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PubMed1988

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.

Adult↗
PubMed1993

Rewarming, ultraprofound hypothermia and cardiopulmonary bypass.

Rewarming, a key event in resuscitation from accidental, experimental and clinical hypothermia, is sometimes followed by neurologic, cardiac, and respiratory sequelae and may lead to death. The rate of rewarming has been implicated but not quantified as etiologic in these sequelae. Under anesthesia fifteen dogs were cannulated and connected to an extracorporeal circuit for oxygenation, core cooling and rewarming. They were subjected to ultra-profound hypothermia with a core (esophageal) temperature as low as 1.3 degrees C, cardiac arrest, blood substitution, and continuous low flow perfusion. After 2-3 hours of cardiac arrest, rewarming began. Mechanical activity of the heart was seen between 10 degrees and 28 degrees C and respiration resumed at 29 degrees C. The rewarming rates of the 15 dogs were retrospectively studied. They were placed into three categories (G) based on the outcome. G-I (N=2):no neurological complications, G-II (N=8):transient neurological problems, and G-III (N=5):death, mainly from cardiovascular and respiratory complications confirmed at death by autopsy. Heat gain by each animal was recorded as a function of time for all experiments. The time it took each dog to reach 35 degrees C was determined and a mean was calculated (rewarming rate). Normal body temperature for a dog is 37.8 degrees C. Statistical analysis (ANOVA) was performed ex post facto to determine the relationship between rewarming rate and outcome. Our data contradicts the notion that slow core rewarming from nadir to normal temperature offers better outcome.(ABSTRACT TRUNCATED AT 250 WORDS)

Analysis of Variance↗
PubMed1987

[Acral rewarming. I: "Normal data" of a healthy adult population].

The acral rewarming test was investigated in 285 healthy subjects (mean age: 44.1; 20-71) to establish "normal" or reference values as a basis for interpreting patient data. The study was disposed in a manner to look also for possible diurnal and seasonal variations of the rewarming parameters. Healthy controls show a considerable interindividual variability in the speed and the pattern of acral rewarming, with a striking bimodal distribution of the individual values. This variability is mainly due to the factors "season" and "gender", while "age" and "daytime" are more related to basal finger temperature as to the rate of rewarming. According to these findings seasonal variations must necessarily be included in the definition of normal reference values of the rewarming test. In the healthy subjects neither personality characteristics (Freiburger personality inventory) nor the individual's psycho-social situation (Life Event questionnaire) and "depressivity" (Beck inventory) correlate with rewarming parameters. However, momentary "fatigue" (Visual Analogue Scale) correlates negatively and the sum of "somatic complaints" positively with acral rewarming time. The issue of variability in normative data is discussed with reference to clinical applications of the rewarming test in part II.

Adult↗
PubMed1978

Laboratory comparison of technique for rewarming hypothermic casualties.

The efficacy of inhalation, hot bath, piped suit and spontaneous rewarming have been directly compared under controlled conditions. Hot bath rewarming was significantly more effective at raising deep body temperature than the piped suit technique and both were more effective than the other two methods. The effect of inhalation rewarming was not significantly different from that of spontaneous rewarming. All techniques gave rise to afterdrops of core temperature of widely varying degrees and durations. It is concluded that inhalation rewarming should not be employed if it entails a delay in transporting a patient to a facility for rapid external rewarming. Piped suit rewarming is a convenient field alternative to the use of a hot bath and a simple apparatus for carrying this out is described. The sluggish response of rectal temperature to cooling and rewarming in this study suggests that it should not be relied upon as the sole indicator of a patient's thermal state during treatment. Auditory canal temperature is a more valid substitute.

Adolescent↗
PubMed1998

Computer-controlled cardiopulmonary bypass increases jugular venous oxygen saturation during rewarming.

