature in neuronal damage or death during CA needs to be determined. However, few studies have investigated the effect of regional temperature variation on survival rate and neurological outcomes. In this study, adult male rats (12 week-old) were used under the following four conditions: (i) whole-body normothermia (37 ± 0.5 °C) plus (+) no asphyxial CA, (ii) whole-body normothermia + CA, (iii) whole-body hypothermia (33 ± 0.5 °C)+CA, (iv) body hypothermia/brain normothermia + CA, and (v) brain hypothermia/body normothermia + CA. The survival rate after resuscitation was significantly elevated in groups exposed to whole-body hypothermia plus CA and body hypothermia/brain normothermia plus CA, but not in groups exposed to whole-body normothermia combined with CA and brain hypothermia/body normothermia plus CA. However, the group exposed to hypothermia/brain normothermia combined with CA exhibited higher neuroprotective effects against asphyxial CA injury, i.e. improved neurological deficit and neuronal death in the hippocampus compared with those involving whole-body normothermia combined with CA. In addition, neurological deficit and neuronal death in the group of rat exposed to brain hypothermia/body normothermia and CA were similar to those in the rats subjected to whole-body normothermia and CA. In brief, only brain hypothermia during CA was not associated with effective survival rate, neurological function or neuronal protection compared with those under body (but not brain) hypothermia during CA. Our present study suggests that regional temperature in patients during CA significantly affects the outcomes associated with survival rate and neurological recovery.