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

To define the part played by mild-to-moderate hypothermia in neuroprotection, it is necessary to take into account the thermoregulatory responses that occur in the normal human as the change in central temperature exceeds 0.2 degrees C. The mechanisms induced by cold are cutaneous vasoconstriction and shivering. They must be suppressed before starting controlled hypothermia. In these conditions, controlled moderate hypothermia between 32 and 35 degrees C does not seem to have deleterious side-effects, especially on coagulation. Caution is needed with the analysis of the numerous papers reporting experiments concerning the effects of moderate hypothermia in animals with induced cerebral ischaemia because of significant differences in the study designs. These differences concern mainly the time of onset of hypothermia, viz before or after ischaemia, the fact that the ischaemia is either global or focal, that it is caused by vascular occlusion posttraumatic or initiated by hypo or hyperglycemia. Some differences are also existing in the criteria used to appreciate the neuronal damage, as well as in the level of temperature and the site where it is measured. The mechanism of neuroprotection from moderate hypothermia seems to be not only a decrease in cerebral metabolism, but also involves a specific action on some intra-cellular events such as the blocking of the release of glutamate and of lipid peroxydation in brain tissue. An indirect proof of the neuroprotective effect of moderate hypothermia is the increase in the neuronal damage induced by moderate hyperthermia. It is conceivable that moderate hypothermia could exert a better neuroprotective effect than the drugs having this reputation, such as barbiturates, isoflurane and propofol.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Mild hypothermia and cerebral protection]. 767 76

Carbon monoxide (CO) and cyanide (CN), commonly found in exhaust fumes and smoke, act as hypoxic agents in eliciting morbid and lethal effects. This study explored the effects of these two toxicants on the ECG in a controlled and well-characterized animal model. Levine-prepared awake female rats were treated with 1500 and 2400 ppm CO for 90 min, CN at 4 mg/kg, or 1500 ppm CO plus 4 mg/kg CN. As in past studies, CO initially induced hyperglycemia and many-fold increases in blood lactate concentration, and rebound increases in blood glucose during recovery. CN produced hyperglycemia, however, there was no glucose rebound, nor was there a significant increase in lactate. CN plus 1500 ppm CO produced glucose changes similar to that of CO alone. CO exposure also induced hypothermia and hypotension, while CN produced little change in these parameters. CO increased heart rate, while CN tended to decrease heart rate. PR interval was increased significantly 4.5-17.0 ms by exposure to CO, with or without combination with CN, while CN alone produced minimal change in the PR interval. QT interval was increased up to 20 ms by exposure to CO, with or without combination with CN. CN alone produced no change in the QT interval. T wave duration was increased up to 22.5 ms by exposure to 1500 ppm CO, with or without combination with CN. CN alone produced minimal changes in T wave duration. There were no changes in duration of the (Q)RS complex or of the R wave. QT interval lengthening was positively correlated with the decrease in systolic blood pressure (0-30 min, r = 0.657, P < 0.05; 0-60 min, r = 0.704, P < 0.05). Hypothermia was correlated with increase in lactate concentration (r = 0.73, P < 0.05) and with decrease in blood pressure (r = 0.69, P < 0.05). No correlation between body temperature and QT interval was observed. The results indicate that CO at the concentrations used in the Levine-prepared rat has major effects on the ECG in slowing AV conduction and ventricular repolarization. In contrast, CN at 4 mg/dl has little or no effect on either conduction or repolarization in this animal model. These findings are discussed in light of past animal and human studies.
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PMID:Electrocardiographic responses to carbon monoxide and cyanide in the conscious rat. 821 56

A research program in cerebral ischemia was initiated by our laboratory to determine optimal strategies for cerebroprotection. Four studies relating to cerebroprotection using nuclear magnetic resonance spectroscopy in a sheep model of hypothermic cardiopulmonary bypass are summarized. These showed, first, that low-flow bypass, with a flow as low as 10 mL.kg-1 x min-1, maintained normal cerebral metabolism; second, that hypothermia increases the high-energy phosphate content and the intracellular pH of the brain; third, that hyperglycemia causes a profound intracellular acidosis; and, finally, that barbiturates prevent the normal increase in high-energy phosphates associated with hypothermia.
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PMID:Low-flow cardiopulmonary bypass and cerebral protection: a summary of investigations. 826 75