BACKGROUND: Conventional roller pump apulsatile cardiopulmonary bypass (CPB) was compared with computer-controlled pulsatile bypass, which was designed to recreate biological variability (return of beat-to-beat variability in rate and pressure with superimposed respiratory rhythms). The degree of jugular venous oxygen saturation (SjvO2) less than 50% during rewarming from hypothermic CPB was compared for the two bypass techniques. An SjvO2 less than 50% during rewarming from hypothermic CPB is correlated with cognitive dysfunction in humans. METHODS: Pigs were placed on CPB for 3 hours using a membrane oxygenator with alpha-stat acid-base management and arterial filtration. After baseline measurements and normothermic CPB, the animals were randomized to apulsatile CPB (n = 12) or computer-controlled pulsatile CPB (roller pump speed adjusted by an average of 2.9 voltage output modulations/s; n = 12). The animals were then cooled to a nasopharyngeal temperature of 28 degrees C. During rewarming to stable normothermic temperatures, SjvO2 was measured at 5-minute intervals. The mean and cumulative areas for an SjvO2 less than 50% were determined for all animals. RESULTS: No between-group differences in temperature were noted during hypothermic CPB or during rewarming. The rate of rewarming was not different between groups. Mean arterial pressure, partial pressure of oxygen in arterial blood, and partial pressure of carbon dioxide in arterial blood also did not differ between groups. The hemoglobin concentration was within 0.4 g/dL between groups at all time periods. Mean pulse pressure was 10.0 +/- 4.8 mm Hg in the apulsatile CPB group and 20.7 +/- 5.2 mm Hg in the pulsatile CPB group (p = 0.0002; unpaired t test). Markedly greater mean and cumulative areas under the curve for SjvO2 less than 50% were seen with apulsatile CPB (164 +/- 209 versus 1.9 +/- 3.6% x min, p = 0.021; and 1,796 +/- 2,263 versus 23 +/- 45% x min, p = 0.020, respectively). CONCLUSIONS: Computer-controlled pulsatile CPB was associated with significantly greater SjvO2 during rewarming from hypothermic CPB. Both the mean and cumulative areas under the curve for SjvO2 less than 50% exceeded a ratio of 75:1 for apulsatile versus computer-controlled pulsatile CPB. These experiments suggest that cerebral oxygenation was better preserved during rewarming from moderate hypothermia with computer-controlled pulsatile CPB, which returned biologic variability to the flow pattern.

Animals↗
PubMed1999

Forced air surface rewarming in patients with severe accidental hypothermia.

Methods of rewarming patients with severe accidental hypothermia remain controversial. This paper reports our experience with the use of forced air rewarming in patients with severe accidental hypothermia and a body core temperature below 30 degrees C. Fifteen hypothermic patients (body core temperature 24-30 degrees C) were successfully treated with forced air rewarming to a body core temperature above 35 degrees C (mean rewarming rate 1.7 degrees C/h, range from 0.7 to 3.4 degrees C/h). An afterdrop phenomenon was not observed in any of the patients. Nine hypothermic patients (group 1) had no prehospital cardiac arrest, all nine were long-term survivors and made a full recovery. Six patients (group 2) had prehospital cardio circulatory arrest with restoration of spontaneous circulation. None of the group 2 patients survived long-term. Group 1 and group 2 patients did not differ in core temperature (26.6+/-1.6 degrees C group 1 and 27.0+/-1.8 degrees C group 2). Group 2 patients needed catecholamine support during rewarming more frequently (83 versus 22%) and had higher lactate levels and lower pH values at all points of observation. In conclusion our preliminary data indicate that forced air rewarming is an efficient and safe method of managing patients with severe accidental hypothermia. The poor outcome of patients with a history of prehospital cardiopulmonary resuscitation is probably due to irreversible ischaemic brain damage in primarily asphyxiated avalanche and near-drowning victims, rather than the consequence of the rewarming method used.

Adolescent↗
PubMed2002

Comparison of fast versus slow rewarming following acute moderate hypothermia in rats.

