Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020672 (hypothermia)
17,327 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Neuropsychological and neurological deficits are still major causes of mortality and morbidity after cardiac operations and are thought to be caused by embolism and cerebral hypoxia. Near-infrared spectrophotometry (NIRS) is a promising method for non-invasive monitoring of cerebral oxygenation and hemodynamics. Different devices provide information on changes of oxygenated (HbO2) and deoxygenated hemoglobin (Hb), oxidized cytochrome aa3 (CytOx) or regional oxygen saturation (rSO2). NIRS has been applied to patients during adult and pediatric cardiovascular surgery with and without deep hypothermic circulatory arrest (DHCA). In most of the studies, significant changes in cerebral oxygenation were detected by NIRS. NIRS measurements were influenced by the cerebral oxygen metabolism and the operative management. However, clinical, experimental, and theoretical issues raise doubts as to the clinical relevance of the hemoglobin saturation (HbO2, Hb, rSO2 signals) during hypothermia and alkalosis, because the oxygen affinity of hemoglobin increases and a high saturation might simply reflect the inadequate oxygen transport into cells. In contrast, recent experiments have proved a high correlation between the CytOx signal and the MRS parameters nucleoside triphosphate and phosphocreatine. Histological damage was significantly related to the lowest CytOx value; in a clinical study it predicted impaired neuropsychological outcome. Therefore, the CytOx signal is of great interest for future studies. NIRS must prove its ability to diagnose cerebral hypoxia consistently during cardiac surgery in a large patient study before this method is brought into routine clinical practice. Absolute quantification and definitions of critical oxygenation margins will be helpful for this goal.
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PMID:Near-infrared spectrophotometry of the brain in cardiovascular surgery. 971 98

Hypothermic cardiopulmonary bypass (CPB) is associated with a high incidence of neuropsychological defects, marked cerebral swelling immediately after surgery and jugular bulb desaturation during rewarming. This suggests cerebral ischaemia may occur, but evidence is indirect. We studied four patients with 31P magnetic resonance spectroscopy (MRS) and four with 1H MRS before and immediately after coronary surgery. There was no visible lactate in 1H MR spectra. In 31P MR spectra, the ratio of phosphocreatine to adenosine triphosphate was maintained (before: 2.13 +/- 0.86 vs after: 2.57 +/- 1.31; mean +/- 1 SD) and there was no intracellular acidosis (intracellular pH: 7.1 +/- 0.04 vs 7.16 +/- 0.08), while phosphocreatine/inorganic phosphate was increased immediately after the operation (2.92 +/- 0.37 vs 6.39 +/- 2.67, p = 0.03). This suggests rebound replacement of energy stores following recovery from temporary cerebral ischaemia during CPB: intra-operative studies would be needed to test this hypothesis further.
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PMID:Magnetic resonance spectroscopy of high-energy phosphates and lactate immediately after coronary artery bypass surgery. 977 17

The rubidium efflux from hypothermic rat hearts perfused by the Langendorff method at 20 degreesC was studied. At this temperature 87Rb-NMR efflux experiments showed the existence of two 87Rb pools: cytoplasmic and mitochondrial. Rat heart mitochondria showed a very slow exchange of mitochondrial Rb+ for cytoplasmic K+. After washout of cytosolic Rb+, mitochondria kept a stable Rb+ level for >30 min. Rb+ efflux from mitochondria was stimulated with 0.1 mM 2, 4-dinitrophenol (DNP), by sarcolemmal permeabilization and concomitant cellular energy depletion by saponin (0.01 mg/ml for 4 min) in the presence of a perfusate mimicking intracellular conditions, or by ATP-sensitive K (KATP) channel openers. DNP, a mitochondrial uncoupler, caused the onset of mitochondrial Rb+ exchange; however, the washout was not complete (80 vs. 56% in control). Energy deprivation by saponin, which permeabilizes the sarcolemma, resulted in a rapid and complete Rb+ efflux. The mitochondrial Rb+ efflux rate constant (k) decreased in the presence of glibenclamide, a KATP channel inhibitor (5 microM; k = 0.204 +/- 0.065 min-1; n = 8), or in the presence of ATP plus phosphocreatine (1.0 and 5.0 mM, respectively; k = 0.134 +/- 0.021 min-1; n = 4) in the saponin experiments (saponin only; k = 0.321 +/- 0.079 min-1; n = 3), indicating the inhibition of mitochondrial KATP channels. Thus hypothermia in combination with 87Rb-NMR allowed the probing of the mitochondrial K+ pool in whole hearts without mitochondrial isolation.
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PMID:Measurements of mitochondrial K+ fluxes in whole rat hearts using 87Rb-NMR. 988 35

