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

We investigated the effect of moderate whole body hypothermia (30 degrees C) on transient middle cerebral artery occlusion (MCAO) in the rat. Male Wistar rats were subjected to 2 h of ischemia by inserting a suture into the lumen of the internal carotid artery and occluding the origin of the MCA. Experimental groups were (a) MCAO induced at 37 degrees C body temperature (n = 15); (b) 30 degrees C body temperature induced prior to ischemia and maintained for 2 h of MCAO and 1 h of reperfusion (n = 12); and (c) MCAO with regional brain and body temperatures measured in normothermic (n = 3) and hypothermic MCAO rats (n = 2). Histopathological evaluation was performed 96 h after reperfusion. All normothermic MCAO animals exhibited ischemic infarct involving the ipsilateral cortex and basal ganglia with infiltration of neutrophils, macrophages, and microvascular proliferation. Hypothermic MCAO animals exhibited minor ischemic damage ranging from selective neuronal injury to small focal areas of infarct with minimal inflammatory response. Our data demonstrate that transient ischemia induced by using the intra-arterial suture method to occlude the MCA results in a reproducible brain lesion and that moderate hypothermia has a profound protective effect on the brain injury after transient MCAO.
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PMID:The effect of hypothermia on transient middle cerebral artery occlusion in the rat. 161 41

Transcranial Doppler sonography (TCD) was used to determine the mean blood flow velocity of the middle cerebral artery (Vm-MCA) and pulsatility (systolic/diastolic flow velocity = S/D) in 25 patients undergoing aortocoronary bypass grafting before, during, and after extracorporeal circulation (ECC). Preoperatively, none of the patients had signs or symptoms of cerebrovascular disease. ECC was performed with 2.4 l/min per m2 under mild hypothermia (34 degrees C) using membrane oxygenators. After 20 min of nonpulsatile perfusion, ECC was switched to the pulsatile mode for 20 min. Nonpulsatile perfusion was applied for the remaining ECC period. Vm-MCA, S/D, mean arterial blood pressure (MABP), and nasopharyngeal temperature (T.np) were recorded continuously throughout the operation. Hematocrit and paCO2 were determined before, during, and after ECC. Following hemodilution after the introduction of ECC, Vm-MCA was significantly increased compared with the baseline values before ECC. With hematocrit and paCO2 varying insignificantly during ECC, the onset of pulsatile ECC decreased Vm-MCA and MABP simultaneously. After the re-establishment of nonpulsatile ECC, both Vm-MCA and MABP increased again. However, a linear relationship between the two variables could not be documented statistically. During pulsatile ECC, pulsatility (S/D) of the obtained TCD wave forms did not reach baseline values. In 4 cases, TCD showed cessation of diastolic blood flow velocity after induction of ECC or onset of pulsatile ECC. An increase in MABP or changes in ECC regimen promptly restored diastolic TCD signals in these cases. Our results support the concept of increased cerebral blood flow under mild hypothermic ECC. Compared with the nonpulsatile perfusion mode, we found Vm-MCA reduced during pulsatile ECC.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Transcranial Doppler sonography during pulsatile and non-pulsatile extracorporeal circulation]. 218 73

The purpose of this study was to develop a primate model for assessing EEG, behavior and histology, and to test the effect of NMDA receptor blockade in transient focal ischemia. Squirrel monkeys (Saimiri sciureus) under halothane anesthesia were subjected to 110 min of transient focal ischemia (n = 15) by temporary clip occlusion of the MCA. An eight-lead EEG was recorded. Neurobehavioral testing was done in a subgroup of animals (n = 6). Brain temperature (37.5 degrees C) was monitored and controlled to avoid hypothermia or intergroup temperature differences, and blood pressure was regulated to 60 mmHg. The entire brain was subserially sectioned, and 52 standardized coronal sections encompassing the infarct were examined histologically 2 wk after the ischemia. Animals were randomized to receive either (+)-5-methyl-10,11-dihydro-5H-dibenzo[a,d]cyclohepten-5,10-imine (MK-801) 1 mg/kg of maleate salt or carrier solution, 20 min and again at 12 h after the onset of ischemia. Cingulate and retrosplenial cortex were examined for NMDA-antagonist-induced neuronal necrosis. No reduction, or trend toward reduction of neurobehavioral deficit was seen with MK-801. MCA occulsion reduced EEG power over the ischemic hemisphere. MK-801 appeared to cause brain activation, and globally increased power at several frequencies. MK-801 did not reduce infarction in either neocortex (p > 0.05) or striatum (p > 0.05). No selective neuronal necrosis was seen in the cingulate or retrosplenial cortex. We conclude that MK-801 given 20 min after the onset of transient ischemia offers no significant neuroprotective effect against either neurobehavioral deficit or ischemic infarction in this model of transient focal ischemia. Further experiments in unanesthetized animals are necessary to determine if MK-801-induced necrosis exists in the gyrencephalic brain, but the enhancement of primate brain electrical activity by MK-801 suggests that brain activation occurs in primates as it does in rodents.
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PMID:Postischemic therapy with MK-801 (dizocilpine) in a primate model of transient focal brain ischemia. 897 96