BACKGROUND: The aim of this study was to compare the biochemical and physiological responses of fast vs. slow rewarming from moderate hypothermia in anaesthetized rats. METHODS: Anaesthetized rats were surface cooled to 28 degrees C, for 20 min, then rewarmed either quickly over 30 min or slowly over 120 min with monitoring of vital signs, systemic vascular resistance (SVR), cardiac output, biochemical changes and activity for 31 days. RESULTS: At hypothermia, cardiac output decreased to 77 +/- 38 ml x min(-1) and lactate increased to 4.62 +/- 4.73 mmol x l(-)1. Fast rewarming caused an abrupt increase in cardiac output (270 +/- 24 ml x min(-1)) and a sharp drop in SVR (325.6 +/- 23.3 dyne x s(-1) x cm(-5)), compared with a smoother course with cardiac output (142 +/- 18 ml x min(-1), P < 0.01) and SVR (662.8 +/- 41.0 dyne x s(-1) x cm(-5), P < 0.01), measured during slow rewarming. Lactate failed to return to normal values (upon returning to normothermia) (2.5 +/- 0.75 mmol x l(-1)) only in the fast rewarming group. In both groups, activity in the open field was not different from control rats. CONCLUSIONS: In rats, moderate hypothermia for 20 min does not appear to cause lasting biochemical or behavioural consequences, whether rewarming lasted over 30 or 120 min. However, there was a greater early change in cardiac output and heart rate, due to systemic vasodilatation in the fast rewarming animals. These acute changes may have consequences in patients with compromised cardiovascular reserves.

Anesthesia, General↗
PubMed2000

Thermal energy balance as a measure of adequate rewarming from hypothermic cardiopulmonary bypass.

OBJECTIVE: To determine whether the amount of heat (thermal energy) used actively to rewarm patients on cardiopulmonary bypass (CPB) was a better indicator of adequate rewarming from hypothermic CPB than core temperature. DESIGN: Prospective study. SETTING: Single hospital. PARTICIPANTS: Fifty-four sequential patients undergoing hypothermic CPB. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: Thermal energy balance (TEB) (net heat supplied to or removed from the body, from initiation to termination of CPB) was measured using previously validated apparatus. Adequacy of rewarming was assessed by measuring the coldest postoperative core (tympanic membrane) temperature and the time to rewarm postoperatively to a core temperature of 37.0 degrees C. Core temperature on termination of CPB did not correlate with the degree of postoperative hypothermia as judged by time to rewarm postoperatively to 37.0 degrees C (r = 0.14; p = 0.33), but did correlate with coldest postoperative core temperature (r = 0.47; p = 0.0003). TEB correlated better with time to rewarm to 37.0 degrees C (r = 0.43; p = 0.001) and coldest postoperative core temperature (r = 0.58, p = 0.0001). CONCLUSION: TEB is a better predictor than corresponding values of core temperature on termination of CPB in predicting the coldest postoperative temperature and time to rewarm to 37 degrees C.

Adult↗
PubMed2002

The rewarming rate and increased peak temperature alter neurocognitive outcome after cardiac surgery.

UNLABELLED: Neurocognitive dysfunction is a common complication after cardiac surgery. We evaluated in this prospective study the effect of rewarming rate on neurocognitive outcome after hypothermic cardiopulmonary bypass (CPB). After IRB approval and informed consent, 165 coronary artery bypass graft surgery patients were studied. Patients received similar surgical and anesthetic management until rewarming from hypothermic (28 degrees -32 degrees C) CPB. Group 1 (control; n = 100) was warmed in a conventional manner (4 degrees -6 degrees C gradient between nasopharyngeal and CPB perfusate temperature) whereas Group 2 (slow rewarm; n = 65) was warmed at a slower rate, maintaining no more than 2 degrees C difference between nasopharyngeal and CPB perfusate temperature. Neurocognitive function was assessed at baseline and 6 wk after coronary artery bypass graft surgery. Univariable analysis revealed no significant differences between the Control and Slow Rewarming groups in the stroke rate. Multivariable linear regression analysis, examining treatment group, diabetes, baseline cognitive function, and cross-clamp time revealed a significant association between change in cognitive function and rate of rewarming (P = 0.05). IMPLICATIONS: Slower rewarming during cardiopulmonary bypass (CPB) was associated with better cognitive performance at 6 wk. These results suggest that a slower rewarming rate with lower peak temperatures during CPB may be an important factor in the prevention of neurocognitive decline after hypothermic CPB.

