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)

The measurement of lactate dehydrogenase (LDH) release into perfusates after hypothermic storage was found to be a reliable index of ischemic injury of rabbit kidneys. Kidneys were exposed to warm and cold ischemia for varying periods. Each kidney was perfused before and after storage at simple hypothermia with 25 ml of a modified Collins solution. The venous effuent was collected in 5 ml fractions. Total LDH activity was measured in the first fraction after storage and used as a measure of ischemic tissue damage. It was confirmed that increasing the period of cold ischemia result in significant increases in LDH activity. The release of LDH into perfusates was then used to compare kidney damage after preservation with various fluids. With this method, it was not possible to demonstrate any difference in the extent of tissue damage after preservation with sodium-rich vs. potassium-rich perfusion fluid. Addition of steroids, vitamins and essential amino acids did not prevent or reduce tissue damage, estimated in this way. The effects of adding cryoprotectants to the perfusion fluid varied; LDH release following addition of 5% DMSO was significantly greater, and after addition of 5% glycerol smaller than the release after perfusion with a modified Collins solution alone. Stepwise addition of DMSO up to 20% resulted in serious tissue damage with a large LDH release into the perfusate.
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PMID:LDH release into perfusates of preserved kidneys. 78 32

Cytotoxicity resulting from the interaction of fluorescent light from a flow hood with Hepes-buffered cell culture medium at room temperature was demonstrated. Toxicity was prevented by keeping both cells (V79 Chinese hamster) and medium shielded from direct fluorescent light ("dark conditions") or by supplementing the medium with 10 micrograms/ml catalase; this suggests that extracellular hydrogen peroxide is a major cause of the lethal effect under "lighted conditions." No sensitization resulted from the exposure of cells in a sodium bicarbonate (SBC)-buffered medium to fluorescent light, nor in a catalase supplemented SBC-buffered medium. The Hepes/light reaction during routine cell manipulations presensitized cells to hypothermia damage in the dark with the presensitization being more severe for 5 than for 10 degrees C hypothermic exposure. Presensitization was prevented by performing the complete experiment under dark conditions or by supplementing the medium with 10 micrograms/ml catalase. However, catalase did not improve the hypothermic survival when experiments were performed under dark conditions. Hence, 10 micrograms/ml catalase does not protect cells from hypothermic (5 and 10 degrees C) damage per se, but rather from Hepes/light sublethal damage which interacts with hypothermic sublethal damage to result in lethal lesions. Additionally, under dark conditions, superoxide dismutase (SOD), allopurinol, catalase plus SOD, DMSO, or mannitol did not improve survival when present during hypothermic storage, suggesting that extracellular superoxide anion, hydrogen peroxide, or hydroxyl radicals are not the cause of cell killing under conditions of pure hypothermia uncomplicated by prehypothermic ischemia or hypoxia.
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PMID:Factors influencing survival of mammalian cells exposed to hypothermia. V. Effects of hepes, free radicals, and H2O2 under light and dark conditions. 201 62

An animal model for anticancer drug-induced hair loss has been developed using the Angora rabbit given i.v. doxorubicin, 2 mg/kg, twice weekly for 3 weeks. There was a 167% increase in the weight of hair collected by grooming between weeks 2 and 5, and a 72% inhibition of new hair growth at week 6 compared with non-treated animals. The hairs that grew in the doxorubicin treated rabbits did so at the same rate as in non-treated rabbits and appeared normal by light microscopy. Topical application of dimethylsulfoxide (DMSO), of 10% alpha-tocopherol in DMSO, of 0.5% naphthazoline hydrochloride in DMSO, of 0.1% fluocinolone acetonide in a propylene glycol base and local hypothermia did not provide any protection against doxorubicin-induced hair loss. Angora rabbits fed an alpha-tocopherol-deficient diet for 6 weeks showed decreased hair growth compared with animals fed a normal diet or a diet supplemented with 100 mg alpha-tocopherol acetate twice a week for 6 weeks. Some rabbits fed the alpha-tocopherol-deficient diet died when given doxorubicin. Rabbits fed the alpha-tocopherol-supplemented diet showed evidence of protection against doxorubicin-dependent inhibition of new hair growth.
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PMID:Doxorubicin-induced hair loss in the Angora rabbit: a study of treatments to protect against the hair loss. 369 Aug 2

