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

Platelet dysfunction and loss of procoagulants and platelets leads to impaired hemostasis after cardiopulmonary bypass (CPB). Preoperative platelet sequestration delays surgery, and the large volume shifts, necessary to harvest therapeutically effective components, may be associated with hemodynamic instability. We performed platelet and plasma sequestration after the initiation of CPB during the cooling period in patients undergoing surgery in deep hypothermic cardiac arrest. Five patients who underwent major vascular surgery in deep hypothermia were enrolled in this pilot study. Platelet and plasma sequestration was performed during cooling with the CATS cell saver using the plasma sequestration set. Before processing, 2 x 1,000 ml of blood were concentrated by means of hemofiltration to reduce dilution effects of CPB. The autologous platelet concentrates were rotated at 24 degrees C, and the plasma was stored at room temperature. The harvested plasma and platelets were re-transfused during modified ultrafiltration after CPB. Platelet count, 20 mmol/L ADP stimulated platelet aggregation, and fibrinogen levels were measured preoperatively in the harvested material and in patient blood before and after transfusion. A heparinase thromboelastogram (TEG) was performed preoperatively before and after re-transfusion. There was a significant increase in the ADP stimulated platelet aggregation, platelet count, fibrinogen level, and maximum amplitude of the TEG after re-transfusion of the harvested material. No patient needed transfusion of fresh frozen plasma or random donor platelet concentrates. No patient needed re-exploration due to hemorrhage. The data presented provide evidence that autologous plasma and platelet sequestration during CPB initiation is effective. The harvested material reveals a high platelet count and fibrinogen level and preserves functional integrity.
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PMID:Autologous plasma and platelet sequestration at the beginning of cardiopulmonary bypass: a pilot investigation in five patients undergoing extended vascular surgery in deep hypothermia. 1181 86

The purpose of the study is to comparatively evaluate the impact of normo- and hypothermic perfusion on acid-base balance (ABB), gas blood composition, metabolic parameters, and hemostasis. Fifty patients undergone multiple aortocoronary bypass under extracorporeal circulation (EC) were examined. Twenty four patients and 26 (Groups 1 and 2, respectively) had been operated on under normo- and hypothermia. The groups did not differ in age, body weight, the duration of an operation, the number of shunts, the time of EC, and myocardial ischemia. ABB, gas blood composition, the concentrations of hemoglobin, lactate, fibrinogen, prothrombin time, thrombin time, activated partial thromboplastin time, activated coagulation time, blood coagulation time as described by Leigh-White, the count of platelets, and ADP-induced platelet aggregation in the early postperfusion and postoperative periods, following 24 and 48 hours after surgery. There were no significant differences in the values of ABB, gas blood composition, blood lactate levels in patients from both groups. However, metabolic acidosis, elevated blood lactate concentrations were more frequently encountered in Group 2 patients, which suggests that hypothermia prduces a more aggressive effect on systemic homeostasis. Impact of normo- and hypothermia on the coagulative link of homeostasis was not revealed. Nevertheless, hypothermic EC halved the functional activity of platelets, which has a substantial effect on the size of postoperative blood loss.
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PMID:[Temperature regimen of extracorporeal circulation during aortocoronary bypass surgery]. 1261 Dec 98

Isolated hepatocytes in suspension provide a number of advantages for use in bioartificial liver device, however, poor stability of this cell preparation at physiological temperatures is an apparent barrier preventing their use. We therefore investigated the integrity and differentiated function of isolated rat hepatocytes under conditions of mild hypothermia. Isolated hepatocytes were suspended in a bicarbonate buffered saline medium, supplemented with glucose and bovine serum albumin (BSA), and maintained for 48 h at 25 degrees C on a rotary shaker under an atmosphere of 95% O2 and 5% CO2. Under these conditions there was no significant decline in cell viability and good preservation of cellular morphology on transmission electron microscopy for at least 24 h. Isolated hepatocytes in suspension at 25 degrees C were also able to maintain normal Na+ and K+ ion gradients. The cellular energy status ([ATP], ATP/ADP ratio, cytoplasmic and mitochondrial redox potentials), metabolic function (urea synthesis and ammonia removal), albumin synthesis and phase I and phase II drug detoxification activity of these cells were also maintained for at least 24 h post isolation. These observations demonstrate the robust nature of mildly hypothermic isolated hepatocytes in suspension and encourage further studies re-examining the feasibility of using this cell preparation in bioartificial livers.
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PMID:Maintenance of integrity and function of isolated hepatocytes during extended suspension culture at 25 degrees C. 1295 84

Endovascular cooling was assessed as a potential treatment for percutaneous coronary intervention in patients with acute myocardial infarction. Here we show that mild hypothermia: (1) inhibits platelet aggregation; (2) augments eptifibatide- and tirofiban- but not abciximab-induced inhibition of platelet aggregation; (3) increases the formation of adenosine diphosphate-induced leukocyte-platelet aggregates; and (4) diminishes the glycoprotein IIb/IIIa antagonist-induced decrease in leukocyte-platelet aggregates.
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PMID:Combined effects of mild hypothermia and glycoprotein IIb/IIIa antagonists on platelet-platelet and leukocyte-platelet aggregation. 1458 64