Body Temperature↗
PubMed2006

Vascular smooth muscle cell apoptosis induced by "supercooling" and rewarming.

PURPOSE: The underlying mechanisms for the reduction in restenosis caused by cryoplasty for peripheral atherosclerotic lesions are not well understood. Because vascular smooth muscle cells (SMCs) are known to play a critical role in restenosis and neointimal hyperplasia, the aim of this study was to determine SMC survival under conditions of "supercooling" and/or rewarming. MATERIALS AND METHODS: Bovine aortic SMCs were supercooled to -10 degrees C for 0, 60, or 120 seconds with a custom-designed conduction cooling stage and then rewarmed to 37 degrees C in an incubator for 0, 12, or 24 hours. A terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling assay was used to measure the degree of apoptosis. Activation of Akt (ie, protein kinase B), a key signal protein involved in cell survival, was assessed by Western blot analysis. RESULTS: An increase in apoptotic SMCs was observed with increasing supercooling and rewarming time. Akt was significantly activated at only the most severe condition (120 seconds of supercooling and 24 hours of rewarming), which showed a 2.03-fold increase compared with the group without rewarming. CONCLUSIONS: The data suggest that SMC apoptosis occurs with supercooling and rewarming. Protective cell survival mechanisms were activated only late in the rewarming phase. This may partially explain the long-term patency observed with cryoplasty of atherosclerotic peripheral lesions.

Analysis of Variance↗
PubMed2005

Effects of rapid rewarming on cerebral nitric oxide production and cerebral hemodynamics after hypothermia therapy for kainic acid-induced seizures in immature rabbits.

BACKGROUND: The aim of the present study was to investigate whether rapid rewarming after hypothermia therapy during seizures alters the endogenous nitric oxide (NO) production in and around hippocampus, cortical cerebral blood flow (cCBF), and mean arterial blood pressure (MABP) in immature rabbits. METHODS: The hypothermic rabbits (rectal temperatures, 33 degrees C) were given kainic acid (KA; 12 mg/kg, i.v; at 0 min), followed by cooling (33 degrees C) for 60 min (at 60 min), then either rewarming (RW; 33-37 degrees C) was started (KA[+]RW[+] group, n = 7) or cooling was continued (KA[+]RW[-] group, n = 7) for another 60 min (at the end 120 min). In the KA(-)RW(+) group (n = 5), 0.5 mL normal saline was given (at time 0 min), followed by cooling (33 degrees C) for 60 min (at 60 min), then rewarming to 37 degrees C was started with observation for another 60 min (at the end 120 min). NO production in and around hippocampus was continuously measured by an NO-selective electrode, cCBF by laser Doppler flowmetry, cortical electroencephalogram (EEG), rectal and cerebral temperatures, and MABP during the experiment. Comparisons were made of these parameters between the values at 60 min and 120 min after the KA administrations. RESULTS: KA administration induced abnormal discharges in both KA(+)RW(+) and KA(+)RW(-) groups at the same degree. The KA(+)RW(+) group had a significant increase in %NO, and significant decreases in %cCBF and MABP after rapid rewarming, compared with before rewarming. In the KA(+)RW(-) group, there were no significant changes in %NO, %cCBF, and MABP between values at 60 and 120 min. These changes after rapid rewarming in the KA(+)RW(+) group were different from those with only elevation in brain temperature from 33 to 37 degrees C without seizures (KA[-]RW[+] group). CONCLUSIONS: These results suggest that rapid rewarming after hypothermia therapy induces an increase in the NO production in and around hippocampus and the decreases in cCBF and MABP during seizures in immature rabbits.

Animals↗
PubMed2002

Accidental hypothermia and active rewarming: the metabolic and inflammatory changes observed above and below 32 degrees C.

