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

Hypothermia frequently accompanies cardiopulmonary bypass (CPB) and myocardial protection strategies during cardiac surgery. With CPB, the blood/artificial surface interface activates components of the humoral and cellular inflammatory cascades and may contribute to postoperative end organ dysfunction including the heart or multiple other organ systems. The endothelial cell (EC) monolayer normally mediates components of solute transport, vasomotor function, coagulation, cell differentiation/growth, and immune/inflammatory processes. E-selectin is a vascular adhesion molecule that mediates neutrophil adherence and that is inducible in ECs by inflammatory mediators such as cytokines. Tissue factor (TF) is similarly an inducible procoagulant factor in ECs that contributes to thrombosis. The induction, transcription, and expression of both molecules were studied in cultured human umbilical vein cells at normothermic (37 degrees), hypothermic (25 degrees), and rewarmed (37 degrees) conditions after stimulation with the cytokines tumor necrosis factor alpha and interleukin-1. Hypothermia reversibly inhibits the transcription and expression but not the induction of both E-selectin and TF.
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PMID:Hypothermia reversibly inhibits endothelial cell expression of E-selectin and tissue factor. 757 38

Mild hypothermia reduces secondary damage after traumatic brain injury (TBI) in rodent models; however, the mechanisms involved in this beneficial effect remain unclear. We previously reported that TBI induces the upregulation of adhesion molecules and infiltration of neutrophils (PMN) in brain. Since PMN accumulation may be associated with the development of hyperemia and blood-brain barrier injury, we hypothesized that hypothermia would reduce acute inflammation after TBI in rats. To test this hypothesis, rats were anesthetized and subjected to TBI by controlled cortical impact to left parietal cortex. Brain temperature was controlled at 32 degrees C, 37 degrees C, or 39 degrees C (n = 8 per group) for 4 h after TBI, then rats were sacrificed and brain were harvested. Immunohistochemistries were performed on brain sections using antibodies that recognize the adhesion molecules E-selectin and intercellular adhesion molecule-1 (ICAM-1), and PMN. PMN were also quantified using a myeloperoxidase (MPO) assay. PMN accumulation in injured brain was decreased in rats maintained at 32 degrees C vs 39 degrees C (4-fold by immunohistochemistry and 8-fold by MPO, p < 0.05). E-selectin was induced after TBI, but not attenuated by hypothermia. ICAM-1 was not up-regulated at this early time after TBI. Based on these preliminary data, we conclude that mild hypothermia reduces PMN accumulation in injured brain during the initial 4 h after TBI, without decreasing adhesion molecule expression.
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PMID:The relationship between brain temperature and neutrophil accumulation after traumatic brain injury in rats. 941 40

Mild hypothermia is an established neuroprotectant against cerebral ischemic injury. Studies have shown that inflammation potentiates cerebral ischemic injury, particularly in the setting of reperfusion. To further elucidate the mechanism by which mild hypothermia attenuates the inflammatory response, we assessed endothelial intercellular adhesion molecule-1 (ICAM-1) expression, neutrophil and monocyte infiltration, and microglial activation following 2 h of transient focal cerebral ischemia under normothermic and mildly hypothermic conditions. Ischemia was induced using the intraluminal suture method in Sprague-Dawley rats. Immunohistochemistry was used to detect endothelial ICAM-1, infiltrating neutrophils and monocytes, and microglia at 1, 3, and 7 days post-ischemia. Immunopositive cell and vessel densities were measured in the peri-infarct region. Mild hypothermia was associated with decreased neutrophils at 1 and 3 days post-ischemia, decreased ICAM-1-positive vessels at 1, 3, and 7 days, and decreased monocytes/activated microglia at 3 and 7 days, but not at 1 day. These data demonstrate that mild hypothermia significantly reduces endothelial adhesion molecule expression, acute (neutrophil) and subacute (monocyte) leukocyte infiltration, and microglial activation up to 7 days following insult in a rodent model of transient focal cerebral ischemia.
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PMID:Mild hypothermia reduces ICAM-1 expression, neutrophil infiltration and microglia/monocyte accumulation following experimental stroke. 1237 61

