Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Rewarming”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 163 records · Page 9Linked to original sources
PubMed1979

An improved method for inducing hypothermia and rewarming.

A hypothermia and rewarming system combining body surface and ventilatory heat exchange is described. The method utilizes body surface heat exchange through conduction, convection, and black body radiation, and ventilatory heat exchange across the lung surface through conduction, convection, and water evaporation. The system consisted of a chamber in which the temperature was maintained at a desired level (+/- 2.5 degrees C) using a refrigeration-heat pump unit. Chamber temperatures during cooling and rewarming were -15.5 +/- 2.7 degrees C and 43.2 +/- 2.3 degrees C, respectively. Inhalate temperatures during cooling were -8.2 +/- 6.5 degrees C and during rewarming they were 41.5 +/- 0.3 degrees C. Helium (100%) was supplied to the chamber, while the animal was ventilated with 20% O2 + 80% He. Under these conditions, the cooling and rewarming rates were 0.33 +/- 0.06 degrees C/min and 0.20 +/- 0.04 degrees C/min, respectively, at 38--21 degrees C. The system provided for rapid cooling and rewarming with no evidence of any untoward effects.

Animals↗
PubMed1983

A review of the literature concerning resuscitation from hypothermia: Part II--Selected rewarming protocols.

In Part I of this paper, a description of the problems confronted in resuscitation from immersion hypothermia was presented and the debate between passive and active rewarming approaches was summarized. In this paper, a review of the literature concerning selected specific rewarming protocols is given. The protocols considered are: peritoneal irrigation, gastrointestinal rewarming, extracorporeal blood rewarming, airway rewarming, and diathermy.

Animals↗
PubMed1978

Effect of rewarming at various water bath temperatures in experimental frostbite.

Studies have been conducted on 72 rats to determine the most suitable temperature at which rapid rewarming should be done as an immediate treatment for frostbite. Animals were put in a harness containing arrangements for warming the body. Their hind limbs were left out of the harness. They were then exposed to -15 degrees +/- 1 degrees C in a deep freeze for 60 min, during which paw temperature was recorded every 5 min. After this, the animals were taken out, the left hind limb was rapidly rewarmed in a water bath maintained at 35 degrees, 37 degrees, 39 degrees, 41 degrees, 43 degrees, or 45 degrees C for different batches and the right hind limb was left free for slow rewarming at room temperature (27 degrees -29 degrees C). The severity of cold injury in the two limbs was compared. The paw temperature showed a drop on cold exposure, followed by a rapid rise and then a second fall. The degree of injury was related to the duration of exposure after the rise in the paw temperature. The rapid rewarming was effective only at water bath temperature of 37 degrees-39 degrees C and was harmful at 45 degrees C. This shows that rewarming at about body temperature is most effective as immediate treatment for frostbite.

Animals↗
PubMed1983

Regional differences in body temperature in hypothermic and rewarmed young calves.

One- to 7-day-old Holstein bull calves were anesthetized and cold-stressed until their core body temperature (CBT; colonic) was lowered by 10 C. The calves were then rewarmed in warm water, by heat pads or heat lamps, or allowed to recover naturally (unassisted). Temperatures of peripheral tissues, muscles, and the body core were recorded. The time required to lower the CBT of the cold-stressed calves was 168 +/- 11.7 minutes (mean +/- SE). Cold exposure caused a linear decrease in blood, colonic, rectal, and oral temperatures, whereas temperature decreases in the thigh and pectoral muscles, dorsal and ventral thoracic regions, and the hock joint region were generally of greater magnitude and were curvilinear in pattern. By the time the CBT had decreased 1 C, tissue temperatures during cooling were less than (P less than 0.01) the respective temperatures obtained before cooling. The mean time required to rewarm the calves in warm water (47.1 +/- 3.5 minutes) was less than (P less than 0.05) that for the other rewarming methods. The mean rewarming times for the heat pad (128 +/- 12.8) and heat lamp (125.4 +/- 10.9) methods were greater than (P less than 0.05) that for the warm water method, but less than (P less than 0.05) that for the unassisted calves (190.7 +/- 23.1). In general, there was a linear increase in most of the tissue temperatures during recovery although temperatures in the hock joint region were variable. Temperature differences were observed between the thigh and pectoral muscles and between subcutaneous tissues during cooling and recovery. There was poor correlation between the ages of the calves and the time required to decrease their CBT during cooling and also the time required to increase their CBT, regardless of the rewarming method used.

