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

Since hypothermia may be a potential treatment for perinatal cerebral hypoxic-ischemic injury, we used an established neonatal model of hypoxia-ischemia to determine the time after injury at which cooling had the best protective effect. Fourteen-day-old Wistar rats were subjected to right carotid artery ligation and hypoxia (8% O(2) for 90 min). Immediately at the end of hypoxia (defined as 0h), animals were either maintained at normal body temperature until sacrifice (normothermia) or subjected to hypothermia. In a preliminary study, the effects of a reduction in temperature and the duration of such cooling were investigated; animals were cooled (until brain temperature reached 33 degrees C or 30 degrees C) for 2, 4, or 6 h commencing immediately after hypoxia. In a second study, animals were cooled (brain temperature 30 degrees C) for 6 h commencing at either 0, 2, 4, or 6 h after the end of hypoxia. Sham-operated animals were used as controls. Twenty-four hours after hypoxia-ischemia, cerebral energy metabolism was measured by phosphorus magnetic resonance spectroscopy, and at 5 d cerebral infarction was measured by planimetry. In normothermic animals the ratio of phosphocreatine/inorganic phosphate (PCr/Pi) had fallen markedly 24 h following hypoxia-ischemia. In contrast, animals cooled between 6 and 12 h displayed high PCr/Pi ratios similar to those in control animals. Similarly, after 5 d, infarct area was significantly reduced only in animals cooled between 6 and 12 h after injury. These results indicate that cooling between 6 and 12 h after hypoxia-ischemia is more effective in reducing cerebral injury than other cooling regimes and suggest that the physiologic events during this period are critical for understanding cerebral infarction.
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PMID:Improved neuroprotection with hypothermia delayed by 6 hours following cerebral hypoxia-ischemia in the 14-day-old rat. 1175 34

Hypothermia may be an ideal neuroprotective intervention in hypoxic-ischemic encephalopathy after perinatal asphyxia. The present study describes the long-term effects of prolonged resuscitative whole-body hypothermia initiated 2 h after hypoxic-ischemic injury on brain morphology and neuropsychological behavior in 7-d-old rats. After right common carotid artery ligation and exposure to hypoxia of 8% O(2) for 105 min, 10 animals were kept normothermic at 37 degrees C and 10 animals were cooled to 30 degrees C rectal temperature for 26 h, starting 2 h after the hypoxic-ischemic insult. All hypoxic-ischemic animals were gavage fed to guarantee long-term survival. Neuroprotection was evaluated by magnetic resonance imaging and behavioral testing. Hypothermia significantly reduced the final size of cerebral infarction by 23% at 6 wk after the insult. The most extended tissue rescue was found in the hippocampus (21%, p = 0.031), followed by the striatum (13%, p = 0.143) and the cortex (11%, p = 0.160). Cooling salvaged spatial memory deficits verified at 5 wk of recovery with Morris Water Maze test; whereas circling abnormalities after apomorphine injection and sensory motor dysfunctions on rotating treadmill improved, yet did not reach statistical significance. When compared with controls, hypoxic-ischemic animals performed worse in all behavioral tests. Hypothermia did not influence functional outcome in controls. Significant correlations between behavioral performance and corresponding regional brain volumes were found. We conclude that 26 h of mild to moderate resuscitative hypothermia leads not only to brain tissue rescue, but most important to long-lasting behavioral improvement throughout brain maturation despite severity of injury and delayed onset of cooling.
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PMID:Delayed postischemic hypothermia improves long-term behavioral outcome after cerebral hypoxia-ischemia in neonatal rats. 1186 42

