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Query: UMLS:C0020672 (hypothermia)
 17,327 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Four fatal cases following scorpion sting in children are presented. Two victims had rectal temperature above 41 degrees C, the third exhibited a temperature of 40.9 degrees C from the combined effects of scorpion sting and heat stroke, while the fourth was hypothermic. All victims developed hypothermia 48 hr following the sting. The hyperthermia was effectively treated by acetaminophen suppositories, ice packs and water sponges. All victims showed late hypotension that was refractory to dopamine infusion. This was explained by bradykinin released by the venom blocking the dopaminergic receptors. Deterioration of the cortical activity of the victims maintained on mechanical ventilation before the incidence of asystole suggests a central component in the cardiovascular manifestations of envenomation. A. amoreuxi venom was selected as a model for the pharmacokinetic and quantitative toxicological studies since it has no effect on body temperature. In hyperthermic rabbits injected with labelled lethal fraction of A. amoreuxi venom, there was a significant decrease in the elimination half-life, t1/2 beta, the apparent volume of the tissue compartment, Vt, the apparent volume of distribution, Vdss, and the intercompartmental rate constant, kCT. Hypothermic rabbits showed a significant decrease in the apparent first-order elimination rate constant, kd, and a significant increase in the elimination half-life. In both states a higher concentration of the lethal fraction in the blood was calculated. This would explain the rapidity of onset of the electrocardiographic effects and the decreased survival time in both the hyperthermic and hypothermic rabbits injected with venom when compared to normothermic animals. The s.c. LD50 in mice and the i.v. MLD in rats were significantly reduced in the hypothermic mice and hypothermic and hyperthermic rats.
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PMID:Do changes in body temperature following envenomation by the scorpion Leiurus quinquestriatus influence the course of toxicity? 208 94

An accumulation of experimental data suggests that N-methyl-D-aspartate (NMDA) receptor antagonists will prevent ischemic neuronal injury following transient global ischemia and reduce infarct volumes following focal ischemic insults. The excitotoxic hypothesis states that the excitatory amino acid neurotransmitter L-glutamate has neurotoxic properties that can be attenuated by antagonism of the NMDA receptor. In vitro work has shown that a variety of NMDA antagonists will prevent the death of neurons grown in culture and subsequently exposed to either brief periods of hypoxia or glutamate exposure. In vivo it has been shown that glutamate is released following ischemia, that the NMDA receptors remain functional both during and following ischemia, and that the concentration of NMDA receptors is highest in those regions that are most sensitive to ischemic neuronal injury. Once stimulated, these receptors mediate a lethal influx of calcium. Experiments with global ischemia have reported a cytoprotective effect by either prior removal of glutamate afferents or pretreatment with either competitive or noncompetitive receptor antagonists. Some of these data have been challenged and one suggestion that has been made is that the observed pharmacoprotection may be the result of coincidental drug-induced hypothermia. Numerous studies using a variety of models of focal ischemia have shown that the volume of a cortical infarct can be reduced with NMDA antagonists given either before or after an ischemic insult. These data are more consistent than those achieved for models of global ischemia and have led to proposals for clinical trials. Novel compounds that antagonize the NMDA receptor are now the subject of phase I clinical studies that are envisaged as a prelude to randomized acute stroke trials. The hypothesis that blockade of excitatory amino acid receptors will prevent neuronal death presages a new era in acute stroke treatment.
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PMID:Do NMDA antagonists protect against cerebral ischemia: are clinical trials warranted? 214 95