The relative role of different adhesion molecules in the ischemia-reperfusion injury after cardioplegic arrest in the clinical setting is unknown, because of protective effects of cardioplegia and hypothermia. The aim of this study is to determine the relationship between the method of the cardioplegia and endothelial derived soluble adhesion molecules; soluble vascular adhesion molecule-1 (sVCAM-1) and soluble intercellular adhesion molecule-1 (sICAM-1) in myocardial ischemia- reperfusion injury. Fourteen male patients who underwent aortocoronary bypass surgery with cardiopulmonary bypass were included in this study. They were randomised to be given blood or crystalloid cardioplegia for myocardial protection. Group I (n=7) received blood cardioplegia and group II (n=7) received crystalloid cardioplegia. The cross-clamp times were not significantly different between the two groups, 49.4+/-4.6 min for group I and 54.8+/-2.5 min for group II. Mean age of patients was 58+/-2.1 years for group I and 54+/-2.6 years for group II. Blood samples were taken from both the aorta and coronary sinuses of all patients before cross-clamp, after cross-clamping and at 30th min of reperfusion. Plasma were obtained from blood samples and then stored at -70 degrees C. sVCAM-1 and sICAM-1 levels were measured by ELISA in the samples. There were no significant differences in the levels of sICAM-1 and sVCAM-1 at the beginning of reperfusion and at 30th min of reperfusion in coronary sinus of group I patients. But, increased sICAM-1 and sVCAM-1 levels were observed at 30th min of reperfusion in blood taken from coronary sinuses of group II patients compared with beginning of reperfusion (respectively p=0.01, p=0.03). In conclusion, these results have shown that ischemia-reperfusion injury is more likely to occur in patients protected by crystalloid cardioplegia, and suggest that blood cardioplegia may be preferred especially in borderline myocardial functioned patients.
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PMID:The relationship between the method of cardioplegia and vascular endothelial cell derived soluble adhesion molecules in myocardial ischemia-reperfusion injury. 1266 54

The neuroprotective effect of hypothermia has long been recognized. Use of hypothermia for stroke therapy, which is currently being induced by whole body surface cooling, has been largely limited because of management problems and severe side effects (i.e., pneumonia). Our recent studies have demonstrated the significant therapeutic value of local brain cooling in the ischemic territory prior to reperfusion in stroke. The goal of this study was to determine if cerebral local cooling infusion could reduce stroke-mediated brain injury by inhibiting inflammatory responses. A hollow filament was used to block the middle cerebral artery (MCA) for 3 hours, and then to locally infuse the ischemic territory with 6 ml cold saline (20 degrees C) for 10 min prior to 48-h reperfusion. This cold saline infusion significantly ( P<0.01) reduced temperature of the MCA supplied territory (in cerebral cortex from 37.2+/-0.1 degrees C to 33.4+/-0.4 degrees C, in striatum from 37.5+/-0.2 degrees C to 33.9+/-0.4 degrees C), with the hypothermia remaining for at least 45 min after reperfusion. Consequently, significant ( P<0.01) reductions in endothelial expression of intracellular adhesion molecule-1 (ICAM-1), the key step for inflammatory progress, as well as leukocyte infiltration, were evident in both cortex and striatum after reperfusion. As a control, ischemic rats received the same amount of cold saline systemically through a femoral artery. A mild hypothermia was induced in the cerebral cortex (35.3+/-0.2 degrees C) but not in the striatum (36.8+/-0.2 degrees C). The reduced cortical temperature returned to normal within 5 min. Brain temperature in ischemic rats perfused locally with saline at 37 degrees C remained normal. Intensive expression of ICAM-1 and accumulation of leukocytes was observed in ischemic control groups without brain cooling infusion. In conclusion, brain hypothermia induced by local pre-reperfusion infusion ameliorated brain inflammation from stroke.
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PMID:Regional brain cooling induced by vascular saline infusion into ischemic territory reduces brain inflammation in stroke. 1469 33

Contributions from the neurosciences to Critical Care in 2011 covered an array of topics. We learned about potential biomarkers for, and the effect of cerebral oxygen metabolism on, delirium, in addition to treatment of the latter. A group of investigators studied surface cooling in healthy awake volunteers, and incidence of infection associated with therapeutic hypothermia. The effects of statin and erythropoietin on stroke were revisited, and the role of adhesion molecule in the inflammatory reaction accompanying intracerebral hemorrhage was scrutinized. Biomarkers in subarachnoid hemorrhage and their relationship to vasospasm and outcome, and effect of daylight on outcome in this patient population, as well as a new meta-analysis of statin therapy were among the research in subarachnoid hemorrhage. Moreover, 2011 witnessed the publication of a multidisciplinary consensus conference's recommendations on the critical care management of subarachnoid hemorrhage. Results of studies regarding the diagnosis and vascular complications of meningitis were reported. Traumatic brain injury received its share of articles addressing therapy with hypertonic saline and surgical decompression, the development of coagulopathy, and biomarkers to help with prognostication. Finally, research on the treatment of Guillain-Barre syndrome in children, prediction of long-term need of ventilatory support, and pathophysiology of critical illness polyneuropathy and myopathy were reported.
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PMID:Year in review 2011: Critical Care--Neurocritical care. 2325 71