It is unknown whether immediate early gene (IEG) induction and subsequent late gene regulation after ischemia is beneficial or deleterious. The aim of this study was to examine the effect of hypothermia on expression of c-Fos and c-Jun, and AP-1 DNA binding activity, after transient focal cerebral ischemia in rat brain, and clarify the role of IEGs and AP-1 after insults. Male Wistar rats underwent right middle cerebral artery occlusion for 1 h with the intraluminal suture method. During ischemia, animals were assigned to either normothermic (NT) or hypothermic (HT) groups. In the NT group, brain temperature was observed to spontaneously increase to 40 degrees C during ischemia. In the HT group, brain temperature decreased to 30 degrees C. Infarct volume in cortex was decreased in the HT group, compared with that in the NT group (P<0.001). Increased c-Fos immunoreactivity in the cortex was observed at 3 h after reperfusion in the HT, but not the NT group, while c-Jun expression was not affected by HT treatment. There was also a significant increase in AP-1 DNA binding activity at 3 h in the HT group when compared to the NT group (P<0.01). In conclusion, hypothermia decreased cerebral infarction in association with early increases in c-Fos expression and AP-1 DNA binding activity in peri-infarct cortex. It remains to be established whether such responses are a cause or consequence of cell survival, but these results clearly establish that altered transcription is a key feature of tissue spared following hypothermic focal ischemia.
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PMID:Effect of intra-ischemic hypothermia on the expression of c-Fos and c-Jun, and DNA binding activity of AP-1 after focal cerebral ischemia in rat brain. 1276 3

Stressful, preconditioning stimuli can elicit rapid and delayed forms of tolerance to ischemic injury. The identification and characterization of preconditioning stimuli that are effective, but relatively benign, could enhance the clinical applicability of induced tolerance. This study examines the efficacy of brief hypothermia as a preconditioning stimulus for inducing rapid tolerance. Rats were administered hypothermic preconditioning or sham preconditioning and after an interval of 20-120 min were subjected to transient focal ischemia using a three-vessel occlusion model. The volume of cerebral infarction was measured 24 h or 7 days after ischemia. In other experiments, the depth or duration of the hypothermic stimulus was manipulated, or a protein synthesis inhibitor (anisomycin) was administered. Twenty minutes of hypothermia delivered 20 or 60 (but not 120) min prior to ischemia significantly reduces cerebral infarction. The magnitude of protection is enhanced with deeper levels of hypothermia, but is not affected by increasing the duration of the hypothermic stimulus. Treatment with a protein synthesis inhibitor does not block the induction of rapid tolerance. Hypothermic preconditioning elicits a rapid form of tolerance to focal ischemic injury. Unlike delayed tolerance induced by hypothermia, rapid tolerance is not dependent on either de novo protein synthesis or the duration of the preconditioning stimulus. These findings suggest that the mechanisms underlying rapid and delayed tolerance induced by hypothermia differ fundamentally. Brief hypothermia could provide a rapid means of inducing transient tissue protection in the context of predictable ischemic events.
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PMID:Hypothermic preconditioning induces rapid tolerance to focal ischemic injury in the rat. 1278 1

The purposes of this review are to clarify the effect of hypothermia therapy on focal cerebral ischemia in rats, and to consider the relevancy of its application to human focal cerebral ischemia. Since 1990, 26 reports confirming the brain-protecting effect of hypothermia in rat focal cerebral ischemia models have been published. Seventy-four experimental groups in these 26 reports were classified as having transient middle cerebral arterial occlusion (MCAO) with mild hypothermia (group A; 43 groups), permanent MCAO with mild hypothermia (group B; 14 groups), permanent MCAO with deep hypothermia (group C; 8 groups) and transient or permanent MCAO with mild hyperthermia (group D; 9 groups). The results were evaluated as the % infarct volume change caused by hypothermia or hyperthermia compared with the infarct volume in normothermic animals. The effectiveness was confirmed in 36 (83%) of the 43 groups in group A, 10 (71%) of the 14 in group B, and six (75%) of the eight in group C. The infarct volume of eight of the nine groups in group D was markedly aggravated. The percent infarct volume change was 55.3% +/- 27.1% in group A, 57.6% +/- 24.7% in group B, 60.8% +/- 45.5% in group C, and 189.7% +/- 89.4% in group D. For effective reduction of the infarct volume, hypothermia should be started during ischemia or within 1 h, at latest, after the beginning of reperfusion in the rat transient MCAO model. However, it is not clear whether this neuroprotective effect of hypothermia can also be observed in the chronic stage, such as several months later. Keeping the body temperature normothermic in order to avoid mild hyperthermia seems to be rather important for not aggravating cerebral infarction. Clinical randomized studies on the efficacy of mild hypothermia for focal cerebral ischemia and sophisticated mild hypothermia therapy techniques are mandatory.
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PMID:Effect of mild hypothermia on focal cerebral ischemia. Review of experimental studies. 1286 92

