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

Extracellular potassium activity, [K+]0, was continuously measured using potassium specific microelectrodes in the cerebral cortex of cats before and after hypoxic or anoxic insults. Two patterns of [K+]0 increase were seen. A slow, linear rise occurred during hypoxia and hypothermia and was correlated with changes in mean blood pressure (B/P). A fast, complex, exponential rise resembling spreading depression occurred during anoxia and was unassociated with B/P changes. The fall of [K+]0 after reversal of the insult was described by a single exponential function with rate constants from 0.009 to 0.0194 sec-1. It is suggested that the linear rise is primarily a result of sodium pump inhibition and that the exponential rise is due to a superimposed sudden increase in cell membrane permeability perhaps secondary to transmitter release. The kinetics of the fall of [K+[0 is consistent with the normalization of the sodium and potassium gradients across the cell membranes secondary to Na+-K+ATPase activity.
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PMID:The kinetics of extracellular potassium changes during hypoxia and anoxia in the cat cerebral cortex. 84 9

Cold preservation of donor organs induces hypothermia-related tissue edema as a result of a reduced activity of the ATP-dependent sodium pump at low temperatures. Hypothermia-induced tissue edema occurs in kidney preservation and is a significant risk factor for delayed graft function (DGF) after transplantation. DGF remains a major problem in kidney transplantation and is significantly associated with preservation injury. The state of hydration of cold-stored organs can be assessed from a biopsy for determination of the wet/dry weight ratio. As a non-invasive method to determine tissue hydration MRI T1 and T2 relaxometry can be used. In this study we have compared changes in tissue hydration in UW-preserved porcine kidneys with increasing cold ischemia times (CIT) using wet/dry weight ratio and MR ralaxometry. The results of the two techniques were correlated to evaluate the use of MR relaxometry. Wet/dry weight ratios of the renal cortex decreased with prolonged CIT (P < 0.01) whereas those of the medulla did not change significantly. T1 values of the cortex decreased with prolonged CIT (P < 0.01). T2 values of the cortex showed a non-significant decline with increased CIT. No significant changes in T1 and T2 were found in the medulla. The correlation between T1 and the wet/dry weight ratio of the cortex was significant (P = 0.05, linear correlation coefficient 0.8698). We conclude that MR relaxometry can be a valuable noninvasive technique to assess tissue hydration in cadaveric donor kidneys before transplantation.
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PMID:Tissue hydration in kidneys during preservation: a relaxometric analysis of time-dependent differences between cortex and medulla. 895 84

Release of neurotransmitters, including dopamine (DA), plays a central role in neuronal death during cerebral ischaemia. We investigated the effects of changes in energy demand and supply on DA release in cerebral ischaemia in vitro. Rat striatal slices were superfused (400 ml/h) with an artificial cerebrospinal fluid at 34 degrees C, unless otherwise stated. Ischaemia were mimicked by removal of O2 and reduction in glucose concentration from 4 to 2 mM. DA release was monitored by voltammetry. The profile of ischaemia-induced DA release was temperature-dependent. Hypothermia (to 24 degrees C) delayed, slowed, and reduced ischaemia-induced DA release relative to 34 degrees C. Pretreatment of the slices for 3 h with creatine (25 mM) delayed and slowed ischaemia-induced DA release. Conversely, blockade of Na+/K+ ATPase with ouabain induced an anoxic depolarisation and rapid DA release similar to ischaemia. In summary, the onset of DA release in this model is controlled by the balance between energy supply and utilisation. Strategies that increase availability of energy substrates for the membrane sodium pump (i.e., pre-incubation with creatine) or decrease their utilisation (hypothermia) slow and delay DA release. Hypothermia may owe part of its neuroprotective effect to a delay and slowing of ischaemia-induced release of DA and/or other neurotransmitters.
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PMID:Effects of metabolic alterations on dopamine release in an in vitro model of neostriatal ischaemia. 1035 71