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

This investigation evaluated the effect of oxygenated perfluorochemical (PFC) perfusion on the viability of ischemic skeletal muscle compared to hypothermic preservation. Twenty-five hindlimbs of 13 white rabbits were divided into five groups: a PFC group (7 hr of ischemia with 6 hr of PFC perfusion), a PFC/ reperfusion group (8 hr of ischemia with 6 hr of PFC perfusion and 1 hr reperfusion), a hypothermia group (7 hr of ischemia with 6 hr of 4 degrees C cold preservation), a hypothermia/reperfusion group (8 hr of ischemia with 6 hr of 4 degrees C cold preservation and 1 hr of reperfusion), and a control group. The levels of adenine nucleotides, creatine phosphate, hypoxanthine, xanthine, and lipid peroxide were determined in each group. In the PFC and PFC/reperfusion groups, the ATP level remained at 90% of that in the control group. The hypoxanthine level in the hypothermia/reperfusion group was decreased to 70% of that in the hypothermia group and the xanthine level was increased to 130%. In the PFC and PFC/reperfusion groups, hypoxanthine and xanthine levels were much lower and were similar to those in the control group. Lipid peroxide levels were also lower in the PFC and PFC/reperfusion groups than in the hypothermia/reperfusion group. Electron microscopy showed that endothelial cells from the PFC/reperfusion groups were not swollen. These results suggest that PFC perfusion is superior to hypothermia in inhibiting the generation of free radicals and in preventing ischemia-reperfusion injury of skeletal muscle.
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PMID:A perfluorochemical prevents ischemia-reperfusion injury of muscle. 880 79

Effects of chronic depletion of high-energy phosphate compounds by feeding beta-guanidinopropionic acid (beta-GPA) with or without hindlimb suspension (HS) on body temperature were studied in rats. Lower rectal and skin temperatures were observed in rats after 10 d of HS. Suspension-related enlargement of the interscapular brown adipose tissue (BAT), associated with adrenal hypertrophy, was seen. Feeding beta-GPA also caused a hypothermia and BAT enlargement. It is suggested that the hypothermic response to HS may be due to decreased contractile activity and metabolic rate in skeletal muscles, associated with stress. It is also speculated that the changes in the thermogenesis in rats fed beta-GPA might be related to a stimulated ATP synthesis with sacrificed heat production, but not associated with stress.
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PMID:Thermogenic responses to high-energy phosphate contents and/or hindlimb suspension in rats. 883 35

Rewarming from accidental hypothermia is associated with fatal circulatory derangements. To investigate potential pathophysiological mechanisms involved, we examined heart function and metabolism in a rat model rewarmed after 4 h at 15-13 degrees C. Hypothermia resulted in a significant reduction of left ventricular (LV) systolic pressure, cardiac output, and heart rate, whereas stroke volume increased. The maximum rate of LV pressure rise decreased to 191 +/- 28 mmHg/s from a control value of 9,060 +/- 500 mmHg/s. Myocardial tissue content of ATP, ADP, and glycogen was significantly reduced, whereas lactate content remained unchanged. After rewarming, heart rate returned to control value, whereas LV systolic pressure, cardiac output, and stroke volume all remained significantly depressed. The posthypothermic maximum rate of LV pressure rise was 5,966 +/- 1.643 mmHg/s. The posthypothermic myocardial lactate content was significantly increased (to 13.3 +/- 3.2 nmol/mg from control value of 5.7 +/- 1.9 nmol/mg), and ATP and glycogen remained significantly lowered. Creatine phosphate or energy charge did not change significantly during the experiment. The finding of deteriorated myocardial mechanical function and a shift in energy metabolism shows that the heart could be an important target during hypothermia and rewarming in vivo, thus contributing to the development of a posthypothermic circulatory collapse.
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PMID:Experimental hypothermia and rewarming: changes in mechanical function and metabolism of rat hearts. 884 17

