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

Changes in rectal and skin temperatures following intraventricular injection of biogenic amines and related substances were investigated in rats. Intraventricular injection of norepinephrine in a small dose (6 mug) produced a slight elevation of rectal temperature, but in larger amounts (25-50 mug) resulted in a dose-dependent hypothermia which was associated with a marked rise of skin temperature. No change was observed in plasma free fatty acid and glucose levels and oxygen consumption after intraventricular injection of norepinephrine (25 mug). Intraventricular injection of imipramine and safrazine produced a slight fall in the rectal temperature. Norepinephrine-induced hypothermia was more pronounced in rats pretreated with safrazine and less in rats pretreated with alpha-methyl-p-tyrosine, as compared with that in controls. Intraventricular injection of 6-hydroxydopamine (0.75-250 mug) brought about a marked dose-dependent hypothermia. The second injection of 6-hydroxydopamine 5 days after the first injection had no effect on the body temperature. Norepinephrine injection 2 days after the second injection of 6-hydroxydopamine produced a more pronounced hypothermia than the change in control rats without pretreatments. Haloperidol did not affect the hypothermia induced by 6-hydroxydopamine. Intraventricular injection of dopamine and L-DOPA showed less effect that norepinephrine had. Intraventricular injection of phenoxybenzamine prior to norepinephrine blocked the hypothermia and skin temperature elevation which are normally observed following norepinephrine injection, while propranolol given in the same way showed less or no effect. Intraventricular injection of phenylephrine produced a dose-dependent hypothermia, whereas no dose-response relationship was obtained by isoproterenol. These results suggest that in the rat the hypothermic effect of norepinephrine injected intraventricularly is mediated by an action of central alpha-receptor. At high and low ambient temperatures hypothermia was similarly observed following intraventricular injection of 5-hydroxytryptamine (25 mug) as at normal room temperature. On the other hand, norepinephrine (25 mug) produced a rise in rectal temperature at high ambient temperature and a marked fall at low ambient temperature. The hypothermic effect of norepinephrine was not different between cold-adapted ones at room temperature. From the results the role of norepinephrine and other biogenic amines in the brain in thermoregulatory processes was discussed.
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PMID:[Role of brain biogenic amines in the central thermoregulatory mechanism of the rat (author's transl)]. 124 80

Because use of the bubble oxygenator during open-heart surgery is associated with complications such as hemolysis, pulmonary insufficiency and oliguria, a membrane oxygenator was used in conjunction with hypothermia in 37 infants. The main features of the oxygenator are gravitational blood flow, oxygenation into an airless, collapsible blood reservoir, low-flow roller pump flow back to the patient, accurate determination of flows and careful use of a heat exchanger. Gas flow (98% oxygen, 2% carbon dioxide) for the unit of 2 m2 is maintained at 3 to 4 1/min. Specific precautions are taken to ensure absence of bubbles. Three prime solutions are used, the final one having an osmolality of 381 mOsmol and containing 129.9 meq of sodium, 3.8 of potassium and 94.0 of chloride and 2001 mg/dl of glucose. Six patients died, but none of the deaths could be directly related to the use of the oxygenator. Respiratory complications were minimal, as were other complications. The technique is reliable in oxygenating blood in an tracorporeal circulation, but further familiarity with the membrane oxygenator for use in open-heart surgery in infants is desirable before firm conclusions can be drawn as to its value.
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PMID:Use of a membrane oxygenator for open-heart surgery in infants. 126 May 50