Isolated mongrel hearts were preserved for 6 h at 5 degrees C followed by normothermic reperfusion for 2 h. The dogs were divided into three groups; K+-cardioplegic solution alone, group C, n = 7; K+-cardioplegic solution with lidocaine 200 mg/l, group L, n = 7; and K+-cardioplegic solution with betamethasone 250 mg/l and lidocaine 200 mg/l, group B + L, n = 7. Ventricular fibrillation occurred early during reperfusion in all dogs in group C, in one of seven in group L, and in two of seven dogs in group B + L. The serum MB fraction of creatinine kinase (MB-CK), mitochondrial aspartate aminotransferase (m-AAT) and calcium overload were suppressed to a greater extent in both groups L and B + L during reperfusion compared to group C. Myocardial ATP, total adenine nucleotide, and creatine phosphate did not differ between the three groups at the end of reperfusion. Myocardial ADP and AMP declined significantly during reperfusion in group C, however, they remained unchanged in group B + L and increased in group L which showed significantly higher levels compared to group C. Left ventricular functional recovery during reperfusion was consistently better in both group L and B + L compared to group C. These results suggested that membrane stabilization prevents myocardial damage from hypothermia and cardioplegia and provides better myocardial viability and functional recovery in donor heart preservation.
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PMID:The significant role of membrane stabilization in hypothermic cardioplegic cardiac preservation in a canine experimental model. 1462 34

Deep Hypothermic Circulatory Arrest (DHCA) is employed during thoracic aortic and congenital heart surgery, and can induce postoperative neurological damage probably caused by microthrombembolism. Hypothermia has been reported to induce platelet activation and aggregation. The platelet activation marker P-selectin mediates binding of platelets to leukocytes. Tirofiban and eptifibatide, short-acting inhibitors of the platelet fibrinogen receptor GP IIb/IIIa, have recently been shown to protect platelet function without increasing bleeding during heart surgery using cardiopulmonary bypass. The aim of this study was to investigate the effect of tirofiban and eptifibatide on platelets and platelet-leukocyte interaction under DHCA conditions in vitro. Platelet aggregation, binding of the GP IIb/IIIa activation specific antibody PAC-1, P-selectin expression as well as monocyte and granulocyte content of aggregates were investigated in unstimulated and ADP-stimulated samples using flow cytometry. Tirofiban and eptifibatide inhibited massive platelet aggregation and PAC-1 binding which were induced by DHCA conditions. P-selectin expression was inhibited by tirofiban but increased by eptifibatide at hypothermia. Platelet-bound leukocytes were present in all samples. Eptifibatide increased granulocyte content of aggregates at hypothermia in ADP-stimulated samples. We conclude that under conditions of DHCA both tirofiban and eptifibatide inhibit platelet aggregation but have different effects on platelet P-selectin expression and platelet-leukocyte interaction. Application of a short-acting and non-activating GP IIb/IIIa inhibitor should be considered during DHCA in vivo to prevent occlusion of the microvasculature and subsequent organ damage.
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PMID:Glycoprotein IIb/IIIa inhibition reduces prothrombotic events under conditions of deep hypothermic circulatory arrest. 1611 94

The remarkable time-resolution enhancement by deep lethargic hypothermia (15 degrees C rectal temperature, "cold narcosis," "anesthesia by internal cold") of metabolic events in the rat brain after oxygen deprivation has been exploited to monitor metabolic changes by in vivo (31)P-NMR. A correlation was established between the bioenergetic status of the brain and physiological descriptors of tolerance (survival and revival times) determined in parallel experiments with large series of animals. Spectral peak integrals were transformed into absolute concentrations by comparison to biochemically determined time series of data obtained in freeze-trapping experiments conducted under identical conditions. Serial spectra were used to reconstruct the time-course kinetics of intracellular brain pH and of concentration changes of inorganic phosphate, phosphocreatine, ATP, and ADP. Both the biochemical and NMR time series of data were simultaneously fitted by a set of exponential kinetic equations accounting for relationships imposed by the Lohmann and adenylate kinase reactions. Depletion profiles were then computed for a number of descriptors of brain energy status (energy charge, phosphorylation potential, total adenylate, and primary energy stores expressed as the sum of high-energy phosphate-bond equivalents). The results contribute to the understanding of the role of brain energetics in tolerance to oxygen deprivation.
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PMID:Brain energetics and tolerance to anoxia in deep hypothermia. 1615 18