In a previous study we showed that hypothermia of 30 degrees C can expand the time during which retinal neurons in vitro can have their metabolism inhibited without adverse effects. In isolated chick retinae, the first signs of acute toxicity resulting from mild, partial, pharmacological inhibition of metabolism are N-methyl-D-aspartate (NMDA)-mediated histological swelling and gamma-aminobutyric acid release. More prolonged or severe inhibition of metabolism results in involvement of non-NMDA glutamate receptors and voltage-dependent Na+ channels. In this study we examine early cellular events that may be associated with hypothermic protection. The early cellular events thought to follow metabolic stress involve a decrease in ATP, reduced activity of the Na+, K(+)-ATPase, which renders ion leakage unopposed, degradation of the membrane potential and subsequent activation of ionotropic glutamate receptors and voltage-dependent Na+ channels, which leads to acute toxicity. Reduction by hypothermia of the rate of loss of ATP was shown, In past work, to only partially account for neuroprotection. In the present study, inhibition of the Na+, K(+)-ATPase with 10 microM ouabain for 30 min at 37 degrees C led to acute toxicity that was similar to the toxicity produced by severe metabolic stress, i.e., primarily excitotoxic and mediated by NMDA receptors and secondarily involving non-NMDA receptors and voltage-dependent Na+ channels. Swelling and increased gamma-aminobutyric acid release were first evident at 15 min of incubation with ouabain at 37 degrees C. Hypothermia (30 degrees C) delayed the onset of acute excitotoxicity caused by ouabain. This protection was independent of an involvement with ATP loss, because ouabain treatment did not reduce ATP levels. Protection against ouabain suggests that hypothermia can intervene at steps subsequent to decreased Na+, K(+)-ATPase activity. In contrast, reducing the temperature to 30 degrees C did not attenuate NMDA-mediated secondary excitotoxicity caused by lowering of the membrane potential with increasing extracellular K+ concentrations (32-55 mM). However, hypothermia of 30 degrees C was able to reduce the rate of ouabain-induced 86Rb efflux. The findings described above suggest that a critical site of action for hypothermic protection is at a step between decreased Na+, K(+)-ATPase activity and degraded membrane potential, specifically, slowing of the rate of ion leakage.
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PMID:Hypothermia and metabolic stress: narrowing the cellular site of early neuroprotection. 885 11

A method of examining arteriolar function in situ using the in vitro-perfused hydronephrotic rat kidney is described. This approach facilitates direct visualization of arteriolar contractile responses in a well-controlled experimental environment while avoiding the consequences of traumatic microdissection and the accompanying exposure to ischemia, hypothermia, or hypoxia. The preparation has a remarkably well-preserved myogenic reactivity, exhibiting precisely graded vasoconstriction over the range in perfusion pressure subtending normal renal autoregulatory responses (i.e., 80-180 mm Hg). Using this preparation, the inhibitory effects of hypoxia on arteriolar myogenic reactivity have been demonstrated. The range over which reduced pO2 affected arteriolar reactivity in this model corresponded closely to that reported to alter vascular tone in vivo. A technique of adapting the model to incorporate simultaneous monitoring of arteriolar fluorescence measurements and contractile responses is also described. This approach has been used to examine the relationship between arteriolar contractility and NADH autofluorescence during the hypoxia-induced activation of ATP-sensitive K channels. Future applications may include the use of intravital fluorescent dyes to examine, for example, microvascular endothelial calcium signaling in an intact, functioning arteriole.
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PMID:In situ studies of renal arteriolar function using the in vitro-perfused hydronephrotic rat kidney. 886 Sep 40

Bimakalim (Bim), an opener of ATP-sensitive K+ (KATP) channels, was given alone or with 2,3-butanedione monoxime (BDM), a reversible uncoupler of contractility, to protect myocardial function during 1 day of hypothermia. Left ventricular pressure (LVP), coronary flow (CF), percent O2 extraction (%O2E), and cardiac efficiency were measured in 96 isolated, perfused guinea pig hearts divided into seven groups: 1) cold control (no drugs); 2) BDM; 3) Bim; 4) BDM + Bim; 5) BDM + glibenclamide (Glib, a blocker of KATP channels); 6) BDM + Bim + Glib; and 7) time control (6 h warm perfusion only). Drugs were given before, during, and initially after 22 h of low CF at 3.8 degrees C. At 26 h (cold groups) or 4 h (warm group) LVP (mmHg; means +/- SE) was similar for time control (94 +/- 4) and BDM + Bim (92 +/- 4) groups, lower and equivalent in the BDM (65 +/- 7) and BDM + Bim + Glib (64 +/- 7) groups, but LVP was higher than in the Bim group (46 +/- 3), and lowest in the cold control (30 +/- 8) group. In addition, only in the BDM + Bim group were basal CF, %O2E, and cardiac efficiency returned to values obtained in the time control group. Epinephrine increased LVP to that of the time control (106 +/- 3) group only in the BDM + Bim group (106 +/- 3) after hypothermia, and CF increases with adenosine, 5-hydroxytryptamine, and nitroprusside were similar to that of the time control group only in the BDM + Bim group after hypothermia. All of the effects of Bim were reversed by Glib. These results indicate that Bim, given with BDM, effectively preserves myocardial function and metabolism as well as inotropic and vasodilatory reserve during long-term hypothermic preservation as if the 1-day hypothermic state had not been instituted. Because the beneficial effects of Bim are blocked by Glib, the protective effect of Bim likely results from maintained KATP channel opening. Treatment with exogenous KATP openers may prove useful in preserving cardiac function in the transplanted heart.
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PMID:One-day cold perfusion of bimakalim and butanedione monoxime restores ex situ cardiac function. 894 5