Brain death is associated with loss of hypothalamic, pituitary and brain stem function resulting in apnea, bradycardia and hypotension, poikilothermia, and diabetes insipidus. In order to preserve body functions mechanical ventilation is continued with the aim to maintain an arterial partial pressure of oxygen of more than 100 mmHg. Previous fluid restrictions and the application of diuretics during the treatment of high intracranial pressure frequently result in dehydration. Progressive vasodilation may induce severe hypotension and fluid replacement with cristalloids and if necessary colloids may be called for until the central venous pressure reaches 10 cm H2O. Continuous substitution of potassium and the use of hypotonic solutions such as glucose 5% may avoid hypokalaemia and hypernatraemia, respectively. Inotropic support with dopamine (5-10 micrograms/kg.min) or adrenaline (0.01-0.1 micrograms/kg.min) may be needed to maintain normal mean arterial blood pressure (65 mmHg). Polyuria (5000 ml/24 h) can be treated by continuous intravenous infusion of antidiuretic hormone (0.5-2-10 U/h). Hypothermia must be prevented by warming all fluids (37 degrees C) and covering the patient with heat saving blankets.
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PMID:[Management of the organ donor]. 128 68

Recent studies have demonstrated that small (i.e., 2-5 degrees C) reductions in temperature may protect the brain and spinal cord from ischemic injury. The present study evaluated the physiologic response of anesthetized animals to convective-based cooling and warming. Six shaved, isoflurane-anesthetized (1.50% end-expired; 1 MAC), pancuronium-paralyzed dogs were subjected to temperature manipulation. The flow of cool (13-14 degrees C) or warm (39-41 degrees C) air was uniformly applied to the the dorsal and lateral surfaces of the dog using an inflatable blanket with perforations in the interior surface. Convective cooling reduced pulmonary artery temperature (Tpa) from 37.0 +/- 0.2 degrees C (Mean +/- S.D.) to 33.0 +/- 0.0 degrees C over a 93 +/- 18 min period. Thereafter, the active cooling was discontinued and passive cooling resulted in a further reduction in Tpa to 32.4 +/- 0.3 degrees C over the next 60 min. Institution of convective warming resulted in an increase in Tpa from 32.4 +/- 0.3 to 33.0 +/- 0.0 degrees C in 23 +/- 14 min and from 33.0 to 37.0 +/- 0.0 in an additional 137 +/- 26 min. During the periods of active cooling, passive cooling and active warming, there were strong correlations between Tpa and temperature within the brain, cisterna magna, parietal epidural space, lumbar subarachnoid space and other commonly used temperature measurement sites non-invasively monitored (e.g. tympanic membrane, esophagus, rectum) r greater than or equal to 0.97; P less than 0.0001). The combination of isoflurane anesthesia (a potent EEG-suppressor) plus mild hypothermia (less than 34 degrees C) resulted in an EEG attenuation in five dogs, two of which progressed to burst suppression. The magnitude of EEG changes correlated with the degree of temperature reduction. Upon rewarming to 37 degrees C, all dogs had normal EEG activity and normal brain concentrations of high energy phosphates, glucose and lactate. Blood pressure and cardiac output did not change during the study and no dog exhibited acid-based anomalies or blood lactate accumulation. Whole body oxygen consumption and heart rate decreased in a temperature-dependent fashion. Cardiac rhythm disturbances were rare. The authors conclude that convection-based corporeal cooling and rewarming are efficacious methods for non-invasively and uniformly altering CNS temperatures without adversely affecting cerebral or systemic physiology.
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PMID:The effects of convective cooling and rewarming on systemic and central nervous system physiology in isoflurane-anesthetized dogs. 132 72

The effects of plain ischemia (34 degrees C) and the protective role of hypothermia (20 degrees C) alone or in combination with cardioplegia (St Thomas' Hospital [STH] or glucose-potassium-nifedipine [GPN]) on the intracellular kinetics of the activator calcium of cardiac muscle were quantified and compared from the interval-force behaviour (mechanical restitution) of right and left ventricles of the perfused rat heart. Plain ischemia caused a major depression in the restitution of force of contraction of both ventricles, deranged the mixed linear-exponential functions by significantly increasing the time constants of the fitted mechanical restitution curves (MRC) and altered the control right/left ventricle interval-force relationship. The right ventricle was found to be more susceptible to ischemic damage than the left ventricle, and its inotropic reserve was virtually abolished by 1 h of plain ischemia. Hypothermic preservation during ischemia improved the mechanical restitution, salvaged the inotropic reserve and optimized right/left ventricle interval-force relationship, but the time constants of the fitted MRCs were still prolonged. However, both the cardioplegic formulations were equally effective in normalizing the time constants of the fitted curves. In general, right ventricle functions were better preserved by STH cardioplegia and left ventricle functions were better preserved by GPN cardioplegia. Cardioplegic interventions did not further improve the ventricular inotropic reserve compared with hypothermic preservation. Additional beneficial effects of cardioplegic formulations were directed towards stabilizing the linear-exponential functions and hence restitution of force of contraction.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Intracellular kinetics of the activator calcium of rat heart after ischemic arrest and cardioplegia: quantitative comparison of right and left ventricles. 137 92