Infants undergoing open-heart surgery with hypothermic cardiopulmonary bypass experience markedly elevated lactate and glucose levels. Reports in infants less than 10 kg show the elevated lactate to be progressive during the operative period. The pathogenesis of the hyperglycemia is not clear but may be caused by excess glucose administration, inadequate insulin response, or glucose regulatory hormone levels of glucagon, cortisol, and growth hormone. The purpose of this study is to confirm these findings and to investigate their pathogenesis. Serial blood samples were taken preoperatively, intraoperatively, and postoperatively during hypothermic cardiopulmonary bypass in nine infants of less than 10 kg. Samples were analyzed for levels of lactate, glucose, and regulatory hormones insulin, growth hormone, glucagon, and cortisol. Our study did not show a progressive accumulation of lactate. The elevated lactate level appears to come from the pump prime solution. The hyperglycemia is also from the pump prime solution, and there do not appear to be elevated levels of regulatory hormones intraoperatively. Insulin response during hypothermia is blunted; however, on rewarming the patient in the immediate postoperative period, a brisk insulin response is seen. The changes in levels of lactate and glucose and the regulatory hormones return to baseline at 24 hours with no further significant changes in the next 48 hours.
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PMID:Lactic acid changes during and after hypothermic cardiopulmonary bypass in infants. 847 97

From January 1984 to May 1994, 17 of 239 children under 15 years old stung by Tityus serrulatus (15.1%) or Tityus bahiensis (84.9%) presented severe envenoming. Of these 17 patients (1-11 years old; median = 2 yr) 14 were stung by T. serrulatus and three by T. bahiensis. All of them received scorpion antivenom i.v. at times ranging from 45 min. to 5 h after the accident (median = 2 h). On admission, the main clinical manifestations and laboratory and electrocardiographic changes were: vomiting (17), diaphoresis (15), tachycardia (14), prostration (10), tachypnea (8), arterial hypertension (7), arterial hypotension (5), tremors (5), hypothermia (4), hyperglycemia (17), leukocytosis (16/16), hypokalemia (13/17), increased CK-MB enzyme activity (> 6% of the total CK, 11/12), hyperamylasemia (11/14), sinusal tachycardia (16/17) and a myocardial infarction-like pattern (11/17). Six patients stung by T. serrulatus had depressed left ventricular systolic function assessed by means of echocardiography. Of these, five presented pulmonary edema and four had shock. A child aged two-years old presented severe respiratory failure and died 65 h after being stung by T. serrulatus. Severe envenomations caused by T. serrulatus were 26.2 times more frequent than those caused by T. bahiensis (p < 0.001).
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PMID:A comparative study of severe scorpion envenomation in children caused by Tityus bahiensis and Tityus serrulatus. 859 62

Brain damage due to an episode of cerebral hypoxia/ischemia remains a major problem in the human infant, providing impetus for the testing of potential neuroprotective agents in animal models. Although these animal models do not mirror the human pathology exactly (e.g., with respect to regions vulnerable to damage), they usually have the histological characteristics of gray matter hypoxic/ischemic injury in the human. An important factor in comparing models directly is the stage of development of the brain at birth, which varies widely between species. Approaches to prevent or treat cerebral hypoxic/ischemic damage in neonates have paralleled those in adults. However, most of these results should be interpreted cautiously, since neonatal rat models with little concurrent physiological monitoring are often used. As in adults, moderate hypothermia during the insult or a preconditioning stress prior to the insult has prevented hypoxic/ ischemic brain damage. Different from adults is the demonstration that pretreatment with moderate doses of glucocorticoids or hyperglycemia during the hypoxic/ ischemic insult protects the brain against infarction. Partial protection, primarily in neonatal rats, has also been produced by pretreatment with voltage-sensitive calcium channel antagonists, free radical scavengers, growth factors, gangliosides, anticonvulsants, antiinflammatory agents, and nitric oxide synthase inhibitors. Posttreatment has been effective with a few agents. The most consistent has been the protective effect observed with glutamate receptor antagonists administered before but also up to 4 h after the insult. The effects of most of these therapies on blood glucose, body temperature, and/or the systemic circulation should be measured and the protective effects confirmed in larger species prior to considering clinical applications.
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PMID:Brain damage due to cerebral hypoxia/ischemia in the neonate: pathology and pharmacological modification. 872 85

Nesidioblastosis associated with progressive weight loss and hyperglycemia was diagnosed in two mid-adult, wild-caught, male squirrel monkeys (Saimiri sciureus). Hyperglycemia, glucosuria, and abnormal glucose tolerance test results were found when the monkeys were presented for clinical evaluation for chronic weight loss, episodic dehydration, hypothermia, and lethargy. Immunohistochemical studies of the pancreatic tissue demonstrated that the proliferating endocrine cells stained predominantly glucagon-positive in the most severely affected monkey.
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PMID:Nesidioblastosis associated with hyperglycemia in two squirrel monkeys (Saimiri sciureus). 902 1