This study evaluates the effectiveness and potential complications of stent-grafting for the treatment of distal arch aneurysms using profound hypothermia and circulatory arrest with retrograde cerebral perfusion. Between December 1998 and December 2001, 9 consecutive patients with a distal arch aneurysm (6 men and 3 women, mean age 71 years) underwent surgical repair using a stent-graft. Profound hypothermic circulatory arrest and retrograde cerebral perfusion were performed in all patients. Endovascular leakage was screened postoperatively using three-dimensional computerized tomography. The mean follow-up period was 27.4 months. Thirty day mortality was 0%. One patient died 3 months after stent-grafting due to proximal leakage into her aneurysm. The mean postoperative extubation period was 2.1 days. No patients suffered cerebral infarction or paraplegia. Although preliminary outcomes using this technique were good, endovascular leakage is a concern. We suggest that, if major proximal leakage is recognized postoperatively, re-intervention should be performed as soon as possible. Endovascular stent-grafting appears to be a good alternative treatment for distal arch aneurysms, although longer follow-up is necessary to more comprehensively evaluate this procedure.
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PMID:Surgical repair of a distal arch aneurysm with a stent-graft. 1468 Oct 95

Malignant cerebral infarction (MaCI) treated with mechanical ventilation, mannitol, or barbiturates has a mortality of about 80% and survivors show severe disability. When applied for 48 to 72 hours, moderate hypothermia seems to reduce the mortality rate of MaCI. However, even after 72 hours, cerebral edema is still present, and the patient's condition often worsens during rewarming. We here report, as a case series, our experience with the use of prolonged moderate hypothermia to treat patients with MaCI. Twelve MaCI patients 27 to 64 years of age were treated. All presented with middle cerebral artery occlusion and all but one with internal carotid artery occlusion. A cooling blanket was used to lower the patient's core temperature to 32 degrees C to 33 degrees C. Hypothermia was induced within 24 hours of infarction onset and was discontinued when the CT scan showed a subsiding mass effect and was followed by slow rewarming (2-5 days). Patients were mechanically ventilated while sedated with high doses of gamma-hydroxybutyrate, a naturally occurring metabolite of gamma-aminobutyric acid (GABA), which acts on the GABAB receptor. Seven patients survived for 6 months, and 6 were able to walk without assistance; the other 5 died due to early cerebral herniation (2) or progression of infarct size (3). The mean duration of hypothermia for the survivors was 19 days (range, 11-22 days). Side effects observed in all patients were systemic hypotension, thrombocytopenia, and hyperfibrinogenemia. Prolonged hypothermia with gamma-hydroxybutyrate can be used to treat MaCI patients, with a fairly good clinical outcome for survivors.
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PMID:Prolonged moderate hypothermia in massive hemispheric infarction: clinical experience. 1563 43

Perinatal brain injury in the term infant is a relatively uncommon event. The principal lesions are intracranial hemorrhage including subarachnoid, subdural, intraparenchymal, intraventricular, focal cerebral infarction and hypoxic ischemic cerebral injury secondary to intrapartum hypoxia-ischemia. Both intracranial hemorrhage and focal cerebral infarction are invariably identified at the time of clinical symptoms, ie, seizures or apnea. This clearly limits the potential for prevention. The mechanisms contributing to brain injury secondary to intrapartum hypoxia-ischemia have become more clearly defined. Secondary or reperfusion injury is potentially amenable to neuroprotective strategies. Modest hypothermia is one such therapy that has been studied in high-risk newborn infants with some initial success. Future studies need to focus on additional neuroprotective strategies.
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PMID:Brain injury in the term infant. 1569 98

