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

In order to reduce the operative injury of the endothelium in free reversed vein grafts, cultured human endothelial cells were used to test the optimal concentration of the constituents of a flushing solution for improved protection of the endothelium. The following solution proved to be the most suitable when tested at 20 degrees C; mannitol 160 mmol l-1, glucose 15 mmol l-1, NaCl 30 mmol l-1, KHCO3 5 mmol l-1, K2SO4 10 mmol l-1, KH2PO4 4 mmol l-1, MgSO4 20 mmol l-1, CaCl2 1.5 mmol l-1, potassium citrate 1.0 mmol l-1, Pluronic F-68 20 mg l-1, HEPES 4 mmol l-1, HEPES-Na 6 mmol l-1, pH 7.25, osmolality 325 mosmol kg-1 H2O. When endothelial cell injury was measured by a 51Cr-release assay, the new solution protected human endothelial cells in culture during hypothermic incubation better than isotonic NaCl, St Thomas' cardioplegic solution or Krebs-Henseleit's buffer. Transmission and scanning electron microscopy showed that the endothelium of human saphenous vein grafts was well preserved following 6 h of incubation at 20 degrees C with the new solution. As determined by morphometry using scanning electron microscopy, the endothelium of free porcine vein grafts was better preserved after incubation for 2 h at 20 degrees C with the new solution than with either isotonic NaCl (p = 0.02) or diluted, heparinized blood (p = 0.02) as the incubation medium, all cases observed following 2 h of subsequent arterial flow. The present study indicates that the endothelium of free vein grafts can be well protected against hypothermia when the flushing and irrigation fluid has a composition favouring endothelial protection. It appears likely that such treatment of vein grafts will reduce the frequency of vein graft narrowing and occlusion, post-operatively.
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PMID:A new protective solution for hypothermic storage of free vein grafts in cardiovascular surgery. 158

During hibernation the animals decrease their body temperature down to a few degrees above 0 degree C. This means that when entering into and arousing from hibernation their body temperature passes the critical level of 20 degrees C, a temperature region where nonhibernating mammals develop circulatory arrest, usually ventricular fibrillation (VF). We found in other experiments that the hibernator heart is resistant to VF, not only induced by hypothermia, but also when induced by local application of aconitine on the epicardium, addition of 0.55 molar CaCl2 to isolated hearts perfused with a potassium free Tyrode solution, addition of procaine to isolated hearts perfused with Tyrode solution after previous administration of adrenaline, ligation of the proximal part of the left anterior descending coronary artery, and electrical stimulation in the vulnerable phase of the heart cycle. Several mechanisms are at work to explain this resistance to VF of the hibernator heart when compared to the nonhibernator heart. The factors of greatest importance seem to be the different adrenergic innervation pattern, different physico-chemical properties with a lower melting point of the lipids in the hibernator, different enzyme temperature activity curves in the hibernator and a different handling of intracellular calcium resulting in a protection against calcium overload in the hibernator heart, when compared with the nonhibernator heart.
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PMID:The hibernator heart--nature's model of resistance to ventricular fibrillation. 181 81

Hibernators are resistant to ventricular fibrillation (VF) induced by hypothermia. This is in contrast to non-hibernating mammals which develop circulatory arrest, usually VF, in the temperature region 15-20 degrees C. The hedgehog which is a hibernator showed resistance to VF also when VF-evoking procedures other than hypothermia were used, such as local application of aconitine on the epicardium, administration of 0.55 M CaCl2 to isolated hearts perfused with a potassium-free modified Tyrode solution, injection of procaine HCl into isolated hearts perfused with a modified Tyrode solution after previous adrenaline administration, and ligation of the left descending coronary artery. Electrical stimulation in the vulnerable period produced VF in some but not in all the hedgehogs but a greater current was necessary than in guinea-pigs, all of which developed VF. Factors of possible importance to explain this difference in VF resistance are the QT duration which is short in hibernators, adrenergic innervation (ventricular muscle fibres in hibernators lack sympathetic innervation), metabolic factors (different temperature activity curves in hibernators compared to nonhibernating mammals) and ultrastructure (less skeletin filament in the conduction system of the hedgehog heart).
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PMID:Ventricular repolarization and fibrillation threshold in hibernating species. 408 17