The in vivo generation of .OH free radicals in specific brain regions can be measured by intracerebral microdialysis perfusion of salicylate, avoiding many of the pitfalls inherent in systemic administration of salicylate. Direct infusion of salicylate into the brain can minimize the hepatic hydroxylation of salicylate and its contribution to brain levels of 2,5-DHBA. Levels of 2,5-DHBA detected in the brain dialysate may reflect the .OH adduct plus some enzymatic hydroxylation of salicylate in the brain. After minimizing the contribution of enzyme and/or blood-borne 2,5-DHBA, the present data demonstrate the validity of the use of 2,3-DHBA and apparently 2,5-DHBA as indices of .OH formation in the brain. Therefore, intracranial microdialysis of salicylic acid and measurement of 2,3-DHBA appears to be a useful .OH trapping procedure for monitoring the time course of .OH generation in the extracellular fluid of the brain. These results indicate that nonenzymatic and/or enzymatic oxidation of the dopamine released by MPTP analogues in the extracellular fluid may play a key role in the generation of .OH free radicals in the iron-rich basal ganglia. Moreover, a site-specific generation of cytotoxic .OH free radicals and quinone/semiquinone radicals in the striatum may cause the observed lipid peroxidation, calcium overload, and retrograde degeneration of nigrostriatal neurons. This free-radical-induced nigral injury can be suppressed by antioxidants (i.e., U-78517F, DMSO, and deprenyl) and possibly hypothermia as well. In the future, this in vivo detection of .OH generation may be useful in answering some of the fundamental questions concerning the relevance of oxidants and antioxidants in neurodegenerative disorders during aging. It could also pave the way for the research and development of novel neuroprotective antioxidants and strategies for the early or preventive treatment of neurodegenerative disorders, such as Parkinson's disease (Wu et al., this issue), amyotrophic lateral sclerosis, head trauma, and possibly Alzheimer's cognitive dysfunction as well. In conclusion, this in vivo free-radical trapping procedure provides evidence to support a current working hypothesis that a site-specific formation of cytotoxic .OH free radicals in the basal ganglia may be one of the neurotoxic mechanisms underlying nigrostriatal degeneration and Parkinsonism caused by the dopaminergic neurotoxin MPTP. Addendum added in proof: The controversy concerning possible neurotoxic and/or neuroprotective roles of NO. in cell cultures was discussed and debated at the symposium (Wink et al., this issue; Dawson et al., this issue; Lipton et al., this issue).(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:In vivo generation of hydroxyl radicals and MPTP-induced dopaminergic toxicity in the basal ganglia. 783 34

The drugs used in frostbite injury care are: Plasma volume expanders (low molecular weight dextran); vasodilating agents (tolazoline hydrochloride); hypotensive agents (guanethidine monosulfate, reserpine); hemorrheologic agents (oxpentifylline); calcium blocking agents (nifedipine); sympatholytic agents (phenoxybenzamine hydrochloride); anticoagulating agents (heparin); thrombolytic enzymes (streptokinase, tissue plasminogen activator--TPA); an industrial solvent (dimethyl sulfoxide--DMSO); anti-inflammatory agents such as nonsteroidal drugs, and acetylsalicylic acid, Ibuprofen. As yet, no clear treatment policy has been determined for preventing injury secondary to the formation of oxygen free radicals, damaging neutrophils or reperfusion injury. The role of oxygen free radical scavengers and factors causing reperfusion injury is unclear at this date. Since that first reported series of 51 patients in 1960-61, 1,282 patients have been seen. Of that number, 1,026 had a diagnosis of frostbite; 151 were diagnosed as hypothermia; and 105 diagnosed as immersion injury.
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PMID:Comments on this issue of Alaska Medicine--from then (1960) until now (1993). 821 84

Pretreatment by hypothermic (25 degrees C) cycling (PHC) of attached exponential-phase V79 Chinese hamster cells by Method 4 (24 hr at 25 degrees C + 1.5 hr at 37 degrees C + 24 hr at 25 degrees C + trypsin + 3 hr at 37 degrees C) or by Method 3 (48 hr at 25 degrees C + trypsin + 3 hr at 37 degrees C) make mammalian V79 cells significantly more resistant to 43 degrees C hyperthermia. There is no significant difference in the 43 degrees C curves whether Method 3 or 4 is used for pre-exposure. If pre-exposure at 15 or 10 degrees C, the resistance to hyperthermia is significantly reduced. PHC by Method 4 significantly increases survival of cells exposed to 5 degrees C and, to a lesser extent, to 10 degrees C. The increase in hyper- and hypothermic survival after PHC cannot be accounted for by changes in cell cycle distribution. Heat-shock protein synthesis is not induced by PHC; hence, protection does not result from newly synthesized proteins. When cells are made tolerant to hyperthermia by a pretreatment in 2% DMSO for 24 hr at 37 degrees C (Method 8), the cells are not more resistant to subsequent exposures to hypothermia, either at 5 or 10 degrees C. The results imply that there may be two mechanisms of inducing resistance to hyperthermia, only one of which also confers resistance to hypothermia.
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PMID:Induction of tolerance to hypothermia and hyperthermia by a common mechanism in mammalian cells. 831 51

