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

Severely birth-asphyxiated human infants develop delayed ("secondary") cerebral energy failure, which carries a poor prognosis, during the first few days of life. This study tested the hypothesis that mild hypothermia after severe transient cerebral hypoxia-ischemia decreases the severity of delayed energy failure in the newborn piglet. Six piglets underwent temporary occlusion of the common carotid arteries and hypoxemia. Resuscitation was started when cerebral [phosphocreatine (PCr)]/[inorganic phosphate (Pi)] as determined by phosphorus magnetic resonance spectroscopy had fallen almost to zero and [nucleotide triphosphate (NTP)]/[exchangeable phosphate pool (EPP)] had fallen below about 30% of baseline. Rectal and tympanic temperatures were then reduced to 35 degrees C for 12 h after which normothermia (38.5 degrees C) was resumed. Spectroscopy results over the next 64 h were compared with previously established data from 12 piglets similarly subjected to transient cerebral hypoxia-ischemia, but maintained normothermic, and six sham-operated controls. The mean severity of the primary insult (judged by the time integral of depletion of [NTP]/[EPP]) was similar in the hypothermic and normothermic groups. In the normothermic group, [PCr]/[Pi] and [NTP]/[EPP] recovered after the acute insult and then fell again. Minimum values for these variables observed between 24 and 48 h were significantly higher in the hypothermic group and not significantly different from the control values (p < 0.05, analysis of variance). A large reduction in secondary energy failure relative to the extent of the primary insult was shown and no further fall in either [PCr]/[Pi] or [NTP]/[EPP] took place up to 64 h in the hypothermic piglets.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Mild hypothermia after severe transient hypoxia-ischemia ameliorates delayed cerebral energy failure in the newborn piglet. 760 88

Blood acid-base changes were studied during acute hypothermia (4-6 h) induced by cold exposure in the unanesthetized rat. Stewart's quantitative analysis was applied as a complementary approach to determine the relative contributions of several non-respiratory components to the arterial acid-base response. Acute decrease in body temperature (TB) lowered PaCO2 (32.5 to 14.5 mmHg) and [HCO3-]a(24.20 mEq/L to 17.56 mEq/L), increased pHa (7.481 to 7.608) and diminished the [OH-]/[H+] ratio, but had no significant effect on [SID] or [Atot], although both total phosphorus [PT] and inorganic phosphate [Pi] increased. The acid-base changes found were intermediate between those predicted by alpha-stat and pH-stat hypotheses. Deviation from the regulative alpha-imidazole strategy was more apparent in the plasma than in the intraerythrocyte compartment. We conclude that blood pH changes observed were mainly caused by increased relative ventilation (lung ventilation per unit of CO2 removed) and by resulting changes in PCO2, with a minor metabolic component but without significant contribution from ionic shifts or changes in plasma protein concentration.
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PMID:Factors influencing acid-base status during acute severe hypothermia in unanesthetized rats. 762 15

Erythrocyte osmotic fragility and plasma ionic composition were studied in rats subjected to acute hypothermia. A decrease in osmotic fragility and a significant increase in plasma magnesium and total phosphorus were observed in blood from hypothermic rats in relation to control. A decrease in erythrocyte osmotic fragility from hypothermic animals was observed when the test was performed at 37 degrees C, whereas osmotic fragility was unaltered if the test was carried out at body temperature. This could be interpreted as an adaptative response to counteract the opposite effect on erythrocyte osmotic fragility observed at low temperature 'in vitro'.
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PMID:Erythrocyte osmotic resistance during acute hypothermia in awake unrestrained rats. 825 42

The effects of hypothermia on the intracellular pH of human erythrocytes were studied non-invasively using 31P NMR spectroscopy and the endogenous phosphorus-containing compounds glycerate 2,3-bisphosphate and inorganic phosphate. Specifically, the pH dependence of the 31P NMR chemical shifts of these compounds was used to measure the intracellular pH at 25 and 37 degrees C. The possibility of a non-pH-dependent change on the chemical shifts of the 2-P and 3-P resonances of glycerate 2,3-bisphosphate due to the presence of paramagnetic deoxy-haemoglobin (i.e., a pseudo-contact interaction) was investigated and found to have negligible effect under the present experimental conditions. The most probable reasons for this are that the deoxy-haemoglobin concentration was too small and/or the glycerate 2,3-bisphosphate does not get sufficiently close to the paramagnetic centre to be affected. The change in intracellular pH with temperature was consistent with that predicted by the alphastat hypothesis.
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PMID:The effects of hypothermia on the intracellular pH of erythrocytes studied using 31P NMR and endogenous compounds. 839 80

