Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0020672 (hypothermia)
 17,327 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. Adenosine 3',5'-monophosphate (cAMP), its dibutyryl derivative (Db-cAMP) and other adenine nucleotides have been micro-injected into the hypothalamic region of the unanaesthetized cat and the effects on body temperature, and on behavioural and autonomic thermoregulatory activities observed. 2. Db-cAMP and cAMP both produced hypothermia when applied to the pre-optic anterior hypothalamus. With Db-cAMP the hypothermia was shown to be dose dependent between 50 and 500 mug (0-096-0-96 mumole). 3. AMP, ADP and ATP also produced hypothermia when injected into the pre-optic anterior hypothalamus. 4. The order of relative potencies of the adenine nucleotides with respect both to the hypothermia produced and to the autonomic thermoregulatory effects observed were similar. Db-cAMP was most potent and cAMP least. 5. Micro-injection into the pre-optic anterior hypothalamus of many substances including saline produced in most cats a non-specific rise in body temperature apparently the result of tissue damage. Intraperitoneal injection of 4-acetamidophenol (paracetamol 50 mg/kg) reduced or abolished this febrile response. 6. The hypothermic effect of the adenine nucleotides has been compared with the effects produced in these same cats by micro-injections of noradrenaline, 5-hydroxytryptamine, a mixture of acetylcholine and physostigmine (1:1), EDTA and excess Ca2+ ions. 7. It is concluded that as Db-cAMP and cAMP both produce hypothermia, it is unlikely that endogenous cAMP in the pre-optic anterior hypothalamus mediates the hyperthermic responses to pyrogens and prostaglandins.
 ...
PMID:The effects of cyclic adenosine 3',5'-monophosphate and other adenine nucleotides on body temperature. 17 Mar 96

Calcium, other divalent cations, and calcium antagonists were tested for their ability to alter ethanol-induced sleeping time, hypothermia, and behavioral intoxication in mice and rats. Calcium given intraventricularly significantly enhanced sleeping time and behavioral intoxication in a dose-related manner. The ionophores X537A and A23187 accentuated the effect of a low dose of calcium, whereas the calcium chelators EDTA and EGTA decreased sleeping time. Calcium also enhanced tertiary butanol- and chloral hydrate-induced sleeping time. The effects of cations on ethanol-induced hypothermia were less significant. The results suggest the existence of a central calcium pool that is involved in ethanol intoxication in rodents.
 ...
PMID:Ethanol: modifications of acute intoxication by divalent cations. 34 51

Survival of V-79 Chinese hamster cells was assessed by colony growth assay after hypothermic exposure in the presence of iron chelators. At 5 degrees C, maximum protection from hypothermic damage was achieved with a 50 microM concentration of the intracellular ferric iron chelator Desferal. A 3-hr prehypothermic incubation with 50 microM Desferal followed by replacement with chelator-free medium at 5 degrees C also provided some protection. This was not observed when the extracellular chelator DETA-PAC (50 microM) was used prior to cold storage. Treating 5 degrees C-stored cells with Desferal just prior to rewarming was ineffective, but treating cells with Desferal during hypothermia exposure after a significant period of unprotected cold exposure ultimately increased the surviving fraction. Submaximal protection during hypothermia was achieved to various degrees with extracellular chelators at 5 degrees C, including 50 microM DETAPAC and 110 microM EDTA. EGTA (110 microM) had little effect. The sensitization of cells at 5 degrees C with 200 microM FeCl3 could be reduced or eliminated with Desferal in accordance with a 1:1 binding ratio. At 10 degrees C, 50 microM Desferal, 50 microM DETAPAC, and 110 microM EDTA were as or less effective in protecting cells than at 5 degrees C. An Arrhenius plot of cell inactivation rates shows a break at 7-8 degrees C, corresponding to maximum survival for control cells and cells in 50 microM Desferal; however, the amount of protection offered by the chelator increases with decreasing temperature below about 19 degrees C, and sensitization increases above that point. It has not previously been shown that iron chelators protect against cellular hypothermia damage which is uncomplicated by previous or simultaneous ischemia. This may be relevant to the low-temperature storage of transplant organs, in which iron of intracellular origin and in the perfusate may be active and damaging.
 ...
PMID:Factors influencing survival of mammalian cells exposed to hypothermia. IV. Effects of iron chelation. 239 29

