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

Patients with intracerebral hemorrhage (ICH) may deteriorate progressively after the initial ictus because of the brain edema around the hematoma. Recently, thrombin has become known to play an important role in the brain edema formation after ICH. In this study, we examined the effect of brain hypothermia on brain edema formation after hematoma and thrombin injection into the brain in rats and clarified the mechanism of hypothermia on brain damage. Anesthetized Sprague-Dawley rats received an injection of 100 microL of autologous blood or 10 units of bovine thrombin into the basal ganglia. Animals were divided into the normothermic and hypothermic groups, which were housed in a room at 25 degrees C and in a cold room at 5 degrees C respectively, for 24 hours. Brain water content was significantly reduced with hypothermia in the cortex (80.8 vs. 79.7% p < 0.05) after hematoma induction. After thrombin injection, brain water content was also significantly reduced with hypothermia in the basal ganglia (84.5 vs. 82.2%; p < 0.01), accompanied by a significant reduction in blood-brain barrier (BBB) permeability to Evan's blue (29.4 vs. 11.6 ng/g tissue; p < 0.05) and in accumulation of polymorphonuclear leukocytes (3.03 vs. 0.27 U of myeloperoxidase/g tissue; p < 0.01). This study indicates that brain hypothermia significantly reduces brain edema formation after hematoma and thrombin injection into the brain in rats. Inhibition of thrombin-induced BBB breakdown and inflammatory response with hypothermia appear to contribute to brain protection in this model.
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PMID:Effects of brain hypothermia on brain edema formation after intracerebral hemorrhage in rats. 1216 13

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

Opiate addicts have been shown to have a high susceptibility to bacterial infection. We investigated how treatment with morphine alters lipopolysaccharide (LPS)-induced inflammatory responses in the rat. Chronic morphine alone elevated serum endotoxin levels. Animals treated with morphine and LPS (250 microg/kg) developed hypothermia, decreased mean arterial pressure (MAP), increased plasma thrombin anti-thrombin III (TAT) complex, and approximately 67% of animals exhibited progressive intramicrovascular coagulation. Morphine also enhanced LPS-induced leukocyte-endothelial adhesion (LEA), suppressed leukocyte flux, and corticosterone production, and elevated interleukin-1beta, tumor necrosis factor-alpha, and interleukin-6 serum levels. Our study presents both the molecular and cellular mechanisms underlying the potentiated LPS-induced inflammation and accelerated progression to septic shock seen with chronic morphine exposure.
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PMID:Chronic morphine accelerates the progression of lipopolysaccharide-induced sepsis to septic shock. 1502 69

Coagulopathy following massive transfusion is a consequence of post-traumatic and surgical hemorrhage. Bleeding following massive transfusion can occur due to hypothermia, dilutional coagulopathy, platelet dysfunction, fibrinolysis, or hypofibrinogenemia. Transfusion of 15 to 20 units of blood products causes dilutional thrombocytopenia, and both antiplatelet agents (eg, clopidogrel [Plavix, Sanofi, Bridgewater, NJ]) and hemostatic inhibitors (eg, low-molecular-weight heparins, pentasaccharides, and direct thrombin inhibitors) are contributing factors to bleeding. Tests for platelet dysfunction are not readily available. Excessive fibrinolysis and low fibrinogen are also causes of bleeding in these patients. Currently, however, there are several agents that have been reported to be effective for the prophylaxis of hemorrhage in surgical patients, including aprotinin for cardiac surgery, orthopedic surgery, and hepatic transplantation, and the off-label use of recombinant activated factor VII (NovoSeven, Novo Nordisk, Bagsvaerd, Denmark) as rescue therapy for life-threatening hemorrhage.
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PMID:Massive transfusion coagulopathy. 1642 87

