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

The effect of temperature on isolated rat liver perfusion was studied. Livers were perfused for 12 hours with oxygenated Krebs-Henseleit solution at 5, 10, 15, 20, 25 and 30 degrees C, followed by one hour normothermic reperfusion. After each perfusion, oxygen consumption, liver enzyme release, tissue swelling, energy metabolism and histopathological abnormalities were determined. Compared to the oxygen consumption at 37 degrees C, that of 25, 10 and 5 degrees C was 47%, 16% and 12%, respectively. When the liver was perfused at 30 degrees C, higher enzyme release and lower energy status was observed. Tissue swelling was significant only with livers perfused at 5, 10 and 30 degrees C. After normothermic reperfusion, liver injury indicated by enzyme release and bile production was remarkable with 30 degrees C liver, and that of the other groups was essentially the same as the control. ATP of 5, 25 and 30 degrees C liver was significantly lower than the control. Histopathological examination demonstrated abnormalities of sinusoidal cells and hepatocytes in livers perfused at 25 degrees C and 30 degrees C Thus higher temperature (25 degrees C to 30 degrees C) during continuous perfusion were found to induce liver damage. Moderate hypothermia between 10 degrees C and 20 degrees C maintained structure and function of rat livers rather well. These results suggest that, when a machine perfusion of the liver is attempted, a wider temperature range, higher than the conventional, needs to be taken into consideration.
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PMID:Isolated perfusion of rat livers: effect of temperature on O2 consumption, enzyme release, energy store, and morphology. 823 63

We evaluated cerebral metabolism during retrograde cerebral perfusion (RCP) and circulatory arrest under profound hypothermia, and also investigated the effect of pulsatile flow on RCP. Eighteen adult mongrel dogs were placed on cardiopulmonary bypass and were cooled to a nasopharyngeal temperature of 20 degrees C. At this temperature, hypothermic circulatory arrest (HCA; n = 6), non-pulsatile RCP (NP-RCP; n = 6), and pulsatile RCP (P-RCP; n = 6) were performed for 60 minutes. Retrograde cerebral perfusion was performed via the bilateral internal maxillary veins, and retrograde flow rate was regulated to maintain a mean perfusion pressure of 20 mmHg in the external jugular vein. During RCP, the temperature was maintained in a narrow range, oxygen consumption and carbon dioxide excretion could be observed, the excess lactate was maintained at a negative value, and cerebral tissue ATP concentration was significantly higher than in the HCA group. The cerebral tissue water content was significantly lower in the P-RCP group than in the NP-RCP group. These findings suggest that hypothermia of the central nervous system, the supply of oxygen, the excretion of metabolites, aerobic metabolism, and the cerebral ATP level were maintained by RCP. In conclusion, RCP may possibly provide adequate metabolic support for the brain during total circulatory arrest, and pulsatile flow appears to reduce cerebral edema when compared with non-pulsatile flow in dogs.
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PMID:Cerebral metabolism and effects of pulsatile flow during retrograde cerebral perfusion. 830 Jul 12

The metabolic status of rat livers during hypothermia has been studied using 31P magnetic resonance spectroscopy. Perfusion with oxygenated buffer at 6-8 degrees C allowed maintenance of ATP, while pH increased to values in the range 7.7-7.9. In organs depleted of ATP by a short (2 h) period of cold ischemia, pH fell to 6.92 +/- 0.10. If these livers were reperfused with hypoxic buffer at hypothermia, two distinct responses were noted. In one group (responders), there was evidence of ATP resynthesis and in these organs pH returned to 7.90 +/- 0.28. In the second group (non-responders), there was no recovery of ATP synthesis and pH remained depressed at 6.97 +/- 0.07. In another group, adenine nucleotides were severely depleted by 24 h of cold ischemia, and in these livers there was again no significant recovery of ATP synthesis during hypoxic reperfusion and pH remained at 7.03 +/- 0.25. These results suggest that (a) there is an apparent relationship between energy metabolism and control of intracellular pH in the hypothermic mammalian liver, and (b) that intracellular pH may shift in liver at hypothermia to values predicted by the alpha-stat hypothesis.
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PMID:Control of intracellular pH in mammalian liver at hypothermia: evidence for a relationship with energy metabolism. 830 3