Animals↗
PubMed1983

Cardiovascular and shivering responses in hypothermic and rewarmed young calves.

Aortic blood pressure, ECG, electromyogram, and heart rate were recorded in cold-stressed and rewarmed young Holstein bull calves. The calves were anesthetized and then cold-stressed by immersion in cold water until their core body temperature (colonic) was lowered 10 C. Hypothermia was continued for 1 additional hour and then the calves were rewarmed by 3 external rewarming methods or were allowed to recover naturally (unassisted). Aortic blood pressure began to decrease in cold-stressed calves by the time their core body temperature had decreased 2 C and continued to decrease during cooling. Heart rate initially increased then decreased with cooling. Blunting of the systolic blood pressure peaks and appearance of extraneous waveforms that obscured the normal component waveforms of the ECG complex were also observed during cooling. Aortic blood pressure and heart rate of cold-stressed calves increased soon after the start of recovery and eventually returned to base line even though the rate of recovery varied depending on the method of rewarming. The component waveforms of the ECG complex became more discernible as rewarming of the cold-stressed calves progressed.

Animals↗
PubMed1980

Accidental hypothermia: the effect of initial body temperatures and physique on the rate of rewarming.

After cooling in sea water, 14 subjects having varied core temperatures were rewarmed by inhalation of saturated air at 44 degrees C. Multiple linear regression analyses were computed for best possible subsets relating rectal and tympanic rewarming rates, phi i (i = R, T), to physiological and anthropometric measures. It was found that there was a good correlation between phi i and metabolic or ventilatory rates (0.61 less than r less than 0.74). Rewarming rates phi i could be more closely predicted by a combination of initial core temperatures and (height/weight)0.5 or by a combination of initial core temperatures and initial skin temperatures (0.75 less than r less than 0.88). The effectiveness of inhalation rewarming has been challenged and experimental studies appear contradictory. It is shown that the different inhalation rewarming rates measured are predictable and can be explained largely in physiological terms.

Adolescent↗
PubMed1998

Use of leukocyte depletion to decrease injury after lung preservation and rewarming ischemia: an experimental model.

BACKGROUND: Hypothermia is critical for proper lung preservation. Ideally, the lungs should be maintained at the optimal preservation temperature during the entire ischemic interval. Lung rewarming during implantation is commonly observed. This study was undertaken to investigate the severity of rewarming ischemia on preservation injury and the possibility of minimizing this by use of leukocyte depletion during initial reperfusion. METHODS: Four experimental groups were tested as follows: neonatal piglet heart-lung blocks were either (1) placed on an isolated, blood-perfused, working heart-lung circuit without intervening ischemia (control, n = 6), (2) reperfused on the circuit with whole blood (WB, n = 6) after 13 hours of preservation, (3) reperfused with WB after 12 hours of preservation and 1 hour of rewarming (RWB, n = 5), or (4) reperfused with leukocyte-depleted blood for an initial 10 minutes followed by WB, after 12 hours of preservation and 1 hour of rewarming (n = 6). All groups were studied for 4 hours. RESULTS: The partial pressure of arterial oxygen and lung compliance were significantly lower in the RWB group than in controls (113.8+/-33.1 vs 417.3+/-6.2 mm Hg, p < 0.01; and 0.8+/-0.2 vs 2.9+/-0.4 ml/cm H2O, p < 0.05, respectively). Pulmonary vascular resistance and lung wet/dry weight ratios were significantly higher in the RWB group than in controls (15884.1+/-11354.8 vs 6108.3+/-1309.9 dyne x sec x cm[-5], p < 0.05; and 7.13+/-0.24 vs 5.82+/-0.35, p < 0.05, respectively). The WB and leukocyte-depleted groups did not differ significantly from controls for any measured parameter. CONCLUSIONS: This model confirms that rewarming ischemia during lung implantation exacerbates reperfusion injury. Leukocyte-depleted reperfusion as tested for a short period of time (10 minutes) ameliorates this injury and therefore should be considered for clinical lung transplantation.

Animals↗
PubMed2006

Rewarming following accidental hypothermia in patients with acute subdural hematoma: case report.