To test the hypothesis that presence of metalloproteases (MMPs), their inhibitors (TIMPs) and their substrate laminin-5 differs between the ischemic core and the surrounding tissue, we examined the impact of middle cerebral artery occlusion/reperfusion (MCA:O/R) on these molecules in different regions of the infarct. We also investigated the influence of hypothermia on the progression of the ischemic lesion and MMP activity. Brain sections from 64 Wistar rats subjected to MCA:O/R were examined by means of cytohistochemistry and zymography. The artery was occluded for 2 h followed by 3, 5, 8 and 12 h of reperfusion. Well characterized antibodies against laminin-5, MMPs and TIMP-2 were used. A total of 32 rats were treated with hypothermia. The presence of each antigen was related to the following regions of interest: ischemic core with BBB breakdown (I(c)), surrounding ischemic tissue without BBB breakdown (I(r)), and the contralateral non-ischemic region (N). Regions of interest were defined by MRI. The I(c) increased over time at the cost of the I(r). BBB breakdown occurred early in the ischemic core and increased over time. Hypothermia reduced the BBB breakdown at all time points. A graded decreased presence of laminin-5 was observed with 16.5+/-3.7(N)>10+/-2.8(I(r))>4+/-1.4(I(c)) immunopositive microvessels/mm(2) at 3 h of reperfusion. MMP-9 showed a reverse pattern with 0 (N)<4+/-0.8(I(r))<10+/-1.5(I(c)) immunopositive microvessels/mm(2). Hypothermia decreased the MMP activity measured by zymography. Laminin-5 and MMP presence relate directly to the degree of postischemic injury. Hypothermia reduces the conversion from the I(r) to ischemic core and the degree of BBB as well as MMP abundance.
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PMID:Topographically graded postischemic presence of metalloproteinases is inhibited by hypothermia. 1293 40

Hypothermic protection was compared in Long-Evans and spontaneously hypertensive rat (SHR) strains using transient focal ischemia, and in Wistar and SHR strains using permanent focal ischemia. Focal ischemia was produced by distal surgical occlusion of the middle cerebral artery and tandem occlusion of the ipsilateral common carotid artery (MCA/CCAO). Moderate hypothermia of 2 hours' duration was produced by systemic cooling to 32 degrees C, with further cooling of the brain achieved by reducing to 30 degrees C the temperature of the saline drip superfusing the exposed occlusion site. Infarct volume was determined from serial hematoxylin and eosin-stained frozen sections obtained routinely at 24 hours, or in some cases after 3 days' survival. In the SHR, moderate hypothermia was only effective when initiated before recirculation after a 90-minute occlusion period. In contrast, the same intervention was strikingly effective in the Long-Evans rat even when initiated after as long as 30-minute reperfusion after a 3-hour occlusion. This magnitude and duration of cooling was not protective in permanent MCA/CCAO in the SHR, but such transient hypothermia did effectively reduce infarct volume after permanent occlusions in Wistar rats. These results show striking differences in the temporal window for hypothermic protection among rat focal ischemia models. As expected, "reperfusion injury" in the Long-Evans strain is particularly responsive to delayed cooling. The finding that the SHR can be protected by hypothermia initiated immediately before recirculation suggests a rapidly evolving component of injury occurs subsequent to reperfusion in this model as well. Hypothermic protection after permanent occlusion in Wistar rats identifies a transient, temperature-sensitive phase of infarct evolution that is not evident in the unreperfused SHR. These observations confirm that distinct mechanisms can underlie the temporal progression of injury in rat stroke models, and emphasize the critical importance of considering model and strain differences in extrapolating results of hypothermic protection studies in animals to the design of interventions in clinical stroke.
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PMID:Hypothermic protection in rat focal ischemia models: strain differences and relevance to "reperfusion injury". 1468 15

Edaravone, a novel free radical scavenger, has been reported to reduce ischemic damage in rats subjected to transient focal ischemia. The aim of this study is, therefore, to investigate the effect of a combined therapy with edaravone and mild hypothermia of 35 degrees C. Sprague-Dawley rats were subjected to MCA occluding an intraluminal suture technique for 2 hrs. The rats were reperfused for 24 h and decapitated for infarct and edema analysis. Animals were randomly devided into four groups: (I) vehicle + normothermia (control) (II) vehicle + mild hypothermia (III) Edaravone + normothermia (IV) Edaravone + mild hypothermia. Mild hypothermia alone had no reduction of the brain damage. The edaravone alone significantly reduced edema volume. The combined treatment with edaravone and mild hypothermia reduced both infarct and edema volume. In addition, this treatment provided for the best functional outcome. These results demonstrate that free radical scavenger, edaravone attenuates brain edema and that the combined therapy with edaravone and mild hypothermia significantly reduces not only edema but also infarct on transient focal cerebral ischemia in rats. The neuroprotective effects seen in this study may be due to the combined interaction of antiedema activity between edaravone and mild hypothermia, suppressing free radical production.
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PMID:The neuroprotective effect of a free radical scavenger and mild hypothermia following transient focal ischemia in rats. 1475 35

