Altered Ca2+ homeostasis and impaired mitochondrial function in cardiomyopathy

This work investigates whether purine metabolism and release is related to cardioprotection with hyperkalemia and hypothermia. Langendorff guinea-pig hearts were used to either monitor metabolism during ischemia or to measure functional recovery, myocardial injury and release of purine during reperfusion. Hearts underwent 30 min ischemia using one of the following protocols: control (normothermic buffer), hyperkalaemia (high-potassium buffer), hypothermia (20°C) and hyperkalemia + hypothermia. At the end of 30 min ischemia, hyperkalemia was associated with similar metabolic changes (rise in purine and lactate and fall in adenine nucleotides) to control group. Accumulation of purine was due to a rise in inosine, xanthine and hypoxanthine and was largely prevented by hypothermia and hyperkalemia + hypothermia. Upon reperfusion, there was a time-dependent release of all purine, lactate and AMP. A fast (peak in less than 20 sec) release of inosine, xanthine, hypoxanthine and lactate was highest in control followed by hyperkalemia then hypothermia and little release in hyperkalemia + hypothermia. Adenosine and AMP release was slow (peak at 3 min), only significant in control and was likely to be due to sarcolemmal disruption as the profile followed lactate dehydrogenase release. Recovery (left ventricular developed pressure) was 63% control, 82% hyperkalemia, 77% hypothermia and 98% for hyperkalemia + hypothermia. The loss of purine during reperfusion but not their production during ischemia is related to cardioprotection with hyperkalemia. The possibility that the consequences of hyperkalemia modulate a sodium-dependent purine efflux, is discussed. The reduced loss of purine in hypothermia or in hyperkalemia + hypothermia is likely to be due to a lower metabolic activity during ischemia.     

Hypothermia in Preterm Infants in the First Hours after Birth: Occurrence,Course and Risk Factors

BackgroundHypothermia is associated with increased morbidity and mortality rates. Preterm infants frequently have hypothermia when they are admitted to the NICU, but there is no data on the occurrence of hypothermia during the first hours after admission.ObjectiveTo investigate the occurrence of hypothermia in preterm infants in the first three hours of admission and to identify risk factors.MethodsInfants < 32 weeks of gestation included in a randomized trial with admission temperature as primary outcome were retrospectively analyzed for the occurrence of hypothermia (< 36.5°C) in the first three hours after admission. Risk factors were identified using linear regression analysis and logistic regression.ResultsIn total 80 infants were included with a median (IQR) gestational age at birth of 29 (27–30) weeks. In 93% of the infants hypothermia occurred in the first three hours after admission. The median (IQR) duration of hypothermia was 101 (34–162) minutes, of which 24 (7–52) minutes the hypothermia was mild, 45 (4–111) minutes moderate, severe hypothermia hardly occurred. Gestational age and the occurrence of hypothermia at birth were independent risk factors for the occurrence of moderate and severe hypothermia and significantly correlated with duration of hypothermia.ConclusionsHypothermia occurred often and for a long period in preterm infants in the first three hours of life, low gestational age and admission temperature were independent risk factors     

Urban hypothermia and hyperglycemia in the elderly

From December 1993 to March 1999 we treated 18 elderly patients aged 66-87 years, suffering from urban hypothermia: 11 women and 7 men. Ten patients suffered from moderate hypothermia (rectal temperature 32-35 degrees C), and eight from severe hypothermia (rectal temperature < 32 degrees C). Regarding consciousness, in the group suffering from moderate hypothermia, 3 were somnolent and 6 in various degrees of comatose states. In the group suffering from severe hypothermia, 3 patients were somnolent or soporous and 5 in comatose states of various degrees. Values of arterial blood pressure in the group with moderate hypothermia was normal in one, in 3 arterial hypotension was observed and 6 were in a state of shock. In the group with severe hypothermia, 3 presented arterial hypotension and 5 were in a state of shock. In the group with moderate hypothermia the blood glucose level was elevated in six: 9.3-10.2-10.7-17.9-21.3-99.0, and in one patient the blood glucose level was low: 2.3 mmol/L, in correlation with hypoglycemic coma. In the group with severe hypothermia in all eight patients the values were elevated: 6.7-7.4-7.6-8.7-9.1-11.2-12.4-17.9 mmol/L.     