A 57-year-old man was admitted to the Emergency and Critical Care Department with accidental hypothermia (31.5 degrees C) after resuscitation from cardiopulmonary arrest (CPA). Brain CT revealed an acute subdural hematoma. Active core rewarming to 33 degrees C was performed using an intravenous infusion of warm crystalloid. The patient underwent craniotomy soon after admission, with bladder temperature maintained at 33 to 34 degrees C throughout the surgery. Therapeutic hypothermia (34 degrees C) was continued for 2 days, followed by gradual rewarming. After rehabilitation, the patient was able to continue daily life with assistance. Traumatic brain injury (TBI) following CPA is associated with extremely unfavorable outcomes. Very few patients with acute subdural hematomas presenting with accidental hypothermia and CPA have been reported to recover. No suitable strategies have been clearly established for the rewarming performed following accidental hypothermia in patients with TBI. Our experience with this patient suggests that therapeutic hypothermia might improve the outcome in some patients with severe brain injury. It also appears that the method used for rewarming might play an important role in the therapy for TBI with accidental hypothermia.

Hematoma, Subdural, Acute↗
PubMed2004

Apoptosis vs. necrosis: glutathione-mediated cell death during rewarming of rat hepatocytes.

Hypothermia induces injury in its own right, but the mechanisms involved in the cell damage are still unclear. The aim of this study was to test the effects that glutathione (GSH) depletion induces on cell death in isolated rat hepatocytes, kept at 4 degrees C for 20 h, by modulating intracellular GSH concentration with diethylmaleate and buthionine sulfoximine (DEM and BSO). Untreated hepatocytes showed Annexin V stained cells (AnxV(+)), scarce propidium iodide stained cells (PI(+)) and presented a low level of lactate dehydrogenase (LDH) leakage after 20 h at 4 degrees C and rewarming at 37 degrees C. When DEM and BSO were added before cold storage, we observed a few AnXV(+) cells and an increase in PI(+) cells associated with LDH release in the incubation medium. Conversely, the addition of DEM and BSO only during rewarming caused a marked increase in cell death by apoptosis. Production of reactive oxygen species (ROS) and thiobarbituric acid species (TBARS), associated with a decrease in GSH concentrations, was higher when DEM and BSO were added before cold storage. Cells treated with DEM and BSO before cold storage showed lower ATP energy stores than hepatocytes treated with DEM and BSO only during rewarming. Pretreatment of hepatocytes with deferoxamine protected against apoptotic and necrotic morphology in conditions of GSH depletion. These results suggest that pretreatment of hepatocytes with DEM and BSO before cold storage induces necrosis, while the treatment of hepatocytes only during rewarming increases apoptosis. In both conditions, iron represents a crucial mediator of cell death.

Analysis of Variance↗
PubMed1997

Comparison of three rewarming methods in a postanesthesia care unit.

Postoperative hypothermia is problematic because patients in postanesthesia care units (PACUs) often feel very cold, and unrecognized or prolonged postoperative hypothermia can aggravate patients' underlying cardiovascular disorders. The researchers compared three methods of rewarming PACU patients who had undergone laparotomy procedures. Patients were assigned randomly to three groups. Each patient in group one received the standard PACU rewarming intervention (ie, two warmed thermal blankets and a hospital bedspread). Each patient in group two received the standard PACU rewarming intervention plus a reflective blanket. Each patient in group three received the standard PACU rewarming intervention plus a reflective blanket and a reflective head covering. Nurses measured patients' vital signs on admission to the PACU and every 15 minutes thereafter until patients' sublingual temperatures reached 36 degrees C (96.8 degrees F). No significant temperature differences occurred among patients in the three groups, but an inverse relationship existed between patients' PACU admission temperatures and the time they required to reach normothermia.

Adult↗
PubMed1996

Forced air speeds rewarming in accidental hypothermia.