Numerous techniques are used to maintain intraoperative heart viability. The studies presented here evaluated heart function and metabolism after various periods of preservation up to 4 hours with intermittent warm and cold blood perfusion. Using a heterotopic heart model cooled to 10 degrees C and maintained for 1, 2, 3, and 4 hours, various preservation techniques were compared. Changes in myocardial metabolism were determined from substrate uptakes and biopsy samples of the left ventricular muscle for high-energy phosphates. Preservation techniques included: (1) sustained hypothermia, (2) 1 or 2 hours of sustained warm blood perfusion with fibrillation, (3) intermittent cold blood perfusion during 2, 3, and 4 hours of preservation, (4) intermittent warm blood perfusion during 2, 3, and 4 hours of preservation and (5) a control group (no preservation). Normothermic fibrillation had no effect on postpreservation functional or metabolic parameters. Sustained hypothermia reduced functional recovery proportional to the length of ischemia. The cold intermittent procedures maintained function and metabolism better than sustained hypothermia, while warm intermittent preservation maintained function and metabolism at control levels throughout the recovery period for all preservation techniques. Changes in ATP mirrored the functional changes. Creatine phosphate (CP) was markedly reduced during heart isolation and preservation and exceeded the control by 100% during reperfusion. For operative procedures of 2 hours or less, functional and metabolic recovery was not affected by the various preservation methods applied. Warm intermittent perfusion during hypothermic preservation offered the best protection for the myocardium. The warming cycles during hypothermia may provide some degree of preconditioning and protect the myocardium during reperfusion.
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PMID:Comparison of intermittent warm and cold blood perfusion during hypothermic myocardial preservation on functional and metabolic recovery. 1102 71

This study was done to determine the effects of hypothermia on brain cell membrane function and energy metabolism after transient hypoxia-ischemia (HI) in the newborn piglet. Cerebral HI was induced by temporarily complete occlusion of bilateral common carotid arteries with surgical clips and simultaneous breathing with 8% oxygen for 30 min, followed by release of carotid occlusion and normoxic ventilation for 4 hr. Rectal temperature was maintained between 38.0 and 39.0 degrees C in normothermic groups, and between 34.0 and 35.0 degrees C in hypothermic groups for 4 hr after HI. During HI, heart rate, glucose and lactate level in the blood and cerebrospinal fluid increased, and base excess, pH and blood pressure decreased significantly in both normothermic and hypothermic groups. After HI, these abnormalities returned to normal in normothermic group, but lactic acidosis persisted in hypothermic group. Decreased cerebral Na+,K+- ATPase activity and increased lipid peroxidation products, indicative of HI- induced brain injury, were more profound in hypothermic group than in normothermic group. Brain ATP and phosphocreatine levels were not different between normothermic and hypothermic groups. In summary, hypothermia applied immediately after HI for 4 hr did not improve the recovery of brain cell membrane function and energy metabolism in the newborn piglet.
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PMID:Effect of hypothermia on brain cell membrane function and energy metabolism after transient global hypoxia-ischemia in the newborn piglet. 1141 Jun 96