Central A1-receptor activation associated with onset of torpor protects the heart against low temperature in the Syrian hamster

Body temperature drops dramatically during hibernation, but the heart retains the ability to contract and is resistant to induction of arrhythmia. Although adaptive changes in the heart prior to hibernation may be involved in the cold-resistant property, it remains unclear whether these changes are sufficient for maintaining cardiac pulsatility under an extreme hypothermic condition. We forcibly induced hypothermia in Syrian hamsters by pentobarbital anesthesia combined with cooling of the animals. This allows reproduction of a hypothermic condition in the absence of possible hibernation-specific reactions. Unlike hypothermia in natural hibernation, the forced induction of hypothermia caused atrioventricular block. Furthermore, J-waves, which are typically observed during hypothermia in nonhibernators, were recorded on an ECG. The origin of the J-wave seemed to be related to irreversible injury of the myocardium, because J-waves remained after recovery of body temperature. An abnormal ECG was also found when hypothermia was induced in hamsters that were well adapted to a cold and darkened environment or hamsters that had already experienced hibernation. These results suggest that acclimatization prior to hibernation does not have a crucial effect at least on acquisition of cardiac resistance to low temperature. In contrast, an abnormal ECG was not observed in the case of hypothermia induced by central administration of an adenosine A1-receptor agonist and subsequent cooling, confirming the importance of the adenosine system for inducing hibernation. Our results suggest that some specific mechanisms, which may be driven by a central adenosine system, operate for maintaining the proper cardiac pulsatility under extreme hypothermia.     

Role of neurotensin in radiation-induced hypothermia in rats

The role of neurotensin in radiation-induced hypothermia was examined. Intracerebroventricular (ICV) administration of neurotensin produced dose-dependent hypothermia. Histamine appears to mediate neurotensin-induced hypothermia because the mast cell stabilizer disodium cromoglycate and antihistamines blocked the hypothermic effects of neurotensin. An ICV pretreatment with neurotensin antibody attenuated neurotensin-induced hypothermia, but did not attenuate radiation-induced hypothermia, suggesting that radiation-induced hypothermia was not mediated by neurotensin.     

Effects of dopaminergic and serotonergic drugs on ethanol-induced hypothermia

The effects of dopaminergic and serotonergic drugs on ethanol-induced hypothermia were studied in the rat. Pretreatment with haloperidol attenuated the hypothermia in a dose-dependent manner. Apomorphine produced a dose-dependent effect on the hypothermia. At a dose of 2.0 mg/kg, apomorphine potentiated ethanol-induced hypothermia, whereas at 0.1 mg/kg, it produced a delayed attenuation effect between 30 min and 45 min after its injection. The former effect was blocked by haloperidol, whereas the latter was not affected by haloperidol, but blocked by pretreatment with parachlorophenylalanine. It is concluded that both dopamine and serotonin exert modulatory effects on ethanol-induced hypothermia.     

Systematic Review and Meta-Analysis of Therapeutic Hypothermia in Animal Models of Spinal Cord Injury

Background

Therapeutic hypothermia is a clinically useful neuroprotective therapy for cardiac arrest and neonatal hypoxic ischemic encephalopathy and may potentially be useful for the treatment of other neurological conditions including traumatic spinal cord injury (SCI). The pre-clinical studies evaluating the effectiveness of hypothermia in acute SCI broadly utilise either systemic hypothermia or cooling regional to the site of injury. The literature has not been uniformly positive with conflicting studies of varying quality, some performed decades previously.

Methods

In this study, we systematically review and meta-analyse the literature to determine the efficacy of systemic and regional hypothermia in traumatic SCI, the experimental conditions influencing this efficacy, and the influence of study quality on outcome. Three databases were utilised; PubMed, ISI Web of Science and Embase. Our inclusion criteria consisted of the (i) reporting of efficacy of hypothermia on functional outcome (ii) number of animals and (iii) mean outcome and variance in each group.

Results

Systemic hypothermia improved behavioural outcomes by 24.5% (95% CI 10.2 to 38.8) and a similar magnitude of improvement was seen across a number of high quality studies. The overall behavioural improvement with regional hypothermia was 26.2%, but the variance was wide (95% CI −3.77 to 56.2). This result may reflect a preponderance of positive low quality data, although a preferential effect of hypothermia in ischaemic models of injury may explain some of the disparate data. Sufficient heterogeneity was present between studies of regional hypothermia to reveal a number of factors potentially influencing efficacy, including depth and duration of hypothermia, animal species, and neurobehavioural assessment. However, these factors could reflect the influence of earlier lower quality literature.