OBJECTIVES: In accidental hypothermia the underlying physiological mechanisms responsible for poor outcome during rewarming through 32 degrees C remain obscure, although possible associations include changes in acid-base balance, divalent cations, and inflammatory markers. This study investigated the metabolic and inflammatory changes that occur during the rewarming of hypothermic patients. METHODS: Eight patients, four men and four women, age 45 to 85 years, admitted with core temperatures <35 degrees C were included in the study. Patients were rewarmed with dry warm blankets and fluid replaced by crystalloid at 40 degrees C. Bloods for pH, ionised calcium (Ca(2+)) and magnesium (Mg(2+)), parathyroid hormone (PTH), interleukin 1 (IL1), interleukin 6 (IL6), tissue necrosis factor alpha (TNFalpha), were collected at presentation, during rewarming, and at 24 hours. RESULTS: Four patients were admitted with mild (32 degrees -35 degrees C) and four with moderate (28 degrees -32 degrees C) hypothermia. Rewarming to 32 degrees C had no significant effect on the presenting acidosis (p=0.1740), although above 32 degrees C pH increased with temperature (p<0.0001). There was a negative correlation between pH and both Ca(2+) (p=0.0005) and Mg(2+) (p=0.0488) below 32 degrees C; above this temperature the relation was significant only for Ca(2+) (p=0.0494). PTH and Ca(2+) correlated positively (p=0.0041) and negatively (p=0.0039) below and above 32 degrees C respectively. There was no relation between IL1 or TNFalpha with Ca(2+) during rewarming, but IL6 and Ca(2+) correlated positively (p=0.0039) and negatively (p=0.0018) when presentation temperature was below and above 32 degrees C respectively. CONCLUSIONS: During rewarming pH remains unchanged until patient temperature approaches 32 degrees C. Ca(2+) and Mg(2+) decline is associated with the pH increase above 32 degrees C. Poor outcome is associated with presentation temperature (<32 degrees C), non-physiological correlation between IL6-PTH-Ca(2+), and age (>or=84 years).

Aged↗
PubMed2004

Epileptiform activity during rewarming from moderate cerebral hypothermia in the near-term fetal sheep.

Moderate hypothermia is consistently neuroprotective after hypoxic-ischemic insults and is the subject of ongoing clinical trials. In pilot studies, we observed rebound seizure activity in one infant during rewarming from a 72-h period of hypothermia. We therefore quantified the development of EEG-defined seizures during rewarming in an experimental paradigm of delayed cooling for cerebral ischemia. Moderate cerebral hypothermia (n=9) or sham cooling (n=13) was initiated 5.5 h after reperfusion from a 30-min period of bilateral carotid occlusion in near-term fetal sheep and continued for 72 h after the insult. During spontaneous rewarming, fetal extradural temperature rose from 32.5 +/- 0.6 degrees C to control levels (39.4 +/- 0.1 degrees C) in 47 +/- 6 min. Carotid blood flow and mean arterial blood pressure increased transiently during rewarming. The cooling group showed a significant increase in electrical seizure events 2, 3, and 5 h after rewarming, maximal at 2 h (2.9 +/- 1.2 versus 0.5 +/- 0.5 events/h; p <0.05). From 6 h after rewarming, there was no significant difference between the groups. Individual seizures were typically short (28.8 +/- 5.8 s versus 29.0 +/- 6.8 s in sham cooled; NS), and of modest amplitude (35.9 +/- 2.8 versus 38.8 +/- 3.4 microV; NS). Neuronal loss in the parasagittal cortex was significantly reduced in the cooled group (51 +/- 9% versus 91 +/- 5%; p <0.002) and was not correlated with rebound epileptiform activity. In conclusion, rapid rewarming after a prolonged interval of therapeutic hypothermia can be associated with a transient increase in epileptiform events but does not seem to have significant adverse implications for neural outcome.

Adult↗
PubMedDate not supplied

Combined use of isoflurane and sodium nitroprusside during active rewarming on cardiopulmonary bypass: a prospective, comparative study.