We evaluated the anti-inflammatory and neuroprotective effects of hypothermia during the early phase of experimental Escherichia coli meningitis in the newborn piglet. Hypothermia significantly attenuated the meningitis-induced acute inflammatory responses such as increased intracranial pressure, decreased glucose level, increased lactate concentration, increased tumor necrosis factor-alpha level and leukocytosis in the cerebrospinal fluid. Decreased cerebral cortical cell membrane Na+,K+-ATPase activity and increased lipid peroxidation products, indicative of meningitis-induced brain damage, were significantly improved with hypothermia. Hypothermia also significantly improved the meningitis-induced reduction in brain ATP and phosphocreatine levels. In summary, hypothermia significantly attenuated the acute inflammatory responses and the ensuing brain injury in experimental neonatal bacterial meningitis.
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PMID:Effect of hypothermia on brain cell membrane function and energy metabolism in experimental Escherichia coli meningitis in the newborn piglet. 1149 47

Our aim was to assess brain myo-inositol/creatine plus phosphocreatine (Cr) in the first week in term infants with neonatal encephalopathy using localized short echo time proton magnetic resonance spectroscopy and to relate this to measures of brain injury, specifically lactate/Cr in the first week, basal ganglia changes on magnetic resonance imaging (MRI), and neurodevelopmental outcome at 1 y. Fourteen term infants with neonatal encephalopathy of gestational age (mean +/- SD) 39.6 +/- 1.6 wk, birth weight 3270 +/- 490 g, underwent MRI and magnetic resonance spectroscopy at 3.5 +/- 2.1 d. Five infants were entered in a pilot study of treatment with moderate whole-body hypothermia for neonatal encephalopathy; two were being cooled at the time of the scan. T(1)- and T(2)-weighted transverse magnetic resonance images were graded as normal or abnormal according to the presence or absence of the normal signal intensity of the posterior limb of the internal capsule and signal intensity changes in the basal ganglia. Localized proton magnetic resonance spectroscopy data were obtained from an 8-cm(3) voxel in the basal ganglia using echo times of 40 and 270 ms, and the peak area ratios of myo-inositol/Cr and lactate/Cr were measured. Outcome was scored using Griffith's development scales and neurodevelopmental examination at 1 y. MRI and outcome were normal in six infants and abnormal in eight. myo-Inositol/Cr and lactate/Cr were higher in infants with abnormal MRI and outcome (p < 0.01, p < 0.01, respectively). myo-Inositol/Cr and lactate/Cr were correlated (p < 0.01) and were both correlated to the Griffith's developmental scales (p < 0.01, p < 0.01, respectively). In conclusion, these preliminary data suggest that early increases in brain basal ganglia myo-inositol/Cr in infants with neonatal encephalopathy are associated with increased lactate/Cr, MRI changes of severe injury, and a poor neurodevelopmental outcome at 1 y.
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PMID:Early increases in brain myo-inositol measured by proton magnetic resonance spectroscopy in term infants with neonatal encephalopathy. 1172 26

The aim of this study was to evaluate the effects of hypothermia on bilirubin-induced alterations in brain cell membrane function and energy metabolism in the developing brain. Thirty-seven newborn piglets were divided randomly into four groups: normothermic control (NC, n=9); hypothermic control (HC, n=7); normothermic bilirubin infusion (NB, n=11); and hypothermic bilirubin infusion (HB, n=10) groups. In bilirubin infusion groups (NB and HB), a loading dose of bilirubin (35 mg/kg) was given over 5 min, followed by a continuous infusion (25 mg/kg/h) for 4 h. The control groups (NC, HC) received a bilirubin-free buffer solution. Sulfadimethoxine was administered to animals in all experimental groups. Rectal temperature was maintained between 38.0 and 39.0 degrees C in normothermic groups, and between 34.0 and 35.0 degrees C in hypothermic groups for 4 h after the start of bilirubin infusion. The final blood and brain bilirubin concentrations in the bilirubin infusion groups (NB and HB) were not significantly different. Decreased cerebral cortical cell membrane Na(+),K(+)-ATPase activity and increased lipid peroxidation products observed in the NB group, indicative of bilirubin-induced brain damage, were significantly attenuated in the HB group. Hypothermia also significantly improved the bilirubin-induced reduction in brain ATP and phosphocreatine levels and increase in blood and brain lactate levels. In summary, hypothermia significantly attenuated the bilirubin-induced alterations in brain cell membrane function and energy metabolism in the newborn piglet. These findings suggest the possibility that hypothermia could be a good neuroprotective therapeutic modality in neonatal bilirubin encephalopathy.
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PMID:Effect of hypothermia on bilirubin-induced alterations in brain cell membrane function and energy metabolism in newborn piglets. 1174 60