A miniature piglet model that replicates clinical hypothermic (14 degrees C nasopharyngeal) circulatory arrest and low-flow (50 ml/kg per minute) bypass was used to study carotid blood flow with electromagnetic flow probe, cerebral blood flow by microsphere injection, cerebral metabolic rate by arteriovenous oxygen and glucose extractions, lactate production by cerebral arteriovenous difference, and cerebral edema. Data from five animals that underwent circulatory arrest and five animals that underwent low-flow bypass (aged 28.8 +/- 0.4 [mean +/- standard error of the mean] days) were analyzed. The duration of circulatory arrest and low-flow bypass was 1 hour. In a parallel study with the same animal model, phosphorus 31 magnetic resonance spectroscopy was used to assess cerebral phosphocreatine, nucleoside triphosphate (adenosine triphosphate), and intracellular pH. Five animals (aged 31.8 +/- 1.1 days) underwent circulatory arrest, and five underwent low-flow bypass. A brief phase of hyperemic carotid blood flow was seen immediately after the onset of reperfusion in the circulatory arrest group but not in the low-flow group. In the circulatory arrest and low-flow bypass groups, cerebral blood flow (percentage of baseline 71.2% +/- 8.3% and 69.1% +/- 5.8%, respectively), cerebral oxygen consumption (45.6% +/- 10.0%, 44.5% +/- 7.6%), and cerebral glucose consumption (31.5% +/- 30.7%, 83.5% +/- 24.2%) remained depressed after 45 minutes of reperfusion and rewarming to normothermia. However, after 3 more hours of pulsatile normothermic reperfusion, cerebral oxygen consumption and cerebral glucose consumption had returned to baseline. Phosphocreatine, adenosine triphosphate, and pH were maintained at or above baseline levels throughout low-flow bypass and throughout 3 hours of normothermic reperfusion. In contrast, both phosphocreatine and adenosine triphosphate became undetectable 32 +/- 3.7 minutes after onset of circulatory arrest. During and early after circulatory arrest, pH decreased to a minimum of 6.506 +/- 0.129 at 40 minutes after reperfusion. After 3 hours of normothermic reperfusion, phosphocreatine and adenosine triphosphate recovered to 98.6% +/- 9.0% and 90.1% +/- 13.5% of baseline, respectively, and pH was 7.087 +/- 0.051, similar to baseline (7.1755 +/- 0.041). In the low-flow bypass group, the disparity between the depressed level of cerebral oxygen consumption and normal high-energy phosphate levels may reflect incomplete cerebral rewarming or decreased energy consumption. In the circulatory arrest group, the parallel recovery of oxygen consumption and high-energy phosphates eventually achieving baseline levels suggests that the degree of hypothermia used provides adequate protection for acute cerebral recovery after 1 hour of circulatory arrest.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Recovery of cerebral blood flow and energy state in piglets after hypothermic circulatory arrest versus recovery after low-flow bypass. 841 62

Recent studies have shown that mild to moderate (modest) hypothermia decreases the damage resulting from hypoxic-ischemic insult (HI) in the immature rat. To determine whether suppression of oxidative metabolism during HI is central to the mechanism of neuroprotection, 31P nuclear magnetic resonance (NMR) spectroscopy was used to measure high energy metabolites in 7-d postnatal rats under conditions of modest hypothermia during the HI. The rats underwent unilateral common carotid artery ligation followed by exposure to hypoxia in 8% oxygen for 3 h. Environmental temperature was decreased by 3 or 6 degrees C from the control temperature, 37 degrees C, which reliably produces hemispheric damage in over 90% of pups. The metabolite parameters and tissue swelling (edema) at 42 h recovery varied very significantly with the three temperatures. Tissue swelling was 26.9, 5.3, and 0.3% at 37, 34, and 31 degrees C, respectively. Core temperature and swelling were also measured, with similar results, in parallel experiments in glass jars. Multislice magnetic resonance imaging, histology, and triphenyltetrazolium chloride staining confirmed the fairly uniform damage, confined to the hemisphere ipsilateral to the ligation. The NMR metabolite levels were integrated over the last 2.0 h out of 3.0 h of HI, and were normalized to their baseline for all surviving animals (n = 25). ATP was 47.9, 69.0, and 83.0% of normal, whereas the estimator of phosphorylation potential (phosphocreatinine/inorganic phosphorus) was 16.9, 27.8, and 42.6% of normal at 37, 34, and 31 degrees C, respectively. There was a significant correlation of both phosphocreatinine/inorganic phosphorus (p < 0.0001) and ATP levels (p < 0.0001) with brain swelling. Abnormal brain swelling and thus damage can be reliably predicted from a threshold of these metabolite levels (p < 0.0001). Thus for all three temperatures, a large change in integrated high energy metabolism during HI is a prerequisite for brain damage. With a moderate hypothermia change of 6 degrees C, where there is an insufficient change in metabolites, there is no subsequent HI brain damage. In general, treatment for HI in our 7-d-old rat model should be aimed at preserving energy metabolism.
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PMID:Modest hypothermia preserves cerebral energy metabolism during hypoxia-ischemia and correlates with brain damage: a 31P nuclear magnetic resonance study in unanesthetized neonatal rats. 935 46