The ability of hypothermia (34 degrees, 28 degrees) to preserve cardiac metabolism and performance during ischemia, was evaluated in the isolated Langendorff perfused rabbit heart. The hearts, isolated and perfused aerobically for 20', were made ischemic for 90' and their wall temperature maintained either at 37 degrees, 34 degrees and 28 degrees. The hearts were consequently reperfused at 37 degrees for 30'. Some of the hearts were frozen and assayed for ATP and CP. Others were homogenized and their mitochondria harvest, using either an EDTA free or an EDTA-containing extraction medium. The oxidative phosphorylating and ATP generating capacity of these mitochondria were established and their Ca++ content determined. The mechanical performance of the hearts, which were paced, was monitored by means of an intra-ventricular balloon filled with water and connected with a pressure transducer. The hearts that were made ischemic and maintained at 37 degrees were severely depleted in ATP and CP content, their mitochondria accumulated Ca++ and their oxidative phosphorylating activity was impaired. During reperfusion mitochondrial Ca++ was substantially increased, the capacity of the mitochondria to use O2 for state III respiration was further impaired and their ATP generating capacity reduced. Diastolic pressure increased and there was no recovery of the ability of the hearts to develop sistolic pressure. The hearts made ischemic and maintained at 28 degrees were protected. There was a less marked rise in mitochondrial Ca++ concentration after ischemia and during reperfusion; the mitochondria recovered the capacity of utilizing O2 and of generating ATP. That was coincident with and almost complete recovery of mechanical performance. Hypothermia at 34 degrees during ischemia provoked only a partial protection. These results are discussed in accordance with the hypothesis that hypothermia protects heart muscle against the deleterious effects of ischemia not only by reducing the metabolic requirement but also by maintaining intracellular homeostasis with respect to Ca++.
 ...
PMID:[Effect and action mechanism of hypothermia to preserve the ischaemic myocardium (author's transl)]. 720 98

Administration of the EDTA, a substance binding calcium ions, helped to resume thermoregulation functions after their "cold paralysis" at the rectal temperature 17.1 +/- 0.2 degrees C and the brain temperature 19.2 +/- 0.2 degrees C, without warming up the animal. Enhancement of the muscle electrical activity following the EDTA administration was due both to increase in the number of bursts of shivering and to enhancement of their intensity. The findings suggest that, in hypothermia, improvement of conditions of the calcium ion transport from the cell cytosole into interstitial space helps to restoration of the cold muscle shivering as an important function of the thermoregulation.
 ...
PMID:[Resuming of thermoregulation in rats during deep hypothermia with EDTA without rewarming the body]. 984 99

Spontaneous EDTA-independent cold platelet agglutination is a rare phenomenon that produces pseudothrombocytopenia when blood samples are analyzed in automated cell counters. We report a case of platelet cold agglutinins and an analysis by flow cytometry. A 49 year old woman presented with abnormal vaginal bleed secondary to uterine fibroids. Platelet clumping was observed in blood samples taken in EDTA-, heparin- and citrate-containing tubes. In flow cytometric tests, patient serum agglutinated 16% of normal platelets at 22 degrees C, and 7% of platelets after incubation at 37 degrees C; in contrast, 3% and < 1% of platelets were agglutinated at 22 and 37 degrees C, respectively, after incubation with normal serum. Minimal agglutination (< 10%) was observed with patient serum at a titre of 1:5 or at temperatures > 30 degrees C. After incubation at 4 degrees C, IgM antibody and C3 were increased on the patient's platelets; no significant amount of IgM or C3 was detected on normal platelets. The specificity of the platelet cold agglutinin was determined by competitive inhibition by monoclonal anti-CD41(GPIIbIIIa). Before the addition of monoclonal antibody, patient's serum agglutinated 16% of normal platelets at 22 degrees C; after addition of anti-CD41 only 2% of the platelets were agglutinated. This blocking effect was not observed with anti-CD42. The patient's platelets functioned normally as determined by CD62 and CD63 expression in response to thrombin, normal platelet aggregation in response to collagen, ADP, and ristocetin, and a normal template bleeding time. In summary, platelet agglutination by a platelet cold agglutinin was quantitated by flow cytometry, the responsible antibody was characterized as a low titre IgM with minimal activity > 30 degrees C, and competitive binding studies supported the GPIIbIIIa complex as the binding site for the antibody. Since the antibody did not affect platelet function, we believe that these patients will not suffer complications from their platelet cold agglutinin, but it could pose a problem under circumstances such as cardiac surgery with hypothermia.
 ...
PMID:Platelet cold agglutinins: a flow cytometric analysis. 1035 Nov 32