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

Central administration of galanin dose-dependently (minimum effective dose, M.E.D. = 1 nmol) blocked the hypothermia induced by the 5-HT1A receptor agonist 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT, 0.5 mg/kg s.c.), in mice. This inhibitory effect was reversed by pretreatment with the galanin receptor antagonist galantide (0.3 nmol) and also by pretreatment with the ATP-sensitive potassium channel blockers glibenclamide (10 nmol) and gliquidone (10 nmol). The hypothermic response to 8-OH-DPAT was also blocked by the 5-HT1A receptor antagonist (N-(2,4(2-methoxyphenyl)-1-piperazinyl)ethyl-N-(2-pyridinyl)cyclohexane, (WAY 100,635, M.E.D. = 0.01 mg/kg s.c.), and the centrally acting muscarinic receptor antagonist scopolamine (M.E.D. = 10 mg/kg i.p.) but not the peripheral muscarinic receptor antagonist N-methylscopolamine. 8-OH-DPAT (0.5 mg/kg s.c.) also decreased cortical and hypothalamic 5-HT (5-hydroxytryptamine, serotonin) metabolism, an effect which was not blocked by pretreatment with galanin (0.3-3 nmol intracerebroventricular, i.c.v.). Neither did galanin (0.03-3 nmol/5 microliters i.c.v.) affect basal 5-HT metabolism in these brain regions. Furthermore, pretreatment in vitro of mouse cortical membranes with galanin (10 or 1000 nM) had no effect on 5-HT1A receptor affinity, Bmax or pharmacology determined using [3H]8-OH-DPAT. These results suggest that the inhibition of 8-OH-DPAT induced hypothermia by galanin is probably not mediated by an interaction with 5-HT1A receptors but more likely by blocking the indirect activation by 8-OH-DPAT of central cholinergic pathways involved in temperature regulation.
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PMID:Effects of galanin on 8-OH-DPAT induced decrease in body temperature and brain 5-hydroxytryptamine metabolism in the mouse. 899 1

Taurine and glutamine are the most abundant intracellular free amino acids in mammalian hearts where changes in their intracellular concentrations are likely to influence a number of cellular activities. In this study we investigated the effects of ischaemia and reperfusion on the intracellular concentrations of taurine and glutamine in the hearts of patients undergoing coronary artery bypass surgery using cold crystalloid or cold blood cardioplegic solutions. Ischaemic arrest (30 min), using cold crystalloid cardioplegic solution (n = 19), decreased the intracellular concentrations (micromol/g wet weight) of taurine (from 9.8 +/- 0.8 to 7.7 +/- 0.7, P < 0.05) and glutamine (8.7 +/- 0.5 to 7.2 +/- 0.6). After 20 min of normothermic reperfusion the fall in taurine and glutamine was maintained (7.5 +/- 0.5 and 7.4 +/- 0.7 for taurine and glutamine respectively). Myocardial ischaemic arrest with cold blood cardioplegic solution (n = 16) did not cause a significant fall in tissue taurine or glutamine. However, on reperfusion there was a marked fall in the intracellular concentrations of taurine (9.4 +/- 0.5 to 6.5 +/- 0.7) and glutamine (8.0 +/- 0.7 to 5.8 +/- 0.4). The fall in amino acids was associated with a fall in ATP and a rise in tissue lactate. This work demonstrates that irrespective of the cardioplegic solution used to arrest the heart, there is a marked fall in tissue taurine and glutamine which may influence the extent of recovery following surgery. The fall in taurine is largely due to efflux whereas changes in glutamine are due to both transport and metabolism. Ischaemia, hypothermia and changes in the transmembrane concentration gradients are the likely factors responsible for the changes in tissue amino acids.
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PMID:Effect of ischaemia and reperfusion on the intracellular concentration of taurine and glutamine in the hearts of patients undergoing coronary artery surgery. 909 9

The neuroprotective effects of pramipexole, a dopamine agonist, were investigated in 3-acetylpyridine (3-AP)-treated Wistar rats. Bromocriptine was used as a reference compound to compare the results obtained with pramipexole. A significant reduction (P < 0.01) in cerebellar cGMP and ATP was observed 96 h after treatment with 3-AP (500 micromol/kg, i.p.). Both pramipexole and bromocriptine significantly attenuated 3-AP-induced reduction in cerebellar cGMP and ATP. Consistent with the neurochemical effect, both pramipexole and bromocriptine prevented 3-AP-induced loss of motor coordination. 3-Acetylpyridine produced a significant (P < 0.01) loss of neurons in the inferior olivary nucleus. Treatment with pramipexole and bromocriptine partially, but significantly (P < 0.01), prevented the loss of inferior olivary neurons. There was no reduction in the temperature of the animals, indicating that hypothermia was not responsible for neuroprotection.
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PMID:Neuroprotective effects of the dopamine agonists pramipexole and bromocriptine in 3-acetylpyridine-treated rats. 913 74


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