AIMS: To evaluate and compare the effect of isoflurane, sodium nitroprusside (SNP) and combined use of isoflurane and SNP on body rewarming and haemodynamic stability during active rewarming on cardiopulmonary bypass (CPB). SUBJECTS AND METHODS: In a prospective, randomised study 75 adult patients scheduled for coronary artery bypass grafting (CABG) under CPB were studied in three groups of 25 patients each. During active rewarming, patients of group I received SNP infusion in CPB, group-II received isoflurane through vaporiser in gas circuit of the CPB machine and group III received a combination of isoflurane inhalation (0.2-0.5%) + SNP in low doses (<1mg/kg/min). RESULTS: Mean requirements of SNP to achieve maximum pump flow during rewarming were 1.48 -/+ 0.65 mg/kg/min (range 0.3-3.5 mg/kg/min) in group I and 0.75 -/+ 0.25 mg/kg/min (range 0.2-0.85 mg/kg/min) in group III. Mean isoflurane concentration required to achieve maximum pump flow during rewarming was 0.95 -/+ 0.35% (range 0.2-1.5%) in group II and 0.35 -/+ 0.1 (range 0-0.4%) in group III. The requirements of SNP and isoflurane in group III were significantly less than group I and II (p<0.001). The haemodynamic stability was better in SNP + isoflurane group with significantly lesser requirement of inotropes. Four-scaled assessment for rewarming evaluation failed to show significant statistical difference amongst the groups. CONCLUSIONS: All three drug regimens were equally effective in terms of uniform rewarming of the body on CPB. However, combined use of SNP and isoflurane in low doses provides haemodynamic stability during CPB and is superior to either drug alone.

Adult↗
PubMed2006

Cranial-neck and inhalation rewarming failed to improve recovery from mild hypothermia.

INTRODUCTION: Rewarming from hypothermia in a field setting is a challenge due to the typical lack of significant power or heat source, making the targeted application of available heat critical. The highly vascular area of the head and neck may allow heat to be rapidly transferred to the core via blood circulation. At the same time, the warming of only a small skin surface may minimize the rapid rise in skin temperature proposed to attenuate shivering and endogenous heat production. Therefore, we investigated the efficacy of targeting the head and neck for rewarming from mild hypothermia. METHODS: There were 16 participants (9 men, 24.1 +/- 4.5 yr, 15.5 +/- 3.9% body fat; 6 women, 23.0 +/- 5.4 yr, 20.8 +/- 3.2% body fat) who were cooled in 15 degrees C water until rectal or esophageal temperature reached 35.5 degrees C, whereupon they were removed and provided passive (PASS), cranial-neck (CN), or cranial-neck and inhalation (CNIR) rewarming. Heart rate and skin temperature were also measured. RESULTS: The mean cooling times were PASS=83 min (range: 22-295 min), CN=94 min (range: 28-314 min), CNIR=97 min (range: 22-285 min). No significant differences (p > 0.05) were found for magnitude of after-drop (PASS = 0.33 +/- 0.24 degrees C, CN = 0.31 +/- 0.18 degrees C, CNIR = 0.29 +/- 0.28 degrees C esophageal temperature) and duration of afterdrop (PASS = 15.4 +/- 10.2 min, CN = 13.0 +/- 10.1 min, CNIR = 8.8 +/- 6.9 min). No significant differences (p > 0.05) were found for rewarming rate (PASS = 1.85 +/- 1.33 degrees C x h(-1), CN = 1.45 +/- 1.04 degrees C x h(-1), CNIR = 2.24 +/- 1.51degrees C x h(-1) esophageal temperature). DISCUSSION: In summary, neither cranial-neck nor cranial-neck and inhalation rewarming combined have an advantage in reducing the magnitude and duration of after-drop or increasing the rewarming rate over passive rewarming.

Adult↗
PubMed1995

An evaluation of hand immersion for rewarming individuals cooled by immersion in cold water.