Cerebral ischemia produces a disruption of calcium homeostasis in neurons. This may explain the extreme sensitivity of these cells to ischemic insult. Prolonged increases in calcium levels may produce irreversible damage to the cell by altering important calcium-dependent enzyme systems such as calcium/calmodulin-dependent protein kinase II. Five minutes of acute forebrain ischemia in the gerbil produced a significant decrease in calcium/calmodulin-dependent protein kinase II activity as early as 10 seconds postischemia and persisting up to 7 days after insult. Because hypothermia protects against ischemia-induced cell death in the gerbil, we examined the effect of ischemia on cell death and calcium/calmodulin-dependent protein kinase II at different intracerebral temperatures: hyperthermia (39 degrees C), normothermia (36 degrees C), and hypothermia (32 degrees C). In ischemic animals, hyperthermia produced severe loss of neurons in CA1 and moderate loss in CA3-CA4 subregions. Normothermia in ischemic animals produced severe loss of neurons in the CA1 subregion. Hypothermic ischemic animals showed no significant loss of neurons in any hippocampal region. Ischemia produced a severe decrease (17 +/- 6% of control) in calcium/calmodulin-dependent kinase II activity in hyperthermic animals, a moderate decrease (55 +/- 15% of control) in normothermic animals, and no decrease of enzyme activity in hypothermic animals. Thus, lowering and raising intracerebral temperature decreased and increased, respectively, the extent of ischemia-induced damage in the gerbil. Because ischemia-induced effects on calcium/calmodulin-dependent protein kinase II activity are rapid and long-lasting, hypothermia may protect through preservation of calcium/calmodulin-dependent protein kinase II activity.
Stroke 1990 Nov
PMID:Effects of ischemia on multifunctional calcium/calmodulin-dependent protein kinase type II in the gerbil. 217 73

The primary mechanism for maintaining normal body temperature during physical exercise in the heat is the evaporation of sweat. With profuse sweating, water loss far exceeds electrolyte loss. Rigorous exercise in the heat places the athlete at risk for thermoregulatory dysfunction from dehydration. Because children are inherently less efficient thermoregulators than adults, they are at even greater risk for heat illness. The three primary syndromes of heat illness are heat cramps, heat exhaustion, and heat stroke. Treatment of heat illness is based on reduction of body temperature and rehydration. Heat stroke is a true medical emergency with a high mortality rate; immediate reduction of body temperature is critical to the survival of these patients. Prevention of heat illness is based on reducing known risk factors. Physical activity should be modified in the face of high ambient temperature and humidity. The athlete should begin exercise well hydrated; frequent consumption of cold water during exercise decreases likelihood of significant dehydration. After exercise, the athlete should continue drinking to replace fluid losses. Clothing should be lightweight; the more skin exposed, the greater the available evaporative surface. A preseason conditioning program, when combined with an 8- to 14-day period of acclimatization, further reduces the risk of heat injury. Although athletes engaged in endurance sports may benefit from drinking carbohydrate/electrolyte-containing solutions, for the majority of young athletes, cold water remains the preferred choice for fluid replacement during exercise. The relatively greater body surface area of young athletes also places them at risk for hypothermia. Special attention should be given when these athletes are competing under cold environmental conditions.
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PMID:Heat illness. Fluid and electrolyte issues for pediatric and adolescent athletes. 221 56

Moderate hypothermia (30 degrees C) induced before circulatory arrest is known to improve neurologic outcome. We explored, for the first time in a reproducible dog outcome model, moderate hypothermia induced during reperfusion after cardiac arrest (resuscitation). In three groups of six dogs each (N = 18), normothermic ventricular fibrillation cardiac arrest (no blood flow) of 17 minutes was reversed by cardiopulmonary bypass--normothermic in control group I (37.5 degrees C) and hypothermic to 3 hours in groups II (32 degrees C) and III (28 degrees C). Defibrillation was achieved in less than or equal to 5 minutes and partial bypass was continued to 4 hours, controlled ventilation to 20 hours, and intensive care to 96 hours. All 18 dogs survived. Electroencephalographic activity returned significantly earlier in groups II and III. Mean +/- SD best neurologic deficit between 48 and 96 hours was 44 +/- 8% in group I, 38 +/- 12% in group II, and 35 +/- 7% in group III (differences not significant). Best overall performance category 2 (good outcome) between 48 and 96 hours was achieved in none of the six dogs in group I and in four of the 12 dogs in the combined hypothermic groups II and III (difference not significant). Mean +/- SD brain total histologic damage score was 130 +/- 22 in group I, 93 +/- 28 in group II (p = 0.05), and 80 +/- 26 in group III (p = 0.03). Gross myocardial damage was greater in groups II and III than in group I--numerically higher overall and significantly higher in group III for the right ventricle alone (p = 0.02). Moderate hypothermia after prolonged cardiac arrest may or may not improve cerebral outcome slightly and can worsen myocardial damage.
Stroke 1990 Nov
PMID:Moderate hypothermia after cardiac arrest of 17 minutes in dogs. Effect on cerebral and cardiac outcome. 223 54