The Arrhenius plot of inactivation (killing) rates of V-79 Chinese hamster cells exposed to hypothermia contains a break at about 8 degrees C, which corresponds to the minimum inactivation rate, implying that there are distinct hypothermic damage mechanisms above (Range I = 8 to +25 degrees C) and below (Range II = 0 to +8 degrees C) 8 degrees C. Several membrane-permeable hydroxyl free radical scavengers, N-acetylhomocysteinethiolactone (citiolone), dimethylthiourea (DMTU), and dimethyl sulfoxide (DMSO), were tested for their ability to protect cells exposed to hypothermic temperatures of 10 degrees C (Range I) or 5 degrees C (Range II) as a function of time in a system that is uncomplicated by previous hypoxia. Citiolone (3 mM) protected cells in Range I, but not in Range II. To date, citiolone is the only agent that protects in Range I. Adenosine was of no benefit in Range I. Glycine (5 mM) protected cells in Range II, but not in Range I. DMSO (10 mM) was ineffective in Range II, while DMTU (10 mM) protected cells in Range II, but not in Range I. The combination of DMTU and citiolone had a synergistic protective effect on the cells during 10 degrees C exposure (Range I). However, the combination of DMTU and citiolone is neither synergistic nor additive at 5 degrees C (Range II).
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PMID:Further evidence for two modes of hypothermia damage. 837 Mar 18

The influence of hypothermia (2 degrees, 15 degrees and 28 degrees C) upon the effect of X-irradiation on chromatin from human diploid fibroblast cells (AG1518) was studied using the fluorescent halo assay. Rewinding of supercoils was inhibited in a dose-dependent manner when cells were irradiated with 4, 8 or 16 Gy. This inhibition of rewinding was reduced when cells were irradiated at subnormal temperatures compared with cells irradiated at 37 degrees C. One hour's preincubation at low temperature did not influence rewinding. When AG1518 cells were irradiated at 37 degrees C in the presence of the radical scavenger DMSO (0.5 M), the radiation-induced damage was reduced. No additional protection of DMSO in hypothermic cells (2 degrees C) was found, possibly indicating that OH-radical-mediated effects are more temperature dependent. These results are similar to those recently found for the malignant MCF-7 cell line.
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PMID:Radiation and hypothermia: changes in DNA supercoiling in human diploid fibroblasts. 1069 53

A new concept in cryopreservation solution design was developed that focuses on the use of an intracellular-type, hypothermic maintenance medium coupled with additives that inhibit cryopreservation-induced apoptosis. HypoThermosol' (HTS), a hypothermic (4 degrees C) maintenance medium utilized in the long-term storage of cell, tissue, and organ systems, was tested for cryoprotective capability on a renal cell line (Madin-Darby Canine Kidney cells). HTS and HTS derivatives were tested against conventional cell culture medium (Dulbecco's Minimal Essential medium, DME) as the cryoprotectant carrier solution because (1) cells are exposed to an extended state of hypothermia during the freeze-thaw process, and (2) HTS is designed to protect cells exposed to a hypothermic state. Cells separately cryopreserved in either HTS or DME + 5% dimethyl sulfoxide (DMSO) yielded equivalent 24-h postthaw survival (approximately 30%) and 5-d recovery (approximately 90%). Cells cryopreserved in CryoStor CS 5, a HTS derivative containing 5% DMSO, yielded approximately 75% 24-h postthaw survival and recovery to 100% within 3 d. DNA gel electrophoresis was performed to determine the mechanisms of cell death contributing to cryopreservation failure. Cells preserved in DME (DMSO-free) died primarily through necrosis, whereas cells preserved in either DME + 5% DMSO, HTS, or CryoStor CS 5 died through a combination of apoptosis and necrosis. This observation led to the inclusion of an apoptotic inhibitor designed to improve cryopreservation outcome. MDCK cells cryopreserved in CryoStor CS 5 supplemented with an apoptotic inhibitor (Caspase I Inhibitor V), hereafter termed CryoStor CS 5N, resulted in a 24-h postthaw survival and recovery rate exceeding that of any other cryoprotective solution tested (85%). We conclude that: (1) the use of HTS (a dextran-based, intracellular-type solution) without DMSO can yield postthaw viability equivalent to that of standard DMSO-based cryopreservation methods, (2) postthaw viability can be significantly increased through the use of an intracellular-type solution in conjunction with DMSO, (3) the use of HTS allows for cryopreservation to be accomplished with reduced levels of cryoprotectants, and (4) the regulation of apoptosis is essential for the improvement of cryopreservation outcome.
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PMID:Cell viability improves following inhibition of cryopreservation-induced apoptosis. 1085 52

We report on an accidental extravasation of docetaxel given intravenously as chemotherapy in a cancer patient. The extravasate was immediately diluted subcutaneously with saline, in addition to which hypothermia (ice-packs) was implemented and topical dimethylsulfoxide (DMSO) was applied three times every 45 min. Corticosteroids and diclofenac were also administered. Dermatitis developed immediately but had disappeared within 24 h. Notably, dermatopathological changes were absent on days 2-4, minimal on day 5, and increased thereafter. Dermatitis developed as a late symptom, resulting in brown discoloration and skin hyperplasia. No plastic surgical intervention was necessary. We propose that isotonic saline, topical DMSO and local hypothermia may have restricted the inflammation and tissue necrosis induced by the extravasation of docetaxel. Repetitive topical application of DMSO beyond the day of extravasation had no additional benefit.
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PMID:Docetaxel extravasation. 1130 72


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