Since hypothermia may be a potential treatment for perinatal cerebral hypoxic-ischemic injury, we used an established neonatal model of hypoxia-ischemia to determine the time after injury at which cooling had the best protective effect. Fourteen-day-old Wistar rats were subjected to right carotid artery ligation and hypoxia (8% O(2) for 90 min). Immediately at the end of hypoxia (defined as 0h), animals were either maintained at normal body temperature until sacrifice (normothermia) or subjected to hypothermia. In a preliminary study, the effects of a reduction in temperature and the duration of such cooling were investigated; animals were cooled (until brain temperature reached 33 degrees C or 30 degrees C) for 2, 4, or 6 h commencing immediately after hypoxia. In a second study, animals were cooled (brain temperature 30 degrees C) for 6 h commencing at either 0, 2, 4, or 6 h after the end of hypoxia. Sham-operated animals were used as controls. Twenty-four hours after hypoxia-ischemia, cerebral energy metabolism was measured by phosphorus magnetic resonance spectroscopy, and at 5 d cerebral infarction was measured by planimetry. In normothermic animals the ratio of phosphocreatine/inorganic phosphate (PCr/Pi) had fallen markedly 24 h following hypoxia-ischemia. In contrast, animals cooled between 6 and 12 h displayed high PCr/Pi ratios similar to those in control animals. Similarly, after 5 d, infarct area was significantly reduced only in animals cooled between 6 and 12 h after injury. These results indicate that cooling between 6 and 12 h after hypoxia-ischemia is more effective in reducing cerebral injury than other cooling regimes and suggest that the physiologic events during this period are critical for understanding cerebral infarction.
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PMID:Improved neuroprotection with hypothermia delayed by 6 hours following cerebral hypoxia-ischemia in the 14-day-old rat. 1175 34

The aim of this study was to compare the ischemic and postischemic energetic changes of rat skeletal muscle in response to hypothermia or room temperature, monitored noninvasively and continuously by in vivo (31)P-magnetic resonance spectroscopy ((31)P-MRS). A model of pedicled rat rectus femoris muscle was developed and analyzed by in vivo (31)P-MRS at a magnetic field strength of 2.35 T. Measurements were performed at three time points: before ischemia, after 4 hours of ischemia, and after 1 hour of reperfusion. Three groups were studied: (1) sham-operated rats (n = 6); (2) rats subjected to room temperature (24-26 degrees C, n = 6); and (3) rats subjected to hypothermia (9-12 degrees C, n = 6). Blood perfusion was measured by laser Doppler flowmetry (LDF). In the hypothermic group, phosphocreatine (PCr) recovered to 75% and adenosine triphosphate (ATP) to 86%; in the room temperature group, the recovery was 53% and 51%, respectively (P < 0.05). Skeletal muscle subjected to hypothermia (9-12 degrees C) was found to recover to a higher postischemic energetic level compared with skeletal muscle subjected to room temperature. Hypothermia appears to be a simple and effective method with which to reduce the damage related to ischemia and reperfusion.
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PMID:Effect of hypothermia on the ischemic and reperfused rat skeletal muscle, monitored by in vivo (31)P-magnetic resonance spectroscopy. 1175 63


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