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

The metabolic effects of combined antegrade/retrograde and antegrade cardioplegia on myocardial protection were evaluated and compared in 30 patients who underwent myocardial revascularization. All patients had three-vessel coronary artery disease, and the revascularization was done with exclusive use of arterial grafts (internal mammary artery, gastroepiploic artery). Myocardial protection consisted of oxygenated crystalloid cardioplegia, topical slushed ice, and moderate systemic hypothermia (34 degrees C). The patients were randomly separated into two groups: group A (n = 15), who received antegrade cardioplegia, and group A/R (n = 15), who received combined antegrade/retrograde cardioplegia. There was no significant difference between the two groups concerning preoperative and intraoperative data. After the first dose of cardioplegia, right ventricular temperature was significantly lower in group A/R (15 +/- 2 degrees versus 19 +/- 5 degrees C; p < 0.05), and there was no significant difference between the two groups in left ventricular temperature. Coronary sinus blood samples were obtained before bypass and 5, 10, and 15 minutes after reperfusion; there was no difference between the two groups concerning lactates, superoxide dismutase, and glutathione peroxidase. After reperfusion, malondialdehyde levels increased significantly in group A and there was no change in group A/R, with a significant difference between the two groups (at 10 minutes after reperfusion, 0.80 +/- 0.20 versus 0.53 +/- 0.16 mumol/L; p < 0.05). Right and left ventricular myocardial biopsies were performed before bypass and 15 minutes after reperfusion; there was no significant difference between the two groups concerning adenosine triphosphate and creatine phosphate myocardial concentrations.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Antegrade/retrograde cardioplegia in arterial bypass grafting: metabolic randomized clinical trial. 784 66

The current study was undertaken so that the effects of both ischemia and ischemia + hypothermia could be examined in mammalian liver. Particular reference was made to the function of glycolysis, which is the only mechanism for energy production under these conditions. The response of adenylate pools reflected the energy imbalance created during warm ischemia within minutes of organ isolation. ATP levels and energy charge values for control (freshly isolated) livers were 1.20 +/- 0.07 and 0.49 +/- 0.02 mumol/g. Within 5 min of warm ischemia, ATP levels had dropped well below control values and by 30 min warm ischemia, ATP, AMP, and E.C. values were 0.21, 2.01, and 0.17 mumol/g, respectively. Cold ischemic livers (flushed with Marshall's citrate solution and stored on ice) exhibited similar, but more protracted, patterns of adenylate depletion (ATP and ADP) and accumulation (AMP). In both warm and cold ischemic livers, levels of fructose-6-phosphate (F6P) and fructose-1,6-bisphosphate (F1,6P2) indicated a marked activation of glycolysis at the phosphofructokinase (PFK) locus after a certain time of ischemia. Although the activations occurred at different times (30 min and 10 h for warm and cold ischemic livers, respectively), the patterns of change in levels of glycolytic metabolites associated with the PFK-catalyzed reaction were similar; levels of F6P dropped and F1,6P2 increased. Changes in metabolite levels (phosphoenol pyruvate and pyruvate) associated with another key suspect regulatory enzyme, pyruvate kinase, indicated no role in regulatory control of glycolysis during warm or cold ischemia. The activation of PFK at 30 min and 10 h of warm and cold ischemia, respectively, may reflect the accumulating effects of loss of intracellular homeostasis, which leads to impending irreversible damage.
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PMID:Glycolysis and energy metabolism in rat liver during warm and cold ischemia: evidence of an activation of the regulatory enzyme phosphofructokinase. 798 53