Conclusion

Systemic hypothermia appears to be a promising potential method of treating acute SCI on the basis of meta-analysis of the pre-clinical literature and the results of high quality animal studies.     

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.     

A microarray analysis of the effects of moderate hypothermia and rewarming on gene expression by human hepatocytes (HepG2)

The gene expression changes produced by moderate hypothermia are not fully known, but appear to differ in important ways from those produced by heat shock. We examined the gene expression changes produced by moderate hypothermia and tested the hypothesis that rewarming after hypothermia approximates a heat-shock response. Six sets of human HepG2 hepatocytes were subjected to moderate hypothermia (31°C for 16 h), a conventional in vitro heat shock (43°C for 30 min) or control conditions (37°C), then harvested immediately or allowed to recover for 3 h at 37°C. Expression analysis was performed with Affymetrix U133A gene chips, using analysis of variance-based techniques. Moderate hypothermia led to distinct time-dependent expression changes, as did heat shock. Hypothermia initially caused statistically significant, greater than or equal to twofold changes in expression (relative to controls) of 409 sequences (143 increased and 266 decreased), whereas heat shock affected 71 (35 increased and 36 decreased). After 3 h of recovery, 192 sequences (83 increased, 109 decreased) were affected by hypothermia and 231 (146 increased, 85 decreased) by heat shock. Expression of many heat shock proteins was decreased by hypothermia but significantly increased after rewarming. A comparison of sequences affected by thermal stress without regard to the magnitude of change revealed that the overlap between heat and cold stress was greater after 3 h of recovery than immediately following thermal stress. Thus, while some overlap occurs (particularly after rewarming), moderate hypothermia produces extensive, time-dependent gene expression changes in HepG2 cells that differ in important ways from those induced by heat shock.     

Risk of hypothermia in elderly patients with diabetes.

The incidence of admissions of patients with hypothermia was determined to examine whether hypothermia was more common in elderly patients with diabetes than in the general population after diabetic metabolic emergency cases had been excluded. A prospective survey of three accident and emergency departments identified 134 cases of hypothermia admitted from a catchment population of almost 157,000 aged 65 or over during the winters of 1981-2 to 1983-4. The predicted number of patients with diabetes in the population was nearly 5600 (3.5%). Twenty three admissions for hypothermia (17%) occurred in 20 patients with previously diagnosed diabetes. Women made up 87% of the diabetic admissions; the ratio of diabetic to non-diabetic admission rates in women was 7.9 (95% confidence interval 5.3 to 12.0). After excluding diabetic metabolic emergency admissions the ratio was 6.4. The ratio in men was 2.4, but the small number of admissions produced wide confidence intervals. Ten of the admissions with diabetes (43%) had pathological disorders that are associated with an increased risk of hypothermia. The frequency of these conditions is higher in patients with diabetes than in the general population and partly explains the increased risk of hypothermia in these patients.     

Post-ischemic hypothermia promotes generation of neural cells and reduces apoptosis by Bcl-2 in the striatum of neonatal rat brain