STUDY OBJECTIVE: To compare the rates of rewarming of forced-air and passive insulation as a treatment for accidental hypothermia. METHODS: We carried out a prospective, randomized clinical trial in two urban, university-affiliated emergency departments. Our subjects were 16 adult hypothermia victims with core temperatures less than 32 degrees C. A convective cover inflated with air at about 43 degrees C (forced-air group) or cotton blankets (control group) were applied until the patient's core temperature reached 35 degrees C. Members of both groups were given IV fluids warmed to 38 degrees C and warmed, humidified oxygen at 40 degrees C by inhalation. RESULTS: The mean +/- SD initial temperature was 28.8 degrees +/- 2.5 degrees C (range, 25.5 degrees C to 31.9 degrees C) in the patients who underwent forced-air rewarming and 29.8 degrees +/- 1.5 degrees C (range, 28.2 degrees C to 31.9 degrees C) in those given blankets. Core temperature increased about 1 degree C/hour faster in patients treated with forced-air rewarming (about 2.4 degrees C/hour) than in patients given only cotton blankets (about 1.4 degrees C/hour, P = .01). Core-temperature afterdrop was detected in neither group. CONCLUSION: Forced air accelerated the rate of rewarming without producing apparent complications in hypothermic patients.

Adult↗
PubMed1998

The physiological response to norepinephrine during hypothermia and rewarming.

Our purpose was to determine if core hypothermia influences physiological responses to norepinephrine (NE); and if rewarming reverses these effects. Animals were instrumented to measure mean arterial pressure (MAP) and cardiac output (CO). Core temperature was manipulated from 37.5 degrees C (normothermia), to 30 degrees C (hypothermia) and the back to 37.5 degrees C (rewarming) using an external arterial-venous femoral shunt. At each of these temperatures, baseline CO and MAP were measured. Norepinephrine (NE) was infused at rates to deliver 0.2, 1.0, or 5 microg kg(-1) per h. At each dose CO and MAP was measured again. Systemic vascular resistance (SVR) was calculated using the formula (SVR = (MAP/CO) x 80). Eight animals underwent all three phases of the protocol. The response to NE during normothermia was a significant increase in MAP to doses of 1 microg kg(-1) per min (P < 0.01) and 5 microg kg(-1) per min (P < 0.01) and SVR to doses of 1 microg kg(-1) per min (P < 0.01) and 5 microg kg(-1) per min (P < 0.01). The response to NE during hypothermia was a significant increase in MAP only at doses of 1 microg kg(-1) per min (P = 0.03) and 5 microg kg(-1) per min (P = 0.01). The response to NE after rewarming was a significant increase in MAP only at a dose of 5 microg kg(-1) per min (P = 0.03). This study shows that core hypothermia causes a change in physiological response to NE that rewarming does not reverse.

Adrenergic alpha-Agonists↗
PubMed2000

Prolonged rewarming time during allograft implantation predisposes to recurrent hepatitis C infection after liver transplantation.

The majority of patients undergoing orthotopic liver transplantation (OLT) have end-stage liver disease secondary to hepatitis C virus (HCV) infection. Although OLT does not cure the disease and recurrent virus is present in all patients, relatively few patients with recurrent viremia develop clinical disease. When the disease recurs, however, the results can be devastating. Factors associated with increased risk for recurrent HCV disease remain controversial. We hypothesized that preservation injury may predispose to the severity of HCV disease after OLT. We reviewed our series of OLTs performed for HCV cirrhosis between January 1994 and December 1998 (n = 56; 62 transplants). Patients were grouped according to the severity of recurrent hepatitis C. Group 1 had no or mild HCV disease (n = 36), and group 2 had moderate to severe HCV disease (n = 20). The duration of ischemic rewarming during graft implantation was significantly associated with the severity of recurrent hepatitis C (P <.04). The estimated chances of severe disease within the first year post-OLT after 30, 60, or 90 minutes of ischemic rewarming time were 19%, 40%, and 65%, respectively. Cold ischemia time, transaminase levels, and prothrombin time did not correlate with the severity of hepatitis C. In conclusion, our data suggest that the duration of ischemic rewarming predisposes to severe recurrent hepatitis C. This finding warrants the investigation of the pathogenesis of recurrent HCV disease after ischemic injury. Reduction of rewarming time should be stressed in OLT, particularly in patients with HCV cirrhosis.

Adolescent↗
PubMed2006

Arrhythmogenesis in the developing heart during anoxia-reoxygenation and hypothermia-rewarming: an in vitro model.