Amino acid enrichment of cardioplegic solutions has been shown to improve both the metabolic and functional recovery of ischemic myocardium. However, because of the marked systemic vasodilatation involved, use of amino acid enrichment is limited to the periods of induction and reperfusion. Fumarate is a Krebs' cycle intermediate whose conversion to succinate is responsible for the generation of adenosone triphosphate and the oxidation of the reduced form of nicotinamide-adenine nucleotide which is the pathway by which aspartate exerts its effect. Fumarate may also function as a free-radical scavenger and is involved in calcium transport. To determine if fumarate-enriched blood cardioplegia would improve the functional recovery of the neonatal heart, 14 neonatal piglet hearts were isolated and placed on a blood-perfused working heart circuit. After the baseline functional and metabolic assessment was done, cold ischemic arrest was initiated with either standard blood cardioplegic solution (group I; N = 7) or fumarate-enriched (13 mmol/L) blood cardioplegic solution (group II; N = 7). Cardioplegic solution was given at a pressure of 40 mm Hg every 20 minutes for 2 hours, and topical hypothermia was used. Sixty minutes after warm whole blood reperfusion, the functional recovery at left atrial pressures of 3, 6, 9, and 12 mm Hg was 70%, 66%, 66%, and 65%, respectively, in group I, versus 102%, 106%, 105%, and 109%, respectively, in group II (p < 0.05). The tissue creatinine phosphate levels after reperfusion were significantly higher in group II hearts (15.0 +/- 1.2 mumol/g dry heart tissue) than in group I hearts (9.2 +/- 1.9 mumol/g dry heart tissue), although the adenosine triphosphate levels were not significantly different.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Fumarate-enriched blood cardioplegia results in complete functional recovery of immature myocardium. 801 Aug 14

In the present experimental study phospholipid peroxidation after hypothermia and rewarming was investigated in isolated buffer-perfused rat hearts. Stable normotherm perfusion (37 degrees C) for 20 min was followed by cooling to 14 degrees C, 4 h perfusion at 14 degrees C, and rewarming to 37 degrees C followed by 30 min normotherm perfusion. Seven hearts went through the whole protocol, whereas six hearts were subjected only to the initial stabilization period. Mechanical performance was measured by a balloon in the left ventricle (LV) permitting measurements of LV pressure and its derivatives. At the end of perfusion, hearts were freeze clamped in liquid nitrogen for phospholipid peroxidation measurements, phospholipid fatty acid composition, high-energy phosphate content (adenosine tri-, di-, and monophosphate and creatine phosphate), and tissue water content. After rewarming there was a significant reduction in mechanical performance and coronary flow. Tissue content of high-energy phosphates was decreased and tissue water content was increased. Levels of peroxidized polyunsaturated fatty acids (conjugated diens) in phospholipids and nonesterified fatty acids were not significantly changed (135.2 +/- 31.1 vs 74.3 +/- 7.6 nmol/g tissue dry wt and 1212 +/- 203 and 1685 +/- 197 nmol/g in control and rewarmed hearts. However, the amount of peroxidized polyunsaturated fatty acids in phospholipids expressed as a fraction of the phospholipids was significantly reduced by the cooling/rewarming procedure (1.28 +/- 0.22 vs 0.61 +/- 0.09 x 10(-3), P < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Phospholipid peroxidation in isolated perfused rat hearts subjected to hypothermia followed by rewarming: inverse relation to loss of function. 805 Feb 71

Cytosolic Ca2+ concentration of rat ventricular cells was measured under varying experimental conditions by using a fluorescent Ca2+ indicator, Fura-2. Resting [Ca2+]i of rat myocyte was 150 +/- 30 nM (n = 39), and this value was compatible with others. The Perfusion of cardioplegic solution significantly increased [Ca2+]i, and this effect was further augmented by hypothermia (p < 0.05). Application of nifedipine (5 x 10(-7) M) to the perfusate or pretreatment of caffeine (10 mM) had no apparent effect on this cardioplegia-induced [Ca2+]i change. But Ni2+ (5 mM), an antagonist of Na+/Ca2+ exchange mechanism, prevented the [Ca2+]i change during cardioplegia (p < 0.05). Magnitude of cardioplegia-induced [Ca2+]i increase was also dependent on the Ca2+ concentration of cardioplegic solution. These results suggest that Na+/Ca2+ exchange may play an important role in cardioplegia-induced [Ca2+]i change. To rule out the possibility whether the protective effect of hypothermic cardioplegia is due to the preservation of high-energy phosphate store or decreasing the transmembrane ionic fluxes by phase transition, we exhausted a energy store of cardiac cell by application of 2,4 dinitrophenol to the bath and measured its effect on [Ca2+]i change during cardioplegia. Hypothermic cardioplegia delayed the onset of [Ca2+]i increase and decreased its amplitude compared to those of normothermic cardioplegia. From the above results, hypothermic cardioplegia may protect the cardiac cells from ischemic insult by preserving a high-energy phosphate store. Application of Ni2+ to the cardioplegic solution or reduction of external Ca2+ concentration also had some protective effect, since it prevented [Ca2+]i increase during cardioplegia.
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PMID:Effect of hypothermic cardioplegia on cardiac protection--I. Effect of hypothermic cardioplegia on the cytosolic Ca2+ concentration in rat ventricular myocytes. 809 93