Hypothermia is a potential therapy for cerebral hypoxic ischemic injury in adults and neonates. However, the mechanism of hypothermia neuroprotection after hypoxic-ischemia (HI) on the developing rat brain remains unclear. In this research, 7-day-old rats were subjected to left carotid artery ligation followed by 8% oxygen for 2h. They were divided into hypothermia (rectal temperature, 32-33°C for 24h) and normothermia (36-37°C for 24h) groups immediately after hypoxia-ischemia. All rats were given 50mg/kg/day 5-bromodeoxyuridine (BrdU) intraperitoneally at 4-6 days and sacrificed at 1 or 2 weeks after HI. There was a significant decrease in infarct volume in the hypothermia group at 7 days after HI compared with that in the normothermia group. The numbers of nestin-labeled cells did not change greatly, but β-tubulin III (Tuj-1) immuno-positive cells increased significantly in the striatum at 1 and 2 weeks after HI in the hypothermia compared to normothermia group. Neurogenesis was assessed by double immunohistochemical/immunofluorescent labeling of BrdU with nestin, Tuj-1 or microtubule-associated protein 2 (Map-2). Newborn neural progenitors (BrdU(+)-nestin(+)) did not change dramatically, but newborn immature (BrdU(+)-Tuj-1(+)) and mature (BrdU(+)-Map-2(+)) neurons increased significantly in the hypothermia compared with normothermia group. Meanwhile, the apoptosis rate of neural precursors, immature and mature neurons, assessed by double labeling of active Casp-3 with nestin/Tuj-1/Map-2, decreased noticeably in the hypothermia compared with normothermia group. We also found that hypothermia significantly increased expression of Bcl-2, which coexisted with nestin/Tuj-1/Map-2. Inhibition of Bcl-2 expression reversed the decreased apoptosis rate of neural precursors and neurons in hypothermia animal striatum of neonatal rat brain. These results suggest that neuroprotection effects of hypothermia on injured developing rat brain may associate with enhanced generation of neuronal cells and Bcl-2-mediated reduction of apoptosis of these cells. These observations are noteworthy regarding clinical hypothermia therapy following cerebral HI injury during the perinatal period.     

Combination Treatment of Hypothermia and Mesenchymal Stromal Cells Amplifies Neuroprotection in Primary Rat Neurons Exposed to Hypoxic-Ischemic-Like Injury In Vitro: Role of the Opioid System

This study was designed to reveal the therapeutic regimen and mechanism of action underlying hypothermia treatment in combination with stem cell transplantation for ameliorating neonatal hypoxic-ischemic-like injury. Primary rat neurons were exposed to oxygen-glucose deprivation (OGD), which produced hypoxic-ischemic-like injury in vitro, then incubated at 25°C (severe hypothermia), 34°C (moderate hypothermia), and 37°C (normothermia) with or without subsequent co-culture with mesenchymal stromal cells (MSCs). Combination treatment of moderate hypothermia and MSCs significantly improved cell survival and mitochondrial activity after OGD exposure. The exposure of delta opioid human embryonic kidney cells (HEK293) to moderate hypothermia attenuated OGD-mediated cell alterations, which were much more pronounced in HEK293 cells overexpressing the delta opioid receptor. Further, the addition of delta opioid peptide to 34°C hypothermia and stem cell treatment in primary rat neurons showed synergistic neuroprotective effects against OGD which were significantly more robust than the dual combination of moderate hypothermia and MSCs, and were significantly reduced, but not completely abolished, by the opioid receptor antagonist naltrexone altogether implicating a ligand-receptor mechanism of neuroprotection. Further investigations into non-opioid therapeutic signaling pathways revealed growth factor mediation and anti-apoptotic function accompanying the observed therapeutic benefits. These results support combination therapy of hypothermia and stem cells for hypoxic-ischemic-like injury in vitro, which may have a direct impact on current clinical trials using stand-alone hypothermia or stem cells for treating neonatal encephalopathy.     

Moderate hypothermia prevents neural cell apoptosis following spinal cord ischemia in rabbits

Paraplegia is a disastrous complication after operations of descending and thoracoabdominal aortic aneurysm. Regional hypothermia protects against spinal cord ischemia although the protective mechanism is not well know. The objective of this study is to examine whether hypothermia protects the spinal cord by preventing apoptosis of nerve cell and also investigate a possible mechanism involved in hypothermia neuroprotection. Cell apoptosis with necrosis was evident in the spinal cord 24 h after 30 min of ischemia. Moderate hypothermia decreased the incidence of apoptotic nerve cells. Both cell apoptosis and necrosis were attenuated by hypothermia, p53 expression increased and bcl-2 expression declined after ischemia, while hypothermia mitigated these changes. This study suggests that apoptosis contributes to cell death after spinal cord ischemia, and that moderate hypothermia can prevent nerve cell apoptosis by a mechanism associated with bcl-2 and p53 genes.     