This study examined the effect of hypothermia (15 degrees C) alone or combined with various cardioplegic solutions on functional recovery of the neonatal heart after 120 minutes of global ischemia in an isolated working rabbit heart model. Control hearts were preserved with hypothermia alone, and groups 1 to 6 were given different hyperkalemic crystalloid cardioplegic solutions. Each cardioplegic solution differed in Na+ and Ca++ content. Aortic flow, coronary flow, cardiac output, heart rate, peak systolic pressure, and stroke work were measured before ischemia and after 35 and 45 minutes of reperfusion. There were no statistical differences in hemodynamic recovery in the six groups in which cardioplegia was used. However, hearts preserved with multidose hyperkalemic cardioplegia showed significantly better recovery of cardiac output (86% versus 75%; p less than 0.05), coronary flow (88% versus 72%; p less than 0.05), and stroke work (86% versus 75%; p less than 0.05) than those preserved with hypothermia alone. These results suggest that hypothermic hyperkalemic cardioplegia improves preservation of the neonatal rabbit heart but that variations in Ca++ and Na+ content appear not to provide further myocardial protection.
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PMID:Cardioplegia for the immature myocardium. A comparative study in the neonatal rabbit. 224 13

We used brief bilateral carotid artery occlusion in gerbils to examine the effects of temperature on ischemia-induced inhibition of calcium/calmodulin-dependent protein kinase II activity and neuronal death. In normothermic (36 degrees C) gerbils, ischemia induced a severe loss of hippocampal CA1 pyramidal neurons measured 7 days after ischemia (28.4 neurons/mm, n = 10; control density in 10 naive gerbils 262.1 neurons/mm) and a significant decrease in forebrain calcium/calmodulin-dependent protein kinase II autophosphorylation measured 2 hours after ischemia (12.9 fmol/min, n = 6; control phosphorylation in six naive gerbils 23.5 fmol/min). The effect of temperature on these indicators of ischemic damage was examined by adjusting intracerebral temperature before and during the ischemic insult. Hyperthermic (39 degrees C) gerbils showed almost complete loss of neurons in the CA1 region (3.0 neurons/mm, n = 11) and extension of neuronal death into the CA2, CA3, and CA4 regions. In addition, hyperthermia exacerbated ischemia-induced inhibition of calcium/calmodulin-dependent protein kinase II activity (4.2 fmol/min, n = 6). Hypothermia (32 degrees C) protected against ischemia-induced CA1 pyramidal cell damage (257.0 neurons/mm, n = 20) and inhibition of calcium/calmodulin-dependent protein kinase II activity (26.0 fmol/min, n = 6). Our results are consistent with the hypothesis that loss of calcium/calmodulin-dependent protein kinase II activity may be a critical event in the development of ischemia-induced cell death.
Stroke 1990 Dec
PMID:Temperature modulation of ischemic neuronal death and inhibition of calcium/calmodulin-dependent protein kinase II in gerbils. 226 78

During the last decade several studies of cerebral blood flow (CBF) and metabolism in the acute phase of head injury have been published. It is the aim of this review to describe the dynamic changes in CBF, cerebral metabolic rate of oxygen (CMRO2), cerebral autoregulation (CA), and reactivity to PaCO2 and barbiturate (metabolic reactivity) in the acute phase after severe head injury and to discuss the therapeutical consequences with reference to prolonged artificial hyperventilation, hypothermia, barbiturate sedation, and mannitol therapy. On the basis of present knowledge concerning cerebral circulation and its regulation, the author reviews the literature concerning methodology for experimental and clinical CBF measurements and regulation of CBF and cerebral oxygen uptake. Emphasis is placed on studies of the effect of body temperature (hypothermia) as a therapeutic tool in the control of cerebral metabolism, blood flow, and intracranial pressure. Although hypothermia significantly reduces cerebral metabolism and blood flow, the effect of hypothermia on cerebral blood flow, metabolism, ICP, and outcome after acute head injury has never been investigated in clinically controlled studies. Experimental and clinical studies concerning sensitivity of CBF for changes in PaCO2 are reviewed. The normal CO2 reactivity defined as absolute (delta CBF/delta PaCO2) and relative (% change CBF/delta PaCO2) or delta in CBF/PaCO2 mm Hg are mentioned. In awake normocapnic man the relative CO2 reactivity averages 4%/mm Hg and the absolute CO2 reactivity 2ml/mm Hg. Uncontrolled prospective studies show a therapeutic effect of artificially prolonged hyperventilation on outcome. Only one preliminary controlled study indicates that the outcome is poorer and recovery prolonged. Nevertheless, in the acute phase of HI, artificial hyperventilation is used routinely for control of intracranial hypertension and during the intensive care management of the patients. The steal and inverse steal phenomena are reviewed. Although of considerable theoretical interest these phenomena are without clinical significance in patients with head injury, unless clinical CBF measurements are performed. The frequency of the inverse steal phenomenon in studies of rCBF with a 16-channel Cerebrograph (intraarterial approach) is found to be about 10%. During prolonged hyperventilation experimental studies and clinical studies of apoplexy show an adaptation of CBF and CSF-pH and bicarbonate.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Cerebral blood flow in acute head injury. The regulation of cerebral blood flow and metabolism during the acute phase of head injury, and its significance for therapy. 227 29