Many aspects of peri-operative management of the diabetic patient remain controversial, although there are a variety of approaches towards management. These patients are at risk for certain complications related to the severity and chronicity of the disease. The surgeon and the anaesthetist must be conversant with the management of diabetes in elective and emergency situations. Reasonable metabolic control can be achieved within a few hours pre-operatively and clinical assessment can be performed on an out-patient basis. Anaesthetic management consists of assessment of the control of the disease followed by evaluation of diabetic complications and their severity. Different views are expressed regarding tight control of blood glucose level (4-8 mmol/l) versus moderate control (8-12 mmol/l) when managing diabetic patients. The importance of guarding against factors favouring metabolic decompensation in the peri-operative period, is stressed. Minor or major surgery has important implications regarding the management of diabetes. All patients scheduled for major surgery should be treated with intravenous insulin. Blood sugar should be monitored at regular intervals to protect the patient against hypoglycaemia. Emergency surgery is usually associated with an infectious process. Pronounced hyperglycaemia, dehydration and metabolic derangement may be present. The underlying pathology may aggravate the diabetic state and surgery may actually improve the patient's condition. It is unnecessary to postpone surgery to treat ketosis fully, because this may need 12-24 hours. Extreme insulin resistance and greater insulin requirements are present during cardiopulmonary bypass, hypothermia and rewarming. Beware of severe hypoglycaemia after cardiopulmonary bypass.
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PMID:Routine peri-operative management of the diabetic patient. 141 7

We have studied the effects of propofol, given to maintain EEG suppression throughout cardiopulmonary bypass (CPB), in 20 children aged 1-15 yr, in a parallel group comparison. Anaesthesia was produced by fentanyl 50 micrograms kg-1, enflurane or halothane and midazolam 0.1 mg kg-1 at the start of CPB. After randomization, 50% of the children also received propofol during CPB. All children were cooled during CPB (25-28 degrees C) and pump flows (non-pulsatile) were 2.4 litre min-1 m-2, reducing to 1.2-1.6 litre min-1 m-2 during hypothermia. Large rates of infusion of propofol were required to maintain EEG suppression, particularly during rewarming. Compared with control, the propofol group showed significant increases in mixed venous oxygen saturation and significant reductions in systemic oxygen uptake and glucose and cortisol concentrations. There were no differences in triiodothyronine and lactate concentrations, mean arterial pressure during CPB and inotrope requirement after CPB, or in recovery times.
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PMID:EEG burst suppression with propofol during cardiopulmonary bypass in children: a study of the haemodynamic, metabolic and endocrine effects. 141 43