Systemic Administration of the TRPV3 Ion Channel Agonist Carvacrol Induces Hypothermia in Conscious Rodents

Therapeutic hypothermia is a promising new strategy for neuroprotection. However, the methods for safe and effective hypothermia induction in conscious patients are lacking. The current study explored the Transient Receptor Potential Vanilloid 3 (TRPV3) channel activation by the agonist carvacrol as a potential hypothermic strategy. It was found that carvacrol lowers core temperature after intraperitoneal and intravenous administration in mice and rats. However, the hypothermic effect at safe doses was modest, while higher intravenous doses of carvacrol induced a pronounced drop in blood pressure and substantial toxicity. Experiments on the mechanism of the hypothermic effect in mice revealed that it was associated with a decrease in whole-body heat generation, but not with a change in cold-seeking behaviors. In addition, the hypothermic effect was lost at cold ambient temperature. Our findings suggest that although TRPV3 agonism induces hypothermia in rodents, it may have a limited potential as a novel pharmacological method for induction of hypothermia in conscious patients due to suboptimal effectiveness and high toxicity.     

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.     

Shallow hypothermia depends on the level of fatty acid unsaturation in adipose and liver tissues in a tropical heterothermic primate

Optimal levels of unsaturated fatty acids have positive impacts on the use of prolonged bouts of hypothermia in mammalian hibernators, which generally have to face low winter ambient temperatures. Unsaturated fatty acids can maintain the fluidity of fat and membrane phospholipids at low body temperatures. However, less attention has been paid to their role in the regulation of shallow hypothermia, and in tropical species, which may be challenged more by seasonal energetic and/or water shortages than by low temperatures. The present study assessed the relationship between the fatty acids content of white adipose and liver tissues and the expression of shallow hypothermia in a tropical heterothermic primate, the gray mouse lemur (Microcebus murinus). The adipose tissue is the main tissue for fat storage and the liver is involved in lipid metabolism, so both tissues were expected to influence hypothermia dependence on fatty acids. As mouse lemurs largely avoid deep hypothermia (i.e. torpor) use under standard captive conditions, the expression of hypothermia was triggered by food-restricting experimental animals. Hypothermia depth increased with time, with a stronger increase for individuals that exhibited higher contents of unsaturated fatty acids suggesting that they were more flexible in their use of hypothermia. However these same animals delayed the use of long hypothermia bouts relative to individuals with a higher level of saturated fatty acids. This study evidences for the first time that body fatty acids unsaturation levels influence the regulation of body temperature not only in cold-exposed hibernators but also in tropical, facultative heterotherms.     

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.     

The corrected Q-T interval in the elderly with urban hypothermia

During winter time in the period from 1993 to 1998, 18 elderly patients: 11 female and 7 male aged 65-88 years, were treated because of hypothermia. Rectal temperature on admission was 20-34.5 degrees C. Ten patients suffered from moderate hypothermia (35-32 degrees C), and eight suffered of severe hypothermia (< 32 degrees C). Arterial hypotension was recorded in 7, and shock in 11 patients. In all of them, and in 18 controls, an electrocardiogram was analyzed with the special reference to the corrected Q-T interval. Decompensated metabolic acidosis was observed in 7/8 patients with severe hypothermia and in 4/10 with moderate hypothermia. Among patients with moderate hypothermia, sinus tachycardia was present in 2, sinus bradycardia in 2, idioventricular rhythm in 2 and atrial fibrillation in 4/10 patients. In patients with severe hypothermia, sinus tachycardia was present in 2, sinus bradycardia in 3, idioventricular rhythm in one, and atrial fibrillation in 2/8 patients. In moderate hypothermia Osborn's or Tomaszewski's J wave was present in 7/10, and it only appeared in 3/10 patients; in severe hypothermia it was present in 6/8 and only appeared in 2/8 patients. The corrected Q-T interval in the group with hypothermia ranged 0.450-0.688 s, in the control group 0.343-0.444 s. The X minimum (s) in the group with hypothermia was 0.508 +/- 0.079, in the control group it was 0.371-0-139 s, and the difference was statistically significant (p < 0.001). The X maximum (s) in the group with hypothermia was 0.576 +/- 0.067 s, in the control group 0.390 +/- 0.019 s, and the difference was also statistically significant (p < 0.0001). In both groups the most significant prolongation of the corrected Q-T interval in the majority of patients was found in anteroseptal leads. The dispersion of the corrected Q-T interval in the group with hypothermia was 87.19 +/- 28.44 ms, in the control group it was 32.06 +/- 8.94 ms, and the difference was statistically significant (p < 0.001).