The effect of low temperature on cytosolic pH regulation and buffering capacity was evaluated in the isolated rat liver. The pH changes were followed by phosphorus-31 nuclear magnetic resonance. Cooling from 37 to 4 degrees C, with Krebs-Heinseleit perfusion at an external pH of 7.35, induced an alkaline shift in cytosolic pH (pHcyt) of 0.13 or 0.75 pH units in the presence of bicarbonate, respectively (dpH cys/dT values were 0.004 and 0.022 unit/degrees C. With 4 degrees C perfusion, in the presence or absence of bicarbonate, acute changes of external pH (from 7.40 to 5.90) did not affect pHcyt. In contrast, intracellular loading with isobutyric acid or NH4Cl induced rapid pHcyt variations. The intrinsic buffering power value (10 to 50 slykes) measured in the absence of bicarbonate depended on pHcyt. The larger value was observed for pHcyt 7.30, a value near the pK value of the imidazole group of intracellular proteins at 4 degrees C. The presence of bicarbonate modified the amplitude of the pHcyt change by increasing the total buffering power. It was demonstrated that during hypothermia, ionic carriers are inactivated and the charged forms of molecules are unable to cross the cell membrane; thus, the pHcyt homeostasis depends essentially on intracellular buffering power.
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PMID:Cytosolic pH variations in perfused rat liver at 4 degrees C: role of intracellular buffering power. 965 31

Isolated rat hepatocytes were suspended and stored in either Liebovitz-15 medium (37 degrees C or 4 degrees C) or University of Wisconsin (UW) solution (4 degrees C) containing [(3)H] arachidonic acid (AA). At varying times, membrane phospholipids were separated by thin layer chromatography. AA labeled phospholipids similarly at both 4 degrees C and 37 degrees C. Analysis of the ratios of [(3)H] AA and [(14)C] glycerol incorporated into phosphatidic acid or other phospholipids in dual-labeled cells indicated that the deacylation/reacylation cycle was the major route of AA incorporation at hypothermia. This was supported by showing that blocking phospholipase A(2) (PLA(2)) activity by trifluoperazine suppressed AA incorporation into phospholipids. PLA(2) activity, measured by determining the release of AA, was slow during 48-hour cold storage, but increased significantly when ATP was depleted by inhibition of mitochondria and glycolysis. In the whole rat liver, there was no significant loss of phospholipids during 48-hour storage (total phospholipids [micromol phosphorus/L/mg] : 0.197 +/-. 001 at 0 hours) unless energy blockers were used (0.155 +/-.005 at 48 hours) or glycogen depleted by fasting the rat (0.167 +/-.001 at 48 hours). This study shows that a net PLA(2) stimulated hydrolysis of phospholipids is seen only when ATP is depleted and its generation from anaerobic glycolysis inhibited. Thus, PLA(2) hydrolysis of phospholipids is not a significant cause of liver cell injury during cold storage when livers are obtained in optimal condition. However, conditions affecting the generation of ATP during cold storage could alter PLA(2) leading to membrane damage.
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PMID:Phospholipid metabolism of hypothermically stored rat hepatocytes. 1053 45

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

Records of 127 cats with arterial thromboembolism (ATE) were reviewed. Abyssinian, Birman, Ragdoll, and male cats were overrepresented. Tachypnea (91%), hypothermia (66%), and absent limb motor function (66%) were common. Of 90 cats with diagnostics performed, underlying diseases were hyperthyroidism (12), cardiomyopathy (dilated [8], unclassified [33], hypertrophic obstructive [5], hypertrophic [19]), neoplasia (6), other (4), and none (3). Common abnormalities were left atrial enlargement (93%), congestive heart failure (CHF, 44%), and arrhythmias (44%). Of cats without CHF, 89% were tachypneic. Common biochemical abnormalities were hyperglycemia, azotemia, and abnormally high serum concentrations of muscle enzymes. Of 87 cats treated for acute limb ATE, 39 (45%) survived to be discharged. Significant differences were found between survivors and nonsurvivors for temperature (P < .00001), heart rate (P = .038), serum phosphorus concentration (P = .024), motor function (P = .008), and number of limbs affected (P = .001). No significant difference was found between survivors and nonsurvivors when compared by age, respiratory rate, other biochemical analytes, or concurrent CHE A logistic regression model based on rectal temperature predicted a 50% probability of survival at 98.9 degrees F (37.2 degrees C). Median survival time (MST) for discharged cats was 117 days. Eleven cats had ATE recurrences, and 5 cats developed limb problems. Cats with CHF (MST: 77 days) had significantly shorter survival than cats without CHF (MST: 223 days; P = .016). No significant difference was found in survival or recurrence rate between cats receiving high-dose aspirin (> or = 40 mg/cat q72h) and cats receiving low-dose aspirin (5 mg/cat q72h). Adverse effects were less frequent and milder for the lower dosage.
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PMID:Arterial thromboembolism in cats: acute crisis in 127 cases (1992-2001) and long-term management with low-dose aspirin in 24 cases. 1256 30


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