Clinical coagulopathy frequently occurs in the presence of hypothermia. The primary purpose of this study was to investigate the effects of hypothermia on clotting protein fibrinogen metabolism and on coagulation function in a swine model. Twelve pigs were randomly allocated into control and hypothermia groups. Hypothermia of 32 degrees C was induced using a blanket with circulating water at 4 degrees C. Fibrinogen synthesis and breakdown were quantified using a 6-hour stable isotope infusion with subsequent gas chromatograph and mass spectrometry analysis. Clotting enzyme thrombin generation kinetics was quantified at baseline and at the end of the infusion. Changes in fibrinogen metabolism and thrombin generation were correlated with coagulation function assessed by thromboelastography (TEG). Hypothermia decreased fibrinogen synthesis from the control value of 2.6 +/- 0.4 to 1.2 +/- 0.2 mg kg(-1) h(-1) (P < .05), with no effect on fibrinogen breakdown. Thrombin generation at the initiation phase was delayed by hypothermia, but there were no changes at the propagation phase. In thromboelastography measurements, the initial clotting time (R time) was prolonged from the baseline value of 3.01 +/- 0.13 to 4.30 +/- 0.24 minutes (P < .05) and clotting rapidity (angle alpha) was decreased from the baseline value of 72.30 +/- 0.90 to 65.34 +/- 1.07 (P < .05). Hypothermia caused no significant changes in clot strength (maximum amplitude) and clot lysis (LY(60)). We concluded that hypothermia caused a potential deficit in fibrinogen availability and a delay in thrombin generation, consequently inhibiting coagulation function. Our data support the current practices of rewarming and prescribing recombinant factor VIIa for hypothermic patients with coagulation defects.
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PMID:The effects of hypothermia on fibrinogen metabolism and coagulation function in swine. 1722 35

The authors propose that hemostasis occurs in a stepwise process, regulated by cellular components in vivo. The effectiveness of hemostasis in vivo depends not only on the procoagulant reactions but also on the fibrinolytic process. Causes of coagulopathic bleeding include consumption of coagulation factors and platelets, excessive fibrinolysis, hypothermia, and acidosis. Generation of the right amount of thrombin during the coagulation process not only may be essential for effective hemostasis but also may set the stage for effective wound healing.
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PMID:Coagulation 2006: a modern view of hemostasis. 1725 14

We have developed a miniaturized semiclosed cardiopulmonary bypass (CPB) circuit incorporating a centrifugal blood pump (TinyPump) with a volume of 5 ml. The current study was undertaken to evaluate the hemolytic performance of the TinyPump in comparison with the BioPump and to investigate the impact of different CPB circuit volumes on hemodilution, coagulation, and the inflammatory response. Twelve 1-week-old piglets (3.4 +/- 0.2 kg) were used. The circuit comprised a centrifugal pump, a membrane oxygenator, and a cardiotomy reservoir. Cardiopulmonary bypass was conducted with mild hypothermia at 150 ml/kg/min for 3 hours. Transfusion was not performed. Priming volume was 68 ml for the circuit with the TinyPump and 111 ml for the circuit with the BioPump. Although the TinyPump required higher speed, plasma free hemoglobin levels after CPB were not different between the groups. After CPB, the TinyPump group had a significantly higher hematocrit (27% +/- 3% vs. 23% +/- 3%) and lower platelet reduction rate, lower thrombin-antithrombin complex levels, and lower interleukin-6 levels. Better lung compliance with less water content was observed in the TinyPump group. The TinyPump maintained CPB with acceptable hemolysis and lower inflammatory responses. This miniaturized CPB circuit may make transfusion-free open heart surgery feasible in neonates and would help to prevent postoperative organ dysfunction.
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PMID:Efficacy of a miniature centrifugal rotary pump (TinyPump) for transfusion-free cardiopulmonary bypass in neonatal piglets. 1804 45