Mitochondrial very-long-chain acyl-CoA dehydrogenase (VLCAD) deficiency is associated with severe hypoglycemia, cardiac dysfunction, and sudden death in neonates and children. Sudden death is common, but the underlying mechanisms are not fully understood. We report on a mouse model of VLCAD deficiency with a phenotype induced by the stresses of fasting and cold, which includes hypoglycemia, hypothermia, and severe bradycardia. The administration of glucose did not rescue the mice under stress conditions, but rewarming alone consistently led to heart rate recovery. Brown adipose tissue (BAT) from the VLCAD-/- mice showed elevated levels of the uncoupling protein isoforms and peroxisome proliferator-activated receptor-alpha. Biochemical assessment of the VLCAD(/- mice BAT showed increased oxygen consumption, attributed to uncoupled respiration in the absence of stress. ADP-stimulated respiration was 23.05 (SD 4.17) and 68.24 (SD 6.3) nmol O2.min(-1).mg mitochondrial protein(-1) for VLCAD+/+ and VLCAD-/- mice, respectively (P < 0.001), and carbonyl cyanide p-trifluoromethoxyphenylhydrazone-stimulated respiration was 35.9 (SD 3.6) and 49.3 (SD 9) nmol O2.min(-1).mg mitochondrial protein(-1) for VLCAD+/+ and VLCAD-/- mice, respectively (P < 0.20), but these rates were insufficient to protect them in the cold. We conclude that disturbed mitochondrial bioenergetics in BAT is a critical contributing factor for the cold sensitivity in VLCAD deficiency. Our observations provide insights into the possible mechanisms of stress-induced death in human newborns with abnormal fat metabolism and elucidate targeting of specific substrates for particular metabolic needs.
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PMID:Abnormal mitochondrial bioenergetics and heart rate dysfunction in mice lacking very-long-chain acyl-CoA dehydrogenase. 1619 75

Resuscitation from cardiac arrest results in reperfusion injury that leads to increased postresuscitation mortality and delayed neuronal death. One of the many consequences of resuscitation from cardiac arrest is a derangement of energy metabolism and the loss of adenylates, impairing the tissue's ability to regain proper energy balance. In this study, we investigated the effects of adenosine (ADO) on the recovery of the brain from 12 min of ischemia using a rat model of cardiac arrest and resuscitation. Compared to the untreated group, treatment with adenosine (7.2 mg/kg) initiated immediately after resuscitation increased the proportion of rats surviving to 4 days and significantly delayed hippocampal CA1 neuronal loss. Brain blood flow was increased significantly in the adenosine-treated rats 1 h after cardiac arrest and resuscitation. Adenosine-treated rats exhibited less edema in cortex, brainstem and hippocampus during the first 48 h of recovery. Adenosine treatment significantly lowered brain temperature during recovery, and a part of the neuroprotective effects of adenosine treatment could be ascribed to adenosine-induced hypothermia. With this dose, adenosine may have a delayed transient effect on the restoration of the adenylate pool (AXP = ATP + ADP + AMP) 24 h after cardiac arrest and resuscitation. Our findings suggested that improved postischemic brain blood flow and ADO-induced hypothermia, rather than adenylate supplementation, may be the two major contributors to the neuroprotective effects of adenosine following cardiac arrest and resuscitation. Although adenosine did not prevent eventual CA1 neuronal loss in the long term, it did delay neuronal loss and promoted long-term survival. Thus, adenosine or specific agonists of adenosine receptors should be evaluated as adjuncts to broaden the window of opportunity in the treatment of the reperfusion injury following cardiac arrest and resuscitation.
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PMID:Adenosine treatment delays postischemic hippocampal CA1 loss after cardiac arrest and resuscitation in rats. 1641 92

We systematically evaluated the effects of test temperature and storage temperature on platelet aggregation using flow cytometry and impedance aggregometry. Aliquots of citrated whole blood from 27 healthy adult male volunteers were stored at 37 degrees C and 22 degrees C. Aliquots were subjected to impedance aggregometry in response to collagen, adenosine diphosphate, ristocetin, and arachidonic acid performed at 22 degrees C, 34 degrees C, 37 degrees C, and 40 degrees C. The expression of activated fibrinogen receptor was determined on adenosine diphosphate-activated platelets at 22 degrees C and 37 degrees C by whole blood flow cytometry using PAC-1 for fluorescent staining. Aggregation induced by collagen, ristocetin, and arachidonic acid was not significantly different at the test temperatures of 34 degrees C and 37 degrees C but was significantly impaired at 22 degrees C. In contrast, adenosine diphosphate-induced aggregation was significantly increased at both 34 degrees C and 22 degrees C. Hyperthermia exclusively impaired collagen-induced aggregation. Storage temperature of 22 degrees C exclusively enhanced adenosine diphosphate- and collagen-induced aggregation compared with storage at 37 degrees C. The binding of PAC-1 was enhanced at test temperatures below 37 degrees C. Prewarming the antibody above 22 degrees C significantly decreased binding. Our results suggest that mild hypothermic test conditions have no relevant effect, whereas profound hypothermia induces defects in adhesion, thromboxane generation, and activation. The pathomechanism for the increased response to adenosine diphosphate at mild and profound hypothermia remains unclear. Storage temperature considerably affects the aggregation response to the agonists adenosine diphosphate and collagen but not to arachidonic acid and ristocetin. Flow cytometry using the temperature-labile antibody PAC-1 fails to assess temperature effects on platelet aggregability.
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PMID:The effects of test temperature and storage temperature on platelet aggregation: a whole blood in vitro study. 1655 37


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