Enhancement of myocardial recovery with glutamate-enriched cold blood potassium cardioplegia (BPC) was evaluated using an isolated working heart model. Three groups of hearts from immature rabbits were subjected to 20 minutes of warm (37 degrees C) ischemia to allow energy depletion, followed by 90 minutes of hypothermic (10 degrees C) ischemia. Myocardial protection provided during hypothermia consisted of cardioplegia infusion, at 50 mm Hg every 30 minutes at 4 degrees C, of either St. Thomas' Hospital solution (group 1, n = 6), oxygenated BPC (group 2, n = 7), or oxygenated BPC enriched with 20 mmol/L L-glutamate (group 3, n = 7). Percent recovery of aortic flow was 87.6% +/- 6.3% (results expressed as mean +/- standard error of the mean) in group 3, which was significantly better than for either group 1 (63.4% +/- 4.0%) or group 2 (47.0% +/- 3.5%) (p < 0.05 by analysis of variance). Group 3 hearts had significantly better recovery of myocardial energy stores (mumol/g dry weight) compared with group 1 or 2 hearts: adenosine triphosphate, 17.8 +/- 1.1 versus 12.4 +/- 1.5 and 12.1 +/- 0.4; creatine phosphate, 25.9 +/- 1.8 versus 17.8 +/- 1.8 and 20.3 +/- 0.7; and glycogen, 140.7 +/- 12.6 versus 98.7 +/- 9.9 and 60.7 +/- 9.9 (p < 0.05). Glutamate-enriched BPC provided excellent myocardial protection after ischemia in this immature model, and this study quantitatively supports the use of glutamate-enriched BPC in neonatal clinical practice.
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PMID:Improved recovery of immature myocardium with L-glutamate blood cardioplegia. 809 34

Advances in myocardial preservation have led to improved patient survival after open heart operations. However, few studies have detailed the nature of national or regional patterns of cardioplegia use. To determine the regional pattern, all open heart surgery programs in Missouri were surveyed. During 1 year, it was found that cardioplegia was administered to 8,382 patients by 61 cardiothoracic surgeons at ten academic affiliated hospitals and 16 nonteaching hospitals. All cardioplegic solutions were hospital produced. Of 13 crystalloid solutions, 11 differed from one another and eight were intracellular formulations. Of 28 multidose blood-based cardioplegic solutions, there were 23 different mixtures. Most crystalloid (69%) and blood-based (89%) solutions differed substantially from commonly reported formulations. The incidences of the various additives to crystalloid solutions were as follows: bicarbonate, 92%; glucose, 69%; lidocaine, 54%; mannitol, 46%; magnesium, 31%; calcium, 23%; methylprednisolone, 15%; heparin, 8%; and acetate, 8%. Of the common blood-based cardioplegic solution additives, the following incidences were observed: glucose, 79%; bicarbonate, 43%; trishydroxyaminomethane, 36%; acetate, 29%; magnesium, 29%; procaine (or lidocaine), 25%; citrate-phosphate-dextrose, 18%; mannitol/albumin, 14%; nitroglycerin, 11%; glutamate/aspartate, 11%; calcium, 7%; insulin, 3%; and methylprednisolone, 3%. No calcium channel blocker or high-energy phosphate additives were reported. We conclude that many different cardioplegic admixtures that have not been tested experimentally are used routinely in clinical practice, presumably with acceptable results. Because the salutary effects of induced cardiac arrest and hypothermia may mask suboptimal solutions, further study of customized cardioplegia should be considered, particularly with regard to high-risk patients.
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PMID:Lack of cardioplegia uniformity in clinical myocardial preservation. 814 36