Following detailed investigation and definition of some of the critical factors relating to the composition and use of cardioplegic protective solutions, we have formulated the St. Thomas' Hospital cardioplegic solution number 2. This cardioplegic solution (NaCl 110.0 mM, NaHCO3 10.0 mM, KCl 16.0 mM, MgCl2 16.0 mM, CaCl2 1.2 mM, pH 7.8) is designed for routine clinical use combining optimal protection with simplicity of formulation and administration/infusion. In order to characterize the efficacy of this modified solution, experiments have been carried out in two species: the isolated rat heart and the in-situ dog heart. In parallel protocols, hearts were subjected to ischemic arrest of up to 4 hours. Multidose (every 40 minutes) cardioplegic infusion of the St. Thomas' solution combined with topical hypothermia extended the tolerable period of ischemia from less than 30 minutes to about 120 minutes in the rat and from less than 60 minutes to more than 180 minutes in the dog. These conclusions were based on the measurement of functional indices together with biochemical, cellular chemical and ultrastructural assessments. The studies confirmed the additive protective properties of hypothermia and chemical cardioplegia and the utility of the rat heart model in the assessment of protective interventions.
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PMID:The St. Thomas' hospital cardioplegic solution: a characterization in two species. 627 81

Reperfusion of an isolated heart with calcium-containing solution after a short period of calcium-free perfusion may result in irreversible cell damage (calcium paradox). Experiments were undertaken to determine whether rat hearts could be predisposed to the calcium paradox by perfusion with Bretschneider's calcium-free histidine-buffered cardioplegic solution. Creatine kinase (CK) release during the reperfusion phase was used to quantitate cell damage. Perfusion with cardioplegic solution was performed at 37 degrees and 20 degrees C. Reperfusion after 10 minutes of perfusion with this solution at 37 degrees C resulted in a full calcium paradox. After 120 minutes of perfusion with cardioplegic solution at 20 degrees C, CK release during reperfusion amounted to 30% of the release during a full calcium paradox. This CK release could be further reduced by lowering the coronary flow rate or by adding 50 mumol X L-1 CaCl2 to the cardioplegic solution. It is concluded that a combination of hypothermia, a low coronary flow rate, and a limited duration of exposure to Bretschneider's histidine-buffered cardioplegic solution will minimize the risk of evoking the calcium paradox.
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PMID:Bretschneider's histidine-buffered cardioplegic solution and the calcium paradox. 688 57

We examined the properties of Mg2+ transport in rat kidney cortex slices and the effects of diuretics were also studied. Incubation with 1 mM 2,4-dinitrophenol, or under anaerobic conditions, sharply inhibited Mg2+ influx, while markedly stimulating Mg2+ efflux. Under conditions of hypothermia, partial inhibition of Mg2+ influx and significant enhancement of Mg2+ efflux were observed. Mg2+ influx was not affected by ouabain, by altering CaCl2 concentration in the medium, or by a change of Ca2+ content in the slices. Incubation with 1 mM ethacrynic acid or mersalyl depressed Mg2+ influx and stimulated Mg2+ efflux, p-chloromercuribenzoic acid (5 X 10(-4) M) had a similar effect and furosemide had no effect on Mg2+ transport. These results suggest that Mg2+ influx is mediated by an energy-dependent process which is dissociated from ouabain-sensitive Na+ transport and Ca2+ flux. Sulfhydryl groups may be involved in the process of Mg2+ influx.
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PMID:Divalent cation transport in kidney slices II. Magnesium transport in kidney cortex slices and effects of diuretics. 745 66

Lowering myocardial temperature increases contractile force, presumably by increasing intracellular calcium content. To study the mechanisms behind this, we compared the effects of some known inotropic interventions with hypothermia on mechanical restitution and post-rest contractile force in isolated guinea-pig papillary muscles. In four groups (n = 6 per group), the effects of: (1) reducing the ability for Na/Ca exchange to extrude Ca2+ (a) by increasing [Na+]i with ouabain or (b) by increasing [Ca2+]o; and (2) activation of calcium channels with Bay-K 8644, were compared with lowering temperature from 37 to 27 degrees C. Normally (at 37 degrees C and 2 mM CaCl2), mechanical restitution could be described by a rapid recovery phase with a time constant between 180 and 220 ms, followed by a slowly decaying phase with a time constant between 5000 and 8000 ms and post-rest contractions (1-10 min rest) were markedly depressed compared to steady-state contractions. Steady-state developed force was markedly increased at 27 degrees C, after 1 microM ouabain, 6 mM CaCl2 or 0.1 microM Bay-K 8644. At 27 degrees C the rapid recovery phase of restitution was delayed while the slowly decaying phase was not affected. Ouabain and increased [Ca2+]o caused elevation of the slowly decaying phase of restitution and markedly attenuated the post-rest depression of developed force, which may be attributed to a reduced diastolic extrusion of Ca2+ via the Na/Ca exchanger. Hypothermia and Bay-K 8644 on the other hand, augmented this post-rest depression. Hence, this study suggests that increased Ca2+ influx due to delayed inactivation of calcium channels may account for the increased developed force during hypothermia rather than reduced diastolic extrusion of Ca2+ via the Na/Ca exchanger.
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PMID:Mechanisms for hypothermia-induced increase in contractile force studied by mechanical restitution and post-rest contractions in guinea-pig papillary muscle. 769 97