Isolated embryonic retinas were metabolically stressed by inhibition of glycolysis either with iodoacetate (IOA) or by glucose withdrawal plus 10 mM 2-deoxy-D-glucose, and the effects of hypothermia were examined. Incubation at 30 versus 37 degrees C during 30 min of hypoglycemia with IOA completely reduced the rapid swelling-related GABA release [6 +/- 2 vs. 68 +/- 10 nmol/100 mg of protein (mean +/- SEM) for 30 and 37 degrees C, respectively]. Histology of the retina immediately following 30 min of metabolic stress at 30 degrees C appeared normal, whereas that at 37 degrees C showed a pattern of acute edema, characteristic of NMDA-mediated acute excitotoxicity. Coincubation with a competitive or noncompetitive NMDA antagonist, respectively, CGS-19755 (10 microM) or MK-801 (1 microM), during 30 min of hypoglycemia at 37 degrees C completely prevented tissue swelling, whereas extracellular GABA content remained at basal levels, indicating that the cytotoxic effects of IOA treatment for 30 min at 37 degrees C were NMDA receptor mediated. Longer periods of hypoglycemia at 37 degrees C produced acute toxicity that was only partially NMDA receptor mediated. Hypothermia delayed the onset of NMDA-mediated toxicity by 30-60 min. At 30 degrees C, the rate of loss of ATP was slowed during the first several minutes of hypoglycemia (82 and 58% of maximal tissue levels at 30 and 37 degrees C, respectively, at 5 min, but by 10 min, ATP levels were comparably reduced. After a transient exposure of retina to 50 microM NMDA in Mg(2+)-free medium, hypothermia significantly attenuated acute GABA release by 30%.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hypothermia, metabolic stress, and NMDA-mediated excitotoxicity. 837 98

After O2 deprivation, tissue acidosis rapidly self-corrects. This study assessed the effect of this pH correction on the induction, and pathways, of posthypoxic proximal tubular injury. In addition, ways to prevent the resultant injury were explored. Isolated rat proximal tubular segments (PTSs) were subjected to hypoxia/reoxygenation (50/30 or 30/50 minutes) under the following incubation conditions: 1) continuous pH 7.4, 2) continuous pH 6.8, or 3) hypoxia at pH 6.8 and reoxygenation at pH 7.4 (NaHCO3 or Tris base addition). Continuously oxygenated PTSs maintained under these same pH conditions served as controls. Lethal cell injury was assessed by lactate dehydrogenase (LDH) release. pH effects on several purported pathways of hypoxia/reoxygenation injury were also assessed (ATP depletion, lipid peroxidation, and membrane deacylation). Acidosis blocked hypoxic LDH release (pH 7.4, 50 +/- 2%; pH 6.8, 6 +/- 1%) without mitigating membrane deacylation or ATP depletion. During reoxygenation, minimal LDH was released (3-5%) if pH was held constant. However, if posthypoxic pH was corrected, immediate (< or = 5 minutes) and marked cell death (e.g., 55 +/- 3% with Tris) occurred. This was dissociated from lipid peroxidation or new deacylation, and it was preceded by a depressed ATP/ADP ratio (suggesting an acidosis-associated defect in hypoxic/posthypoxic cell energetics). Realkalinization injury was not inevitable, since it could be substantially blocked by 1) posthypoxic glycine addition, 2) transient posthypoxic hypothermia, or 3) allowing a 10-minute reoxygenation (cell recovery) period before base addition. Neither mannitol nor graded buffer Ca2+ deletion conferred protection. Acute pH correction caused no injury to continuously oxygenated PTSs. Conclusions are as follows: 1) Posthypoxic "pH shock" causes virtually immediate cell death, not by causing de novo injury but, rather, by removing the cytoprotective effect of acidosis. 2) This injury can be prevented by a variety of methods, indicating a great potential for salvaging severely damaged posthypoxic PTSs.
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PMID:Physiological pH. Effects on posthypoxic proximal tubular injury. 844 71