We have shown repeatedly that pre-treatment of neonatal rats with dexamethasone provides protection against hypoxic-ischemic brain damage. Although the mechanism of action is not certain, hypothermia, an alteration in cerebral perfusion or an induction of antioxidant enzymes does not readily explain this effect. A relative hyperglycemia is usually observed during hypoxia-ischemia in dexamethasone treated animals, and may provide partial protection, but does not account for the entire response. However, the protective effect is likely mediated by glucocorticoid receptors since alternate glucocorticoids such as methyl prednisolone and corticosterone are also effective. Furthermore, the effect can be inhibited by pre-treatment with a glucocorticoid antagonist RU38486. The neuroprotection also appears to be related to alterations in cerebral metabolism. Glucose utilization is reduced prior to hypoxia-ischemia in dexamethasone compared to vehicle treated animal and is better maintained during hypoxia-ischemia in dexamethasone treated animals. In addition, preliminary studies indicate that high energy phosphates in the brain are higher in dexamethasone animals. Thus, glucocorticoids may provide their protection against hypoxic-ischemic damage by decreasing basal metabolic energy requirements and/or increasing the availability or efficiency of use of energy substrates.
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PMID:Glucocorticoids and the prevention of hypoxic-ischemic brain damage. 906 40

Propranolol has been shown to be effective for as long as 5 days in massively burned children to reduce heart rate and cardiac work. This article describes the use of propranolol given for 10 days to burned children to test whether the drug remains effective and safe in reducing heart rate and cardiac work for longer periods. We prospectively studied 22 children, 1 to 10 years of age with burns covering > or = 40% of their total body surface area. These children were treated with 0.5 to 1.0 mg/kg propranolol given orally or intravenously every 8 hours for 10 days. In both septic and nonseptic patients, propranolol significantly decreased their daily average heart rate (between 10% and 13%, p < 0.05) and rate-pressure product (between 10% and 16%, p < 0.05) compared with their 24-hour mean before propranolol treatment. No significant change in mean arterial blood pressure, or plasma urea nitrogen creatinine or glucose levels could be shown. No hypotension, hypothermia, azotemia, hyperglycemia or hypoglycemia, arrhythmia, bronchospasm, or peripheral ischemia was noted during or after treatment. Whereas propranolol lowered heart rate more per milligram per kilogram body weight when given intravenously, both routes were safe and effective. From these data, we conclude that propranolol can be given to decrease the work of the heart safely and effectively for > or = 10 days.
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PMID:Prolonged use of propranolol safely decreases cardiac work in burned children. 916 45

A retrospective, nonrandomized study of blood glucose levels in very young children under 6 kg was undertaken. Each patient underwent the repair of complex congenital heart defects using hypothermia and nonpulsatile cardiopulmonary bypass (CPB). Hyperglycaemia may cause metabolic changes, resulting in reduced glucose transport and cerebral ischaemia. To evaluate the frequency of the occurrence of hyperglycaemia, samples were evaluated for glucose levels in three groups of patients. Group 1 (n = 5) consisted of infants undergoing standard bypass and moderate hypothermia (26 degrees C). Group 2 (n = 5) were infants undergoing low-flow bypass and profound hypothermia (20 degrees C). Group 3 (n = 5) was comprised of infants undergoing total circulatory arrest and profound hypothermia (18 degrees C). Glucose samples were taken preoperatively, during hypothermic bypass, during rewarming and 1-h postoperatively. In group 1, blood glucose levels remained within the normal range (65-100 mg/dl) throughout bypass and in the 1-h postoperative sample. In group 2, blood glucose levels remained within the normal range preoperatively and during the hypothermic bypass period. However, during the rewarming period, the glucose level rose to 185 +/- 17.2 mg/dl. The 1-h postoperative level was also increased to 168 +/- 16.5 mg/dl. Group 3, like group 2, showed that the preoperative and hypothermic glucose values were within the normal range and the rewarming, 133 +/- 29.4, and the 1 h, 130 +/- 33.3 mg/dl, glucose values were hyperglycaemic. This study indicates that blood glucose levels should be monitored routinely, both during and after CPB.
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PMID:Glucose management in the infant under six kilograms. 930 Apr 75


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