Both clinical and laboratory studies are being undertaken to investigate the deleterious neurologic and developmental effects associated with cardiopulmonary bypass, hypothermia, and circulatory arrest in the neonate and infant. A prospective, randomized clinical study of 171 neonates and young infants compared circulatory arrest with low-flow bypass (50 mL.kg-1.min-1). Circulatory arrest was associated with a higher incidence of early postoperative seizures as well as greater release of creatine kinase-BB. There was a strong correlation between duration of circulatory arrest and seizures (p = 0.004). The late consequences of these findings will be known at the completion of developmental assessment of all patients at 1 and 4 years of age. Laboratory studies have used a miniature piglet model that closely replicates clinical circulatory arrest. High-energy phosphate stores determined by magnetic resonance spectroscopy were maintained in animals undergoing 1 hour of low-flow bypass but became undetectable after 32 minutes of a 1-hour period of circulatory arrest. However, they returned to baseline within 3 hours of reperfusion as did cerebral blood flow and metabolism determined by microsphere studies. Piglets undergoing 1 hour of circulatory arrest showed more rapid recovery of cerebral adenosine triphosphate content and intracellular pH when managed with the pH-stat strategy during hypothermic bypass than with the more alkaline alpha-stat strategy. Other laboratory studies have examined pharmacologic methods of reducing cerebral injury associated with circulatory arrest including aprotinin, anti-CD18, neuronal receptor antagonists (MK801, NBQX), and blockade of glutamate release with adenosine in a cerebroplegia solution. These studies have suggested a number of promising approaches to improving the technique of circulatory arrest.
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PMID:Review of current research at Boston Children's Hospital. 826 70

A research program in cerebral ischemia was initiated by our laboratory to determine optimal strategies for cerebroprotection. Four studies relating to cerebroprotection using nuclear magnetic resonance spectroscopy in a sheep model of hypothermic cardiopulmonary bypass are summarized. These showed, first, that low-flow bypass, with a flow as low as 10 mL.kg-1 x min-1, maintained normal cerebral metabolism; second, that hypothermia increases the high-energy phosphate content and the intracellular pH of the brain; third, that hyperglycemia causes a profound intracellular acidosis; and, finally, that barbiturates prevent the normal increase in high-energy phosphates associated with hypothermia.
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PMID:Low-flow cardiopulmonary bypass and cerebral protection: a summary of investigations. 826 75

The effects of hypothermia on the intracellular pH of human erythrocytes were studied non-invasively using 31P NMR spectroscopy and the endogenous phosphorus-containing compounds glycerate 2,3-bisphosphate and inorganic phosphate. Specifically, the pH dependence of the 31P NMR chemical shifts of these compounds was used to measure the intracellular pH at 25 and 37 degrees C. The possibility of a non-pH-dependent change on the chemical shifts of the 2-P and 3-P resonances of glycerate 2,3-bisphosphate due to the presence of paramagnetic deoxy-haemoglobin (i.e., a pseudo-contact interaction) was investigated and found to have negligible effect under the present experimental conditions. The most probable reasons for this are that the deoxy-haemoglobin concentration was too small and/or the glycerate 2,3-bisphosphate does not get sufficiently close to the paramagnetic centre to be affected. The change in intracellular pH with temperature was consistent with that predicted by the alphastat hypothesis.
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PMID:The effects of hypothermia on the intracellular pH of erythrocytes studied using 31P NMR and endogenous compounds. 839 80


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