Acute stroke is the third most common cause of death and also the most common cause of permanent disability in industrialized countries. Ischemic stroke is caused by occlusion of a cerebral artery leading to a critical reduction in brain perfusion in the respective brain area (penumbra). Most acute stroke treatment strategies are based on the penumbra concept: attaining rapid and persistent reperfusion is followed by the protection of critically ischemic and not yet infarcted (penumbral) tissue by, e.g., neuroprotection. Examination of the acute stroke patient includes a brief history, neurostatus and imaging (CT or MRI) for the exclusion of intracerebral hemorrhage. The diagnostic standard is CT; modern stroke MRI protocols provide an improved selection in later time windows. Intravenous thrombolysis with rt-PA within 3 h of symptom onset is the only approved therapy with a proven significant benefit for the patient. The effect is smaller but still significant if treatment occurs up to 4.5 h, and may still be present in MRI selected patients up to 9 h. More aggressive forms of therapy include interventional reperfusion techniques and therapy of malignant MCA infarction such as hemicraniectomy and hypothermia, which at present, however, are not routine and are only performed in specialized centers.
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PMID:[Acute cerebral circulation problems]. 1597 Oct 52

Cerebral aneurysms are treated by two methods: direct microsurgical clipping and endovascular coiling. Both are selected based on definite guidelines for clinicoradiological criteria as follows: Endovascular therapy comprising of GDC embolization, CSF wash-out with UK or TP A were performed in cases with Hunt and Kosnik grade 4 (GCS 7, 8), and grade 5 (without hydrocephalus or intracranial hemorrhage), age>70 years, subacute stage (4--14 days of vasospasm), basilar aneurysm and peripheral MCA/PCA aneurysms. Microsurgical clipping with a drainage procedure was performed in cases with Hunt and Kosnik grades 0--3, grade 4 (GCS 9--12), age less than 70 years, grade 5 with hydrocephalus or intracerebral hematoma and acute stage (0--3 days after bleed). The patient's outcome was measured using GOS (Glasgow outcome score) at the time of discharge. In our series of severe (poor grade) SAH cases, 120 cases underwent clipping and 59 cases underwent coiling. Although they accounted for 37.8 % and 48 % of total SAH cases, respectively, the outcome was satisfactory. Good recovery and moderate disability, together termed "favorable outcome" was found in 69.16 % of clipping cases and 44.06 % of coiling cases. Clipping had a better outcome than coiling in cases of acute severe SAH in our series. The golden hour resuscitation, pre-hospital care and the adjunctive treatment strategies like hypothermia are discussed. A critical appraisal of the ISAT of microsurgical clipping versus coiling is used for comparison of our results.
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PMID:The effect of clipping and coiling in acute severe subarachnoid hemorrhage after international subarachnoid aneurysmal trial (ISAT) results. 1617 68

Both mild hypothermia (MH) and decompressive craniectomy (CE) have been shown to have neuroprotective effects in brain ischemia. We investigated a possible effect of MH and a combination of CE and MH (CE + MH) on the changes of infarction size, DNA fragmentation, and immunoreactivities for Bcl-2 and Bax after 24 h of permanent middle cerebral artery occlusion (MCAO) in rats. For the estimation of ischemic brain injury, we calculated the infarct size of the MCA region at 24 h after the MCAO. Terminal deoxynucleotidyl transferase-mediated dUTP-biotin in situ nick labeling (TUNEL) staining was performed for the detection of DNA fragmentation. Immunoreactivities for Bcl-2 and Bax were stained. Infarction size after permanent MCAO was significantly reduced by CE+MH treatment (P < 0.01). Infarction size did not change significantly by application of MH alone (P > 0.05). TUNEL staining was remarkably reduced both in MH-treated animals and in CE + MH-treated animals. Immunoreactivity for Bcl-2 was greatly induced both in MH-treated animals and in CE + MH-treated animals. Induction of immunoreactivity for Bcl-2 was obviously inhibited both in MH-treated animals and in CE + MH-treated animals. It suggests that temporary MH delays infarct evolution and ameliorates neuron apoptosis but does not significantly reduce definite infarction size. CE + MH not only ameliorates neuron apoptosis but also remarkably reduces infarction size.
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PMID:Decompressive craniectomy and mild hypothermia reduces infarction size and counterregulates Bax and Bcl-2 expression after permanent focal ischemia in rats. 1640 75

Massive unilateral hemispheric infarction often develops progressive postischemic edema that leads to a malignant course of stroke with mortality of up to 80% with conventional medical therapies. Hypothermia and decompressive hemicraniectomy have shown neuroprotective effects in several animal models of focal transient and permanent MCA occlusion by reducing infarct size and improving neurological outcome. Our aim in this paper was to review the possible mechanisms of both therapies as well as the optimal time window and duration of application of each treatment in animal model and in human malignant MCA infarction reported in the literature.
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PMID:Neuroprotection in malignant MCA infarction. 1665 20


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