Isolated canine hearts were preserved for 6 h at 5 degrees C followed by normothermic reperfusion for 2 h. The dogs were divided into two groups of nine hearts each; group 1 received a nondepolarizing preservation solution in multidose, and group 2 received a single flush of University of Wisconsin (UW) solution. Serum MB-CK and mitochondrial aspartate aminotransferase (m-AAT) concentrations and calcium overload during reperfusion were lower in group 1 than in group 2. At the end of reperfusion, myocardial ATP and total adenine nucleotide concentrations were higher and mitochondrial morphology appeared more intact in group 1 than in group 2. Left ventricular diastolic function was preserved better in group 1 than in group 2. These results suggest that in 6-h heart preservation, a nondepolarizing solution applied in multidose fashion protects the myocardium from the deleterious effects of hypothermia and cardioplegia better than a single flush of UW solution.
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PMID:Comparison of intermittent injection of nondepolarizing solution with a single flush of UW solution for donor heart preservation. 844 26

Hypothermic perfusion of rat livers was investigated by 31phosphorus nuclear magnetic resonance (31P NMR) spectroscopy using a temperature-controlled module that allowed data acquisition at various time points during a 48-h period. The livers were perfused with an oxygenated lactobionate/raffinose-based solution containing adenosine and inorganic phosphate, and changes in tissue oedema were monitored by direct on-line measurements of liver weight changes. Liver tissue ATP concentrations, determined by fluorimetric assay, were low immediately after organ removal, probably reflecting metabolic stress during the removal period, and these increased slightly during the next 3 h. This was reflected by changes in the 31P NMR spectra. However, by 24 h ATP levels had increased significantly, and these were maintained for up to 48 h, suggesting a shift in the balance between energy production and consumption. When inorganic phosphate was replaced by another anion (citrate), ATP was maintained at a constant lower level during perfusion for 48 h. Tissue weight changes were similar in both groups, suggesting that volume control was not affected by the different ATP contents of the livers. By combining the temperature-controlled module with a separate perfusion circuit, NMR spectroscopy can provide a sensitive method for following energy metabolism in the same organ over long periods during hypothermic perfusion.
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PMID:Hypothermic perfusion preservation of liver: the role of phosphate in stimulating ATP synthesis studied by 31P NMR. 857 34

In neonatal and adult animals, modest reduction in brain temperature (2-3 degrees C) during ischemia and hypoxia-ischemia provides partial or complete neuroprotection. One potential mechanism for this effect is a decrease in brain energy utilization rate with consequent preservation of brain ATP, as occurs with profound hypothermia. To determine the extent to which modest hypothermia is associated with a decrease in brain energy utilization rate, in vivo 31P and 1H magnetic resonance spectroscopy (MRS) was used to measure the rate of change in brain concentration of phosphocreatine, nucleoside triphosphate, and lactate after complete ischemia induced by cardiac arrest in 11 piglets (8-16 d). Pre-ischemia metabolite concentrations and MRS-determined rate constants were used to calculate the initial flux of high energy phosphate equivalents (d[approximately P]/dt, brain energy utilization rate). Baseline physiologic and MRS measurements were obtained at 38.2 degrees C and repeated after brain temperature was adjusted between 28 and 41 degrees C. This was followed by measurement of d[approximately P]/dt during complete ischemia at 1-2 degrees C increments within this temperature range. Adjusting brain temperature did not alter any systemic variable except for heart rate which directly correlated with brain temperature (r = 0.95, p < 0.001). Before ischemia brain temperature inversely correlated with phosphocreatine (r = -0.89, p < 0.001), and reflected changes in the phosphocreatine-ATP equilibrium, because brain temperature inversely correlated with intracellular pH (r = -0.77, p = 0.005). Brain temperature and d[approximately P]/dt were directly correlated and described by a linear relationship (slope = 0.61, intercept = -12, r = 0.92, p < 0.001). A reduction in brain temperature from normothermic values of 38.2 degrees C was associated with a decline in d[approximately P]/dt of 5.3% per 1 degree C, and therefore decreases in d[approximately P]/dt during modest hypothermia represent a potential mechanism contributing to neuroprotection.
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PMID:Quantitative relationship between brain temperature and energy utilization rate measured in vivo using 31P and 1H magnetic resonance spectroscopy. 861 94