Hyper-coagulation, hypothermia, systemic inflammatory responses and shock are major clinical manifestations of endotoxin shock syndrome in human. As previously reported, mice primed with heat-killed Propionibacterium acnes are highly susceptible to the action of LPS to induce tumour necrosis factor (TNF)-alpha and to that of TNF-alpha to trigger lethal shock. Here we investigated the mechanisms underlying the P. acnes-induced sensitization to LPS and TNF-alpha and the development of individual symptoms after subsequent challenge with LPS or TNF-alpha. Propionibacterium acnes-primed wild-type (WT) mice, but not naive mice, exhibited hyper-coagulation with elevated levels of thrombin-antithrombin complexes and anti-fibrinolytic plasminogen activator inhibitor 1 in their plasma, hypothermia, systemic inflammatory responses and high mortality rate after LPS or TNF-alpha challenge. Propionibacterium acnes treatment reportedly induces both T(h)1 and T(h)17 cell development. Propionibacterium acnes-primed Il12p40(-/-) and Ifngamma(-/-) mice, while not Il17A(-/-) mice, evaded all these symptoms/signs upon LPS or TNF-alpha challenge, indicating essential requirement of IL-12-IFN-gamma axis for the sensitization to LPS and TNF-alpha. Furthermore, IFN-gamma blockade just before LPS challenge could prevent P. acnes-primed WT mice from endotoxin shock syndrome. These results demonstrated requirement of IFN-gamma to the development of endotoxin shock and suggested it as a potent therapeutic target for the treatment of septic shock.
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PMID:IFN-gamma is a master regulator of endotoxin shock syndrome in mice primed with heat-killed Propionibacterium acnes. 2013 Feb 31

Hemorrhage is a significant pathological feature of some fever or hyperthermia-related diseases, such as dengue fever and heatstroke. Although the mechanisms of hemorrhage in these diseases are thought to be complex, whether there is an association between hemorrhage and hyperthermia or fever remains unclear. Platelets play a central role in maintaining integrity of endothelium and biological hemostasis. To explore the effect of hyperthermia on platelet physiology, platelet-rich plasma or washed platelets were incubated at hypothermia (22 degrees C), normothermia (37 degrees C) or hyperthermia (40 and 42 degrees C) for 1 or 2 hours. ADP and alpha-thrombin induced platelet aggregations were obviously reduced in platelets incubated at hyperthermia. Hyperthermia induced apoptotic events in platelets, including depolarization of mitochondrial inner transmembrane potential, caspase-3 dependent gelsolin cleavage and phosphatidylserine exposure. Furthermore, hyperthermia incurred platelet glycoprotein Ibalpha ectodomain shedding. Thus, these data suggest that hyperthermia induces platelet apoptosis and dysfunction. These findings have important implications for the pathogenesis of hemorrhage in fever or hyperthermia-related diseases, and also suggest that attention should be paid to platelet apoptosis under relatively high temperature conditions.
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PMID:Hyperthermia induces platelet apoptosis and glycoprotein Ibalpha ectodomain shedding. 2015 80

Physical injuries, especially road traffic injuries, are a leading cause of death and morbidity worldwide, ranking fifth among the leading causes of death in the United States. Immediate and early trauma deaths are mainly determined by primary brain injuries and/or hemorrhages, whereas late mortality is caused by secondary brain injuries, host defense failure, and superimposed complications including also disseminated intravascular coagulation (DIC). Trauma patients are particularly susceptible to the early development of coagulopathy, and the most severely injured patients are coagulopathic on hospital admission. The zenith of the problem is typically seen in patients with head injuries and in those who are massively injured and transfused. The resulting coagulopathy is characterized by nonsurgical bleeding from mucosal lesions, serosal surfaces, and wound and vascular access sites. DIC associated with traumatic injury results from multiple independent but interplaying mechanisms, involving tissue trauma, shock, and inflammation. As such, the multifaceted derangement of hemostasis occurring after massive traumatic injuries, especially those involving the brain, is mainly sustained by release of procoagulants (fats, phospholipids) and constitutive tissue factor from the injured tissue into the circulation, associated with a systemic inflammatory response that also promotes tissue factor hyperexpression on monocytes and the other cells. The excessive, non-wound-related thrombin generation is insufficiently antagonized by physiological anticoagulant pathways and amplified by impaired endogenous fibrinolysis. The resulting burst of systemic thrombin generation, coupled with platelet hyperaggregability, shock, hypothermia, and tissue hypoperfusion, further contribute to the development of DIC and microvascular bleeding.
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PMID:Disseminated intravascular coagulation in trauma injuries. 2061 90


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