INTRODUCTION: The spatio-temporal pattern of arrhythmias in the embryonic/fetal heart subjected to a transient hypoxic or hypothermic stress remains to be established. METHODS AND RESULTS: Spontaneously beating hearts or isolated atria, ventricles, and conotruncus from 4-day-old chick embryos were subjected in vitro to 30-minute anoxia and 60-minute reoxygenation. Hearts were also submitted to 30-minute hypothermia (0-4 degrees C) and 60-minute rewarming. ECG disturbances and alterations of atrial and ventricular electromechanical delay (EMD) were systematically investigated. Baseline functional parameters were stable during at least 2 hours. Anoxia induced tachycardia, followed by bradycardia, atrial ectopy, first-, second-, and third-degree atrio-ventricular blocks and, finally, transient electromechanical arrest after 6.8 minutes, interquartile ranges (IQR) 3.1-16.2 (n = 8). Reoxygenation triggered also Wenckebach phenomenon and ventricular escape beats. At the onset of reoxygenation QT, PR, and ventricular EMD increased by 68%, 70%, and 250%, respectively, whereas atrial EMD was not altered. No fibrillations, no ventricular ectopic beats, and no electromechanical dissociation were observed. Arrhythmic activity of the isolated atria persisted throughout anoxia and upon reoxygenation, whereas activity of the isolated ventricles abruptly ceased after 5 minutes of anoxia and resumed after 5 minutes of reoxygenation. During hypothermia-rewarming, cardiac activity stopped at 17.9 degrees C, IQR 16.2-20.6 (n = 4) and resumed at the same temperature with no arrhythmias. All preparations fully recovered after 40 minutes of reoxygenation or rewarming. CONCLUSION: In the embryonic heart, arrhythmias mainly originated in the sinoatrial tissue and resembled those observed in the adult heart. Furthermore, oxygen readmission was by far more arrhythmogenic than rewarming and the chronotropic, dromotropic, and inotropic effects were fully reversible.

Animals↗
PubMed1996

Experimental hypothermia and rewarming: changes in mechanical function and metabolism of rat hearts.

Rewarming from accidental hypothermia is associated with fatal circulatory derangements. To investigate potential pathophysiological mechanisms involved, we examined heart function and metabolism in a rat model rewarmed after 4 h at 15-13 degrees C. Hypothermia resulted in a significant reduction of left ventricular (LV) systolic pressure, cardiac output, and heart rate, whereas stroke volume increased. The maximum rate of LV pressure rise decreased to 191 +/- 28 mmHg/s from a control value of 9,060 +/- 500 mmHg/s. Myocardial tissue content of ATP, ADP, and glycogen was significantly reduced, whereas lactate content remained unchanged. After rewarming, heart rate returned to control value, whereas LV systolic pressure, cardiac output, and stroke volume all remained significantly depressed. The posthypothermic maximum rate of LV pressure rise was 5,966 +/- 1.643 mmHg/s. The posthypothermic myocardial lactate content was significantly increased (to 13.3 +/- 3.2 nmol/mg from control value of 5.7 +/- 1.9 nmol/mg), and ATP and glycogen remained significantly lowered. Creatine phosphate or energy charge did not change significantly during the experiment. The finding of deteriorated myocardial mechanical function and a shift in energy metabolism shows that the heart could be an important target during hypothermia and rewarming in vivo, thus contributing to the development of a posthypothermic circulatory collapse.

Animals↗
PubMed2000

Fatal severe vasospasm due to rewarming following hypothermia--case report.

A 37-year-old female died of cerebral vasospasm as a complication of rewarming following hypothermia therapy for severe head injury. She presented with severe consciousness disturbance and anisocoria after falling down a flight of stairs. Computed tomography (CT) revealed a right acute subdural hematoma and temporal contusion. Following surgery, mild hypothermia was started and rewarming was completed by the 11th day. Neurological examination showed no abnormalities, but intracranial pressure (ICP) suddenly increased and she manifested anisocoria on the 13th day. Repeat CT revealed a low density area in the right middle cerebral artery region and cerebral angiography showed diffuse narrowing of the main arterial trunks. A cerebrospinal fluid (CSF) sample was collected using an intraventricular ICP monitoring catheter. The CSF level of 8-hydroxy-2'-deoxyguanosine was elevated during the rewarming period, indicating substantial deoxyribonucleic acid (DNA) oxidation. She died on the 15th day due to uncontrollable ICP. Histological examination at autopsy of the narrowed artery found the waving phenomenon in the internal elastic lamina and invasion of inflammatory cells into the adventitia. These findings constitute the possible evidence that free-radical-mediated oxidative DNA damage may be important in the genesis of severe vasospasm due to rewarming following hypothermia.