To protect the spinal cord during thoracoabdominal aortic aneurysm repair, motor evoked potentials (MEP) monitoring and cerebrospinal fluid drainage are often employed. Herein, we report a case, where intraoperative diminishment of motor evoked potentials was accompanied by multiple cerebral infarction. A 63-year-old man underwent elective surgery for both thoracoabdominal aortic aneurysm and abdominal aortic aneurysm. He had a past history of cerebral infarction, resulting in Wernicke aphasia but no paralysis. Preoperative magnetic resonance angiography and echocardiography revealed occlusion of the intercostal and lumbar arteries, mild aortic regurgitation, and atherosclerotic lesions at the aortic arch as well as descending aorta. Anesthesia and muscular relaxation were maintained with fentanyl, propofol, and continuous administration of vecuronium at 0.5 mg x kg(-1) x h(-1). The thoracoabdominal aortic aneurysm was repaired under distal aortic perfusion with femorofemoral bypass. After terminating the bypass, we found that the MEP at the lower limb had disappeared. Although we reconstructed intercostal arteries under mild hypothermia and partial bypass, the amplitude of MEP remained very low. Suspecting spinal cord ischemia, we performed cerebrospinal fluid drainage immediately after the operation. On the postoperative day 4, when we stopped the cerebrospinal fluid drainage and propofol administration, his level of consciousness was poor and brain CT revealed multiple cerebral infarction. On the postoperative day 30, he was discharged from an intensive care unit with complications of hemiplagia and paraplegia. Although cerebrospinal fluid drainage may be recommended to protect spinal cord during thoracoabdominal aortic aneurysm repair, we should consider performing brain CT to exclude a risk of brain herniation secondary to cerebrospinal fluid drainage if there is a possibility of cerebral incidents.
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PMID:[A case report of a patient who developed hemiparaplegia with multiple cerebral infarction during thoracoabdominal aortic aneurysm repair]. 1574 19

Hypothermia has been demonstrated to protect the brain from ischemia or traumatic brain injury. Achieving profound hypothermia has relied on techniques requiring total body cooling, which may result in serious cardiovascular and pulmonary complications. A technique to selectively cool the brain could conceivably exert a marked protection on cerebral structures and provide a relatively bloodless operative surgical field without systemic complications. Accordingly, this approach was tried in 7 rhesus monkeys after induction of general anesthesia. The right internal carotid artery and both internal jugular veins were each occlusively cannulated and connected to a circulation pump. The left internal carotid artery, both external carotid arteries, and both external jugular veins were temporarily clamped to establish severe cerebral ischemia. Using a closed-circuit system, cooled Ringer's lactate liquid (4 degrees C) was infused through right internal carotid artery with outflow draining though both internal jugular veins. Cooled perfusate decreased cerebral temperature to the target temperature of 15 degrees C. Thereafter, pump flow was discontinued, and brains were rewarmed spontaneously, while the temporarily clamped carotid arteries and jugular veins were opened to resume normal cerebral blood circulation. Neurological functions were recorded daily and cerebral histology was examined at the conclusion of the experiment. Magnetic resonance (MR) scans were routinely taken before and 3 weeks after ischemia. In the normothermia control group of five rhesus monkeys, Ringer's solution at 37 degrees C was infused in the same manner as the cold solution with cerebral temperature maintained at 36.7 +/- 0.32 degrees C. Right cerebral temperature decreased from 36.5 +/- 0.49 to 15.5 +/- 2.29 degrees C, and simultaneously the left cerebral temperature decreased from 36.4 +/- 0.38 to 16.3 +/- 2.4 degrees C for 62.8 +/- 9.76 min during selective cerebral cooled Ringer's liquid perfusion. In contrast, rectal temperature was only reduced to 32.4 +/- 0.96 degrees C from a baseline of 37.2 +/- 0.76 degrees C. Internal jugular vein hematocrit was 38.2 +/- 0.31% before perfusion and 2.82 +/- 0.46% at the end of perfusion in profound hypothermia group; hematocrit was 39.7 +/- 0.62% before perfusion and 3.42 +/- 0.38% at the end of perfusion in the normothermia group. In the hypothermic group, neurological functions were normal during 6 months of follow-up, and microscopic examination of brain tissue did not show evidence of pathological changes in hippocampus or medulla. MR scans did not show any cerebral infarction. In contrast, none of the monkeys in normothermia group survived for more than several hours, and microscopic examination of the brain revealed extensive neuronal necrosis within the medulla. Selective cerebral profound hypothermia provides significant histologic and neurologic protection after severe cerebral ischemia. In addition, there were no major complications, and the operative field remained relatively bloodless in the profound hypothermic group.
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PMID:Marked protection by selective cerebral profound hypothermia after complete cerebral ischemia in primates. 1718 93


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