Administration of small doses of the EDTA decreased by 15-20% the Ca2+ contentn in the blood plasma of rabbits and rats. The decrease coincided with an abrupt stimulation of the thermoregulation system of cooled animals. Restoration of the Ca2+ content in circulating blood coincided in time with repeated suppression of the system's functions. The findings corroborate the theory of a key role of the Ca2+ in sensitivity of the homoiothermal organism to cold and substantiates the method of restoring physiological functions in deep hypothermia without rewarming the body.
 ...
PMID:[Ca(2+) level in the animal blood and their cold resistance]. 1068 91

The cold inhibited functions of skin thermoreceptors, of the thermoregulation centre, and the respiration centre during deep hypothermia can be restored without rewarming the body. The methods used were developed to test the hypothesis that during deep hypothermia calcium ion concentration [Ca(2+)](i) in the cytoplasm increases. This causes a perturbation of cell metabolism, the impairment of cell membrane function that cause the inhibition of cell functioning, resulting in cell death. Such an increase in [Ca(2+)](i) most likely would result from an energy deficit in a deeply cooled cell, which would compromise the processes that maintain the [Ca(2+)](i) at about 10(-7) M. These processes require large amounts of energy since they occur against a large concentration gradient. With the use of EDTA the extracellular concentration of Ca(2+) has been lowered by 15-27%, so reducing the concentration gradient for Ca(2+) between the cell and the medium and in consequence facilitated the process the extrusion of cell Ca(2+).During a period of cooling, sufficient to impair normal functioning, the experimental lowering of blood Ca(2+) allowed the restoration of normal function without the need to rewarm. In such cases the animals survived after cooling the body to temperatures at which they would normally have succumbed. The data presented support the stated hypothesis that the impairment of cellular function in mammals by low temperatures is the result of an uncorrected rise in [Ca(2+)](i).
 ...
PMID:Physiological blocking of the mechanisms of cold death: theoretical and experimental considerations. 1088 Aug 71

Cold-induced platelet aggregation (CIPA) in PRP has previously been documented in connection with platelet preservation (4-15 degrees C). This report describes hypothermia-induced platelet aggregation (HIPA) in whole blood and at temperatures used in open-heart surgery (24-32 degrees C). HIPA (specifically, the formation of occlusive aggregates) was studied in human whole blood. Fresh heparinized (1.5 U/ml) human blood was cooled and maintained at target temperatures (15, 20, 24, 28, 32, or 37 degrees C) as it flowed (1 ml/min) through 75-cm long 1/32 inches internal diameter polymer conduit. The formation of aggregates in the tubing was verified using optical video microscopy and was quantified by a light-scattering method and a constant-pressure filtration method. Donors were tested at least twice at each target temperature and were classified into three separate response regimes (Low, Medium, and High) on the basis of the number of aggregates and the duration of their appearance. The screening of 121 donors (average age 22.3 +/- 4.3 years) for HIPA at 24 degrees C (the temperature of maximum response) indicated 14% High Responders, 18% Medium Responders, and 68% Low Responders. HIPA was inhibited by EDTA, citrate, PGE1, and Tirofiban, but not by aspirin, and it was enhanced by elevated heparin levels. HIPA was consistently noted in the blood of a subpopulation of donors, and the associated platelet aggregates in the blood of High Responders were rigid and occlusive. It is postulated that such aggregates may contribute to cognitive dysfunction noted in patients undergoing hypothermic open-heart surgery, and that postulus is being investigated.
 ...
PMID:Hypothermia-induced platelet aggregation in heparinized flowing human blood: identification of a high responder subpopulation. 1183 31

Influence of EDTA (C10H14N2Na2O8.2H2O) and EGTA (C14H24N2O10) on physiological functions homoiothermic organisms at deep hypothermia, was studied. White rats during cooling were in special sections without rigid fixing of head and limbs. In reply to intravenous introduction of EDTA and EGTA solutions, similar answers of the organisms were observed: raised breathing frequency and amplitude, intensity of electrical activity of muscles; these signs of activation of physiological functions lasted 8-10 minutes. Besides, of the 20th-30th minute after introduction of the second dose of preparations (at rectal temperature 17.1 +/- 0.5 degrees C), the secondary activation respiratory and thermoregulatory functions were registered. The termination of the cold shivering in experiments with introduction of EDTA and EGTA solutions occurred at lower temperatures in rectum and in a brain (16.7-17.3 degrees and 17.8-18.2 degrees C, resp.) than in control experiments (18.7 +/- 0.6 degrees C and 20.2 +/- 1.5 degrees C). The authors suppose that the activation of the thermoregulatory and respiratory functions is caused by a decrease in concentration of ions Ca2+ in the blood plasma.
 ...
PMID:[Stimulation of thermoregulatory and respiratory functions with the help of EDTA and EGTA during deep hypothermia in rats]. 1475 38


1 2 Next >>