Adult↗
PubMed1995

Influence of body composition on rewarming from immersion hypothermia.

BACKGROUND: This study was conducted to determine if the differences between efficacies of three treatments for immersion hypothermia are affected by body composition. METHODS: Twelve subjects were divided into equally sized low (LF) and high (HF) fat groups. On three occasions subjects were each immersed in cold water until esophageal temperatures (Tes) decreased to approximately 33.2 degrees C (LF) and approximately 35.8 degrees C (HF). They were then rewarmed by: 1) shivering; 2) application of external heat; or 3) treadmill exercise in a balanced design. RESULTS: For HF, the afterdrop during exercise (1.04 +/- 0.2 degrees C) was greater than during shivering (0.35 +/- 0.3 degrees C) and external heat (0.36 +/- 0.1 degree C) (p < 0.01). In LF, however, the exercise afterdrop (0.75 +/- 0.2 degree C) was greater than only external heat (0.35 +/- 0.2 degree C) (p < 0.05) but not shivering (0.58 +/- 0.4 degree C). There was a positive relationship between % fat and afterdrop for the exercise condition with a slope (95% C.I.) of 0.03 (0.01 to 0.05) degree C.% fat-1 (r2 = 0.37, p < 0.05). The exercise rewarming rate (3.48 +/- 1.1 degrees C.h-1) was greater (p < 0.01) than during both shivering (1.80 +/- 0.7 degrees C.h-1) and external heat (2.22 +/- 0.7 degrees C.h-1) in HF while no difference was seen between the three treatments (5.28 +/- 0.4, 4.86 +/- 1.1 and 5.16 +/- 0.7 degrees C.h-1, respectively) in LF. There were inverse relationships between % fat and rewarming rate in the exercise -0.12 (-0.23 to -0.01) degree C.h-1.% fat-1, (r2 = 0.38), shivering -0.27 (-0.38 to -0.16) degrees C.h-1.% fat-1, (r2 = 0.76) and external heat -0.26 (-0.35 to -0.17) degree C.h-1.% fat-1, (r2 = 0.83) conditions (p < 0.05). CONCLUSIONS: The inter-treatment differences between these techniques are accentuated in the HF, and attenuated (afterdrop) or even eliminated (rewarming rate) in the LF subgroup.

Adult↗
PubMed1994

Phospholipid peroxidation in isolated perfused rat hearts subjected to hypothermia followed by rewarming: inverse relation to loss of function.

In the present experimental study phospholipid peroxidation after hypothermia and rewarming was investigated in isolated buffer-perfused rat hearts. Stable normotherm perfusion (37 degrees C) for 20 min was followed by cooling to 14 degrees C, 4 h perfusion at 14 degrees C, and rewarming to 37 degrees C followed by 30 min normotherm perfusion. Seven hearts went through the whole protocol, whereas six hearts were subjected only to the initial stabilization period. Mechanical performance was measured by a balloon in the left ventricle (LV) permitting measurements of LV pressure and its derivatives. At the end of perfusion, hearts were freeze clamped in liquid nitrogen for phospholipid peroxidation measurements, phospholipid fatty acid composition, high-energy phosphate content (adenosine tri-, di-, and monophosphate and creatine phosphate), and tissue water content. After rewarming there was a significant reduction in mechanical performance and coronary flow. Tissue content of high-energy phosphates was decreased and tissue water content was increased. Levels of peroxidized polyunsaturated fatty acids (conjugated diens) in phospholipids and nonesterified fatty acids were not significantly changed (135.2 +/- 31.1 vs 74.3 +/- 7.6 nmol/g tissue dry wt and 1212 +/- 203 and 1685 +/- 197 nmol/g in control and rewarmed hearts. However, the amount of peroxidized polyunsaturated fatty acids in phospholipids expressed as a fraction of the phospholipids was significantly reduced by the cooling/rewarming procedure (1.28 +/- 0.22 vs 0.61 +/- 0.09 x 10(-3), P < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