The objective of this study was to assess the influence of temperature on the coupling among energy failure, depolarization, and ionic fluxes during anoxia. To that end, we induced anoxia by cardiac arrest in anesthetized rats maintained at a body temperature of either 34 degrees C or 40 degrees C, measured extracellular K+ concentration (K+e), and froze the neocortex through the exposed dura for measurements of phosphocreatine (PCr), creatine (Cr), ATP, ADP, and AMP, glucose, glycogen, pyruvate and lactate content after ischemic intervals of maximally 130 s. Free ADP (ADPf) concentrations were derived from the creatine kinase equilibrium. Hypothermia reduced the initial rate of rise in K+e, and delayed the terminal depolarization; however, both hypo- and hyperthermic animals showed massive loss of ion homeostasis at a K+e of 10-15 mM. The initial rate of rise in K+e did not correlate to changes in ATP, or ATP/ADPf ratio, suggesting that temperature changes per se may control the degree of activation of K+ conductances. The results clearly showed that, in both hyper- and hypothermic subjects, energy failure preceded the sudden activation of membrane conductances for ions. The results indicate that temperature primarily influences membrane permeability to ions like K+e (and Na+), and that cerebral energy state is secondarily affected. It is proposed that the higher rate of rise of K+e at high temperatures accelerates ATP hydrolysis primarily by enhancing metabolic rate in glial cells.
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PMID:Changes of labile metabolites during anoxia in moderately hypo- and hyperthermic rats: correlation to membrane fluxes of K+. 142 48

Magnetic resonance (MR) may be used for repeatedly and non-invasively imaging the brain. Until now, no studies have used this approach to study the effects of carbon monoxide (CO) poisoning in a defined animal model. Conscious, Levine-prepared female rats (unilateral carotid artery and jugular vein occlusion) were exposed to 2400 ppm CO for 90 min, with or without the infusion of 50% glucose solution; CO-stimulated increases in blood glucose and lactate occurred in both groups, while blood pressure and body temperature fell. One to four hours following termination of CO exposure, increased cortical pixel intensity, cortical surface area and brain midline shift were observed on the operated side of the brain in some rats of both groups (i.e. responders = R), providing evidence of edema. At sacrifice, 5 h following termination of CO exposure, gross water content was increased on the left side in the corresponding cortical slices in R rats, providing another measure of edema. Significant positive correlations were found between left to right pixel intensity difference and water content difference, and between the extent of midline shift and water content difference. The elevations of blood glucose and lactate concentrations, and the magnitudes of CO-induced hypothermia and hypotension were similar to those in past studies, but appeared to exert no effect on the severity of cortical edema in terms of differences in pixel intensity, surface area, midline shift or gross tissue water content. Thus, the observed differences between the R rats is not explained by the available data.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Magnetic resonance imaging of the rat brain following acute carbon monoxide poisoning. 145 74

To ascertain the alterations in cerebral oxidative and energy metabolism that occur during hypothermic circulatory arrest, nitrous oxide-anesthetized, paralyzed, and artificially ventilated newborn dogs were surface cooled to 18-20 degrees C, after which their hearts were arrested with KCl. At 10, 30, 60, and 105 min of circulatory arrest, their brains were prepared by in situ freezing for the regional analysis of glycolytic intermediates and high-energy phosphate reserves. Hypothermia alone was associated with optimal preservation of labile metabolites in brain, even in caudal brainstem and cerebellum, compared with barbiturate-anesthetized littermates. After onset of hypothermic circulatory arrest, glucose decreased progressively in cerebral cortex, caudate nucleus, hippocampus, and subcortical white matter to negligible levels by 30 min. Pyruvate increased transiently (+50%) at 10 min, whereas lactate increased and plateaued (10-11 mmol/kg) at 30 min. The disproportionate increases in pyruvate and lactate resulted in a progressive rise in the lactate/pyruvate ratio. Phosphocreatine fell precipitously to < 0.5 mmol/kg in all structures, with a preservation of ATP for the first 10 min of cerebral ischemia. Thereafter, ATP decreased to < 0.1 mmol/kg in cerebral cortex and between 0.1 and 0.2 mmol/kg in caudate nucleus, hippocampus, and white matter. Total adenine nucleotides (ATP+ADP+AMP) were partially depleted by 30 min in the gray matter structures but were unchanged from control for 60 min in white matter. The findings showed a direct correlation between preservation of cerebral energy stores during hypothermic circulatory arrest and the selective resistance of subcortical white matter to ischemic damage.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Cerebral oxidative metabolism during hypothermia and circulatory arrest in newborn dogs. 148 Apr 56


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