Mild hypothermia enhances cardiac contractility, and volatile anesthetics depress contractility. Contractile force (tension) and Ca2+ transients were measured in canine Purkinje fibers at 35 and 25 degrees C with and without halothane and isoflurane to examine how anesthetics attenuate the positive inotropic effect of mild hypothermia. Isometric tension and light emitted from the photoprotein aequorin were used to assess contractility and intracellular Ca2+ transients in fibers stimulated at 40-60 pulses/min. At 35 degrees C, each anesthetic depressed peak tension and peak Ca2+ transients and decreased contractile force duration but, for halothane, increased Ca2+ transient duration. Decreases in tension by both anesthetics at 35 degrees C were converted to marked increases in tension at 25 degrees C, whereas Ca2+ transients were little changed. Removal of anesthetics at 25 degrees C greatly increased tension with a small increase in Ca2+ transients that was much lower than that at 35 degrees C. The curve relating peak contractile force as a function of Ca2+ transients at 25 degrees C during stepwise increases in extracellular CaCl2 was shifted steeper and leftward of the curve at 35 degrees C. These studies suggest that the positive inotropic effect of mild hypothermia is due primarily to increased myofibrillar Ca2+ sensitivity and that anesthetics decrease tension during hypothermia by decreasing myofibrillar Ca2+ sensitivity. Reduced influx of transsarcolemmal or sarcoplasmic reticular Ca2+ may also play a role during mild hypothermia.
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PMID:Hypothermia modifies anesthetic effect on contractile force and Ca2+ transients in cardiac Purkinje fibers. 806 28

Cardiac hypothermia alters contractility and intracellular Ca2+ concentration ([Ca2+]i) homeostasis. We examined how left ventricular pressure (LVP) is altered as a function of cytosolic [Ca2+]i over a range of extracellular CaCl2 concentration ([CaCl2]e) during perfusion of isolated, paced guinea pig hearts at 37 degrees C, 27 degrees C, and 17 degrees C. Transmural LV phasic [Ca2+] was measured using the Ca2+ indicator indo 1 and calibrated (in nM) after correction was made for autofluorescence, temperature, and noncytosolic Ca2+. Noncytosolic [Ca2+]i, cytosolic diastolic and systolic [Ca2+]i, phasic [Ca2+]i, and systolic Ca2+ released per beat (area Ca2+) were plotted as a function of 0.3-4.5 mM [CaCl2]e, and indexes of contractility [LVP, maximal rates of LVP development (+dLVP/dt) and relaxation (-dLVP/dt), and the integral of the LVP curve per beat (LVParea)] were plotted as a function of [Ca2+]i. Hypothermia increased systolic [Ca2+]i and slightly changed systolic LVP but increased diastolic LVP and [Ca2+]i. The relationship of diastolic and noncytosolic [Ca2+] to [CaCl2]e was shifted upward at 17 degrees C and 27 degrees C, whereas that of phasic [Ca2+]) to [CaCl2]e was shifted upward at 17 degrees C but not at 27 degrees C. The relationships of phasic [Ca2+]i to developed LVP, +dLVP/dt, and LVP(area) were progressively reduced by hypothermia so that maximal Ca2+-activated LVP decreased and hearts were desensitized to Ca2+. Thus mild hypothermia modestly increases diastolic and noncytosolic Ca2+ with little effect on systolic Ca2+ or released (area) Ca2+, whereas moderate hypothermia markedly increases diastolic, noncytosolic, peak systolic, and released Ca2+ and results in reduced maximal Ca2+-activated LVP and myocardial sensitivity to systolic Ca2+.
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PMID:Modulation of myocardial function and [Ca2+] sensitivity by moderate hypothermia in guinea pig isolated hearts. 1060 Aug 52

In rats, data on influence of i. v. administration of calcium chloride on the level of [Ca2+] in the blood and on process of oppression ofthermoregulatory and respiratory functions in rats in hypothermia. 0.18 or 0.135 mmol Ca2+ on the 3rd minute from beginning of the administration increased [Ca2+] in the blood from 1.01 +/- 0.03 to 2.56 +/- 0.08 mM (or 2.27 +/- 0.06 mM). Then [Ca2+] was reduced gradually, in 20 minutes from administration, solution of CaCh [Ca2+] exceeded the initial level by 20-30 %. The increase of concentration of ionized calcium in the rat blood strengthened the cold oppression of breathing and cold shivering as compared with the control (administration of physiological solution). Arrest of breathing in rats after administration of CaCl2 solution occurred at higher rectal temperatures (21 +/- 0.03 degrees C) as compared with control experiments (18 +/- 0.4 degrees C), p < 0.05. It is suggested that increase of [Ca2+] in the blood strengthens effects of cold in the form of oppression of thermoregulatory and respiratory functions.
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PMID:[Development of hypothermia in rats at increase of [Ca2+] in the blood]. 1807 91


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