Recent advances have led to increased use of ultraprofound hypothermia for cardiopulmonary bypass, organ preservation and trauma patients and have introduced the possibility of targeted pharmacologic intervention during the hypothermic period. In this study, rabbit renal cortex slices were used to examine the effect of administering quinacrine (100 microM) during hypothermia induced after a warm ischemic injury (60 min at 37 degrees C) on recovery of biochemical function during 3.5 hr of simulated warm reperfusion. In ischemic tissue slices, ATP content was reduced to near zero and only recovered about 50% by the end of reperfusion. Hypothermic storage of ischemic slices for 18 hr restored slice ATP content to about 80% of control levels but was followed by a decline during reperfusion to levels similar to ischemic slices. Administering quinacrine (100 microM) during 18 hr of hypothermic storage of ischemic slices resulted in a significant and sustained increase in slice ATP content during warm reperfusion. Slices stored at hypothermia only 3 hr with quinacrine had reduced swelling during reperfusion even though total ATP content was unaffected. Administering quinacrine (100 microM) only during reperfusion after ischemia or hypothermia did not affect tissue ATP content. This study showed that drug administration during hypothermic storage has potential therapeutic benefits for resuscitating tissues after warm ischemia and is more effective than the same drug given only during reperfusion. Tissue pretreatment was not required to obtain improved function in this study which suggests that future adaptations of these principles may have practical applications for specific clinical conditions where ischemic and reperfusion injury are significant factors.
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PMID:The effects of administering quinacrine during ultraprofound hypothermia on warm ischemic kidney cortex tissue. 862 47

The energy state and intracellular pH of the rat brain during and after transient cerebral ischemia was measured by the method of 31P magnetic resonance spectroscopy in vivo for the purpose of the evaluation of the protective effect of hypothermia. The rat's chest was opened and the bilateral subclavian arteries were ligated. The transient cerebral ischemia was induced by occlusion of the bilateral cerebral arteries using the balloon occluders. The rat's brain was cooled to 20 degrees C by the surface cooling using the ice bags and was heated to 37 degrees C in the control group, respectively. The animal's temperature was adjusted and regulated by a water blanket placed under the animal's body. After 30 min cerebral ischemia, the level of phosphocreatine (PC) was decreased to 58 +/- 4% versus to 36 +/- 4%, 20 degrees C versus 37 degrees C, respectively (p < 0.01). ATP was decreased to 73 +/- 5% versus 52 +/- 4% (< 0.01). Intracellular pH was decreased from 7.23 to 6.48 at 20 degrees C, from 7.22 to 6.08 at 37 degrees C (p < 0.01). After 60 min ischemia, PC was decreased to 52 +/- 5% versus to 33 +/- 6%, 20 degrees C versus 37 degrees C (p < 0.01). ATP was decreased to 62 +/- 6% versus 36 +/- 6% (p < 0.01). At 37 degrees C either PC or ATP was not recovered to the pre-ischemic level. Intracellular pH was decreased to 6.38 at 20 degrees C, to 5.80 at 37 degrees C (p < 0.01). It is concluded the hypothermia saved the high energy phosphates and keeps intracellular pH high and this beneficial effects contribute the brain protection during cerebral ischemia.
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PMID:[The protective effect of hypothermia in a new transient cerebral ischemic model of the rat--A 31P magnetic resonance spectroscopy in vivo study]. 868 62


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