The use of hypothermia in cardiac and neurologic surgery is well established, but its use in treating hemorrhagic shock is controversial. Using a modified Wiggers hemorrhagic shock model, we examined the effects of hypothermia (group 1, 33 degrees C, N = 7; group 2, 28 degrees C, N = 12) after inducing hemorrhagic shock. In group 3, N = 6, dogs were maintained at body temperature in hemorrhagic shock and throughout resuscitation (normothermic shock). Sixty minutes after resuscitation (shed blood and lactated Ringer's solution, 50 ml/kg body wt), all hypothermic dogs were rewarmed and studied for an additional 120 min. Comparison of moderately hypothermic, severely hypothermic, and normothermic dogs showed a lower heart rate (80.6 +/- 3.3, 62.5 +/- 4.1, and 136.7 +/- 4.2 beats/min, P less than 0.05), reduced rate of left ventricular pressure fall (938 +/- 125, 700 +/- 75, and 1550 +/- 275 mm Hg/sec, P less than 0.05), a lower arterial pH (7.15 +/- 0.02, 7.10 +/- 0.03, and 7.24 +/- 0.02, P less than 0.05), a lower respiratory rate (18 +/- 1, 14 +/- 1, and 24 +/- 2 breaths/min, P less than 0.05), and a higher arterial pCO2 (36.6 +/- 1.6, 46.9 +/- 4.6, and 20.3 +/- 2.0 mm Hg, P less than 0.05). Left ventricular end-diastolic pressure was lower in the severely hypothermic dogs while stroke volume was higher in this group. Rewarming ablated all differences in cardiovascular performance and acid-base balance. Our data show that moderate hypothermia during hemorrhagic shock increased coronary perfusion, enhanced cardiac contractile performance, and significantly reduced myocardial oxygen requirements.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of different degrees of hypothermia on myocardium in treatment of hemorrhagic shock. 229 84

Twenty-eight patients were studied after uncomplicated aortocoronary bypass surgery with hypothermic cardiopulmonary bypass (CPB). In all patients residual hypothermia was effectively treated by the use of extended rewarming during CPB and postoperatively by an external heat source. This treatment almost eliminated postoperative shivering, and it resulted in the lowering of oxygen uptake, carbon dioxide production, and required ventilatory volumes to stable levels where spontaneous breathing could be used safely. The patients were divided into two groups. In group I (n = 12), intraoperative anesthesia was based on an intravenous (IV) opioid (phenoperidine), which caused persistent respiratory depression and made mechanical ventilation necessary for a mean postoperative time period of 10.7 +/- 3.8 hours even with the rewarming. In group II (n = 16), thoracic epidural analgesia and intraoperative general anesthesia with enflurane were used. In this group, postoperative metabolic and ventilatory requirements were stable and low, finger skin temperature was normalized earlier, systemic vascular resistance was lower, and stroke index was higher. Emergence from anesthesia was uneventful and was achieved early postoperatively in Group II. The patients had good pain relief and were mentally alert. Adequate spontaneous breathing was resumed quickly and endotracheal extubation was performed within the first two postoperative hours (1.6 +/- 0.5 hours). No complications or increased morbidity occurred, and no patient needed to be reintubated in Group II.
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PMID:Early extubation after coronary artery surgery in efficiently rewarmed patients: a postoperative comparison of opioid anesthesia versus inhalational anesthesia and thoracic epidural analgesia. 252 Sep 17


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