The hypothesis that hypothermic individuals can be actively rewarmed in the field by immersion of the extremities in hot water was investigated. Three techniques for rewarming subjects with lowered deep body temperatures were compared: a) whole body immersion to the neck in water at 40 degrees C; b) immersion of two hands plus forearms only in water at 42 degrees C; and c) passive rewarming. The suggestion that the fall in deep body temperature resulting from immersion to the neck in water at 15 degrees C could be arrested by immersing both arms in water at 42 degrees C was also investigated. Results indicated that immersion to the neck in hot water was clearly the most effective rewarming technique. No significant difference (p > 0.05) was observed in the deep body temperature response during passive rewarming or during immersion of both hands and forearms in water at 42 degrees C. In the later condition some increase in peripheral blood flow to the hands may have occurred and resulted in a heat input of approximately 12 W, but any benefit from this was negated by an associated significant decrease (p > 0.05) in intrinsic heat production. Immersing the arms in hot water during immersion to the neck in cold water appeared to accelerate rather than decelerate the rate of fall of deep body temperature. We concluded that hand rewarming, although theoretically attractive, is ineffective in practice and could be detrimental in some circumstances, by suppressing intrinsic heat production or precipitating rewarming collapse.

Adult↗
PubMed1980

Effects of circulatory arrest and rewarming on regional blood flow during surface-induced hypothermia.

Regional blood flow and distribution of cardiac output (CO) were evaluated by the radioactive microsphere technique in rhesus monkeys during surface rewarming following the induction of deep hypothermia (20 degrees C.) under deep ether anesthesia. A comparison of animals subjected to 30 minutes of circulatory arrest and those not arrested revealed cerebral, coronary, and renal vascular resistance and flow patterns consistent with a hyperemic response to circulatory arrest at 20 degrees C. Throughout rewarming cerebral and coronary absolute flows tended to be at or above the flows noted at comparable cooling temperatures in a previous study. Renal flow fraction (% Qt) were well preserved during rewarming to 30 degrees C., but a decrease was observed thereafter. Carcass (muscle, skin, bone) %Qt was also reduced following rewarming, especially in arrested animals. CO appeared to be similar to those noted at comparable cooling temperatures until 30 degrees C. during rewarming; thereafter, CO did not fully recover to awake control levels. These data suggest that regional flow is redistributed from the carcass and renal circulations to cerebral and coronary circulations in response to hemodynamic alterations during surface rewarming. It was concluded that autoregulative responses to both circulatory arrest and hemodynamic factors are elicited during surface rewarming from deep hypothermia to 20 degrees C. with the method described.

Animals↗
PubMed2003

Involvement of the mitochondrial pathway in cold storage and rewarming-associated apoptosis of human renal proximal tubular cells.

The cellular and molecular mechanisms of cold storage-ATN are not well characterized. In our earlier studies, cold storage caused necrosis of human proximal tubular epithelial (RPTE) cells, whereas apoptosis was prominent during rewarming. An intriguing finding was the pronounced swelling of the mitochondria in the cold, which promoted us to further characterize its role in rewarming-associated apoptosis. Human proximal tubular epithelial cells were cold stored in University of Wisconsin (UW) solution for 48 h followed by 24 h of rewarming in regular cell culture medium. During the cold storage, there was no significant change in the Bcl-2 to Bax protein ratio, mitochondrial location of cytochrome C or caspse-3 activity. However, during rewarming, the Bcl-2 to Bax ratio increased, cytochrome C was translocated to cytosol, and caspase-3 was activated: events and timing were consistent with the occurrence of apoptosis during rewarming. In a time-course experiment, mitochondrial swelling was discernable by electron microscopy as early as at 2 h. Cold storage of isolated-mitochondria for 2 h was attended by an increase in the opening of the permeability transition pores (PTP), suggesting PTP opening as an early mechanism for mitochondrial swelling. Addition of antioxidants (deferoxamine or 2-methyaminochroman) to the storage solution suppressed mitochondrial pore opening and swelling, Bcl-2 to Bax ratio increase, cytochrome C translocation, caspase-3 activation as well as rewarming-induced apoptosis. Our data demonstrate for the first time that apoptosis following cold storage and rewarming of human renal tubular cells is accompanied by specific mitochondrial events, and that these events and apoptosis can be suppressed by adding antioxidants to the